Nutrient chapter

Allicin

Diallyl thiosulfinate formed after garlic tissue damage. Thiol reactions, protein modification, redox repair, sensory channels, nutrient interactions and exposure limits; garlic preparations and polysulfides retain separate experimental identities.

125 recorded mechanisms · 4 availability situations · 1 preserved sources. Source recording and scientific verification are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Garlic alliinase is a PLP-dependent plant enzyme; its structural cofactor requirement is not a human B6 supplementation experiment.
PLP → Allium sativum alliin lyase / alliinase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Purified Allium sativum enzyme; X-ray structural study.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Garlic alliinase is a PLP-dependent plant enzyme; its structural cofactor requirement is not a human B6 supplementation experiment.
primary_references
The active principle of garlic at atomic resolution. | 2002 | DOI 10.1074/jbc.m208669200 | PMID 12235163 | https://pubmed.ncbi.nlm.nih.gov/12235163/ | https://doi.org/10.1074/jbc.m208669200
source_locator
Reviewed reference lines 11-11; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 11–11
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified Allium sativum enzyme; X-ray structural study. · Recorded from source · Recorded from source
**Alliinase and vitamin B6.** Garlic alliinase is a plant pyridoxal-5′-phosphate (PLP)-dependent enzyme, not a human enzyme. Structural studies resolved its cofactor-containing active site, an apo form, and a PLP-bound aminoacrylate intermediate. Alliin cleavage produces allylsulfenic acid and an aminoacrylate intermediate; the latter yields pyruvate and ammonia. Two allylsulfenic acid molecules condense to allicin with water loss. This links allicin formation to B6 chemistry in the plant. It does not show that taking B6 increases allicin production in a person. [Kuettner 2002](https://pubmed.ncbi.nlm.nih.gov/12235163/) [Shimon 2007](https://pubmed.ncbi.nlm.nih.gov/17174334/)
Complete structured claim and evidence
PLP-dependent garlic alliinase cleaves alliin to the sulfenic-acid precursor; aminoacrylate formation leads to pyruvate and ammonia.
Alliin / (+S)-S-allyl-L-cysteine sulfoxide → Allylsulfenic acid Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Plant enzyme and structural intermediate; biochemical reaction.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
PLP-dependent garlic alliinase cleaves alliin to the sulfenic-acid precursor; aminoacrylate formation leads to pyruvate and ammonia.
primary_references
Two structures of alliinase from Alliium sativum L.: apo form and ternary complex with aminoacrylate reaction intermediate covalently bound to the PLP cofactor. | 2007 | DOI 10.1016/j.jmb.2006.11.041 | PMID 17174334 | https://pubmed.ncbi.nlm.nih.gov/17174334/ | https://doi.org/10.1016/j.jmb.2006.11.041
source_locator
Reviewed reference lines 11-11; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 11–11
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Plant enzyme and structural intermediate; biochemical reaction. · Recorded from source · Recorded from source
**Alliinase and vitamin B6.** Garlic alliinase is a plant pyridoxal-5′-phosphate (PLP)-dependent enzyme, not a human enzyme. Structural studies resolved its cofactor-containing active site, an apo form, and a PLP-bound aminoacrylate intermediate. Alliin cleavage produces allylsulfenic acid and an aminoacrylate intermediate; the latter yields pyruvate and ammonia. Two allylsulfenic acid molecules condense to allicin with water loss. This links allicin formation to B6 chemistry in the plant. It does not show that taking B6 increases allicin production in a person. [Kuettner 2002](https://pubmed.ncbi.nlm.nih.gov/12235163/) [Shimon 2007](https://pubmed.ncbi.nlm.nih.gov/17174334/)
Complete structured claim and evidence
Two allylsulfenic-acid molecules condense to allicin with water loss.
Allylsulfenic acid → Allicin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Garlic sulfur chemistry; spontaneous condensation follows the enzymatic cleavage.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Two allylsulfenic-acid molecules condense to allicin with water loss.
primary_references
Two structures of alliinase from Alliium sativum L.: apo form and ternary complex with aminoacrylate reaction intermediate covalently bound to the PLP cofactor. | 2007 | DOI 10.1016/j.jmb.2006.11.041 | PMID 17174334 | https://pubmed.ncbi.nlm.nih.gov/17174334/ | https://doi.org/10.1016/j.jmb.2006.11.041
source_locator
Reviewed reference lines 11-11; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 11–11
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Garlic sulfur chemistry; spontaneous condensation follows the enzymatic cleavage. · Recorded from source · Recorded from source
**Alliinase and vitamin B6.** Garlic alliinase is a plant pyridoxal-5′-phosphate (PLP)-dependent enzyme, not a human enzyme. Structural studies resolved its cofactor-containing active site, an apo form, and a PLP-bound aminoacrylate intermediate. Alliin cleavage produces allylsulfenic acid and an aminoacrylate intermediate; the latter yields pyruvate and ammonia. Two allylsulfenic acid molecules condense to allicin with water loss. This links allicin formation to B6 chemistry in the plant. It does not show that taking B6 increases allicin production in a person. [Kuettner 2002](https://pubmed.ncbi.nlm.nih.gov/12235163/) [Shimon 2007](https://pubmed.ncbi.nlm.nih.gov/17174334/)
Complete structured claim and evidence
Alliinase localization to garlic bundle-sheath cells qualifies where precursor-enzyme mixing occurs after tissue damage.
Allium sativum alliin lyase / alliinase → Alliin / (+S)-S-allyl-L-cysteine sulfoxide Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Publisher abstract read through web tool; anatomical localization, not independent full-section microscopy reanalysis.
experimental_model
Garlic-clove anatomical staining; primary publisher abstract.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Spatial localization, not a causal inhibition or universal intracellular arrangement. Precursor is contextual; no human enzyme is implied.
plain_language
Alliinase localization to garlic bundle-sheath cells qualifies where precursor-enzyme mixing occurs after tissue damage.
primary_references
Alliin lyase localization in bundle sheaths of the garlic clove (Allium sativum) | 1994 | DOI 10.1002/j.1537-2197.1994.tb15413.x | https://bsapubs.onlinelibrary.wiley.com/doi/abs/10.1002/j.1537-2197.1994.tb15413.x
source_locator
Reviewed reference lines 13-13; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 13–13
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Garlic-clove anatomical staining; primary publisher abstract. · Recorded from source · Recorded from source
**Plant anatomy.** Alliinase was strongly localized to garlic-clove bundle-sheath cells, particularly around phloem, with little detected in storage mesophyll away from vascular bundles. Tissue disruption permits precursor–enzyme contact, but a uniform arrangement in every garlic cell is an oversimplification. Intact garlic still contains active metabolism and other constituents. [Ellmore and Feldberg 1994](https://bsapubs.onlinelibrary.wiley.com/doi/abs/10.1002/j.1537-2197.1994.tb15413.x)
Complete structured claim and evidence
Allicin transformation and garlic processing involve chemically distinct e-ajoene; this provenance does not transfer the product's effects to allicin.
Allicin → E-Ajoene Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Chemical preparation/transformation scope; media determine product mixture.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
DADS/DATS and ajoene remain distinct. This qualitative preparation relationship does not establish human metabolic yield or tissue exposure.
plain_language
Allicin transformation and garlic processing involve chemically distinct e-ajoene; this provenance does not transfer the product's effects to allicin.
primary_references
Products of Allicin Transformation: Ajoenes and Dithiins, Characterization and their Determination by HPLC*. | 1990 | DOI 10.1055/s-2006-960926 | PMID 17221396 | https://pubmed.ncbi.nlm.nih.gov/17221396/ | https://doi.org/10.1055/s-2006-960926
source_locator
Reviewed reference lines 15-15; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 15–15
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical preparation/transformation scope; media determine product mixture. · Recorded from source · Recorded from source
**Distinct sulfur compounds.** Alliin, allicin, diallyl disulfide (DADS), diallyl trisulfide (DATS), E-ajoene, Z-ajoene, and the two vinyldithiin isomers require separate records. Preparation conditions influence the transformation products and ajoene isomer ratio. S-allylcysteine (SAC) has a thioether linkage; S-allylmercaptocysteine (SAMC) is a mixed disulfide. SAMC can arise by reaction with cysteine, whereas SAC is not another name for allicin. Food processing products, biological reaction products, and metabolites should not be collapsed into one chemical family that inherits every member's effects. [Iberl 1990](https://pubmed.ncbi.nlm.nih.gov/17221396/) [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Allicin transformation and garlic processing involve chemically distinct z-ajoene; this provenance does not transfer the product's effects to allicin.
Allicin → Z-Ajoene Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Chemical preparation/transformation scope; media determine product mixture.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
DADS/DATS and ajoene remain distinct. This qualitative preparation relationship does not establish human metabolic yield or tissue exposure.
plain_language
Allicin transformation and garlic processing involve chemically distinct z-ajoene; this provenance does not transfer the product's effects to allicin.
primary_references
Products of Allicin Transformation: Ajoenes and Dithiins, Characterization and their Determination by HPLC*. | 1990 | DOI 10.1055/s-2006-960926 | PMID 17221396 | https://pubmed.ncbi.nlm.nih.gov/17221396/ | https://doi.org/10.1055/s-2006-960926
source_locator
Reviewed reference lines 15-15; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 15–15
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical preparation/transformation scope; media determine product mixture. · Recorded from source · Recorded from source
**Distinct sulfur compounds.** Alliin, allicin, diallyl disulfide (DADS), diallyl trisulfide (DATS), E-ajoene, Z-ajoene, and the two vinyldithiin isomers require separate records. Preparation conditions influence the transformation products and ajoene isomer ratio. S-allylcysteine (SAC) has a thioether linkage; S-allylmercaptocysteine (SAMC) is a mixed disulfide. SAMC can arise by reaction with cysteine, whereas SAC is not another name for allicin. Food processing products, biological reaction products, and metabolites should not be collapsed into one chemical family that inherits every member's effects. [Iberl 1990](https://pubmed.ncbi.nlm.nih.gov/17221396/) [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Allicin reacted with L-cysteine to form the identified mixed-disulfide product SAMC.
Allicin → S-Allylmercapto-L-cysteine / SAMC Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Cell-free chemical reaction; NMR characterization.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Allicin reacted with L-cysteine to form the identified mixed-disulfide product SAMC.
primary_references
The mode of action of allicin: trapping of radicals and interaction with thiol containing proteins. | 1998 | DOI 10.1016/s0304-4165(97)00104-9 | PMID 9528659 | https://pubmed.ncbi.nlm.nih.gov/9528659/ | https://doi.org/10.1016/s0304-4165(97)00104-9
source_locator
Reviewed reference lines 9-9; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 9–9
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free chemical reaction; NMR characterization. · Recorded from source · Recorded from source
**Chemical identity.** Allicin is diallyl thiosulfinate, C6H10OS2, approximately 162.27 g/mol, with the structure CH2=CH–CH2–S(=O)–S–CH2–CH=CH2. The oxygen-containing thiosulfinate linkage matters: allicin is not diallyl disulfide, and the compounds cannot share target effects merely because both contain sulfur. Primary chemistry identified S-allylmercaptocysteine when allicin reacted with L-cysteine. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Allicin reacts with glutathione to form GSSA, distinct from GSSG.
Allicin → S-Allylmercaptoglutathione / GSSA Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Cell-free product preparation and LC-MS characterization; not human oral metabolism.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Allicin reacts with glutathione to form GSSA, distinct from GSSG.
primary_references
S-allylmercaptoglutathione Is a Substrate for Glutathione Reductase (E.C. 1.8.1.7) from Yeast (Saccharomyces cerevisiae). | 2018 | DOI 10.3390/antiox7070086 | PMID 29986384 | https://pubmed.ncbi.nlm.nih.gov/29986384/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6070820/ | https://doi.org/10.3390/antiox7070086
source_locator
Reviewed reference lines 39-39; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 39–39
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free product preparation and LC-MS characterization; not human oral metabolism. · Recorded from source · Recorded from source
**Thioallylation chemistry.** Allicin reacts with accessible cysteine thiols to form allyl-containing mixed disulfides. For a protein, the simplified first reaction is protein-SH + allicin → protein-S-S-allyl + allylsulfenic acid. Glutathione forms S-allylmercaptoglutathione (GSSA), which is chemically distinct from oxidized glutathione (GSSG). Accessibility, local environment, competing thiols, and exposure determine which targets are modified. An adduct alone does not demonstrate inhibition, phenotype mediation, or dietary target engagement. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/) [Horn 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6070820/)
Complete structured claim and evidence
Allicin and thiamine form thiamine allyl disulfide, identified as allithiamine in the original chemistry report.
Allicin → Allithiamine / thiamine allyl disulfide Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary publisher abstract reviewed; chemical identification only. Detailed reaction conditions, human absorption and therapeutic comparisons were not extracted.
experimental_model
Historical chemical identification; publisher abstract; full reaction conditions not extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No quantified gastrointestinal yield, clinical B1-deficiency rescue, or equivalence to TTFD inferred.
plain_language
Allicin and thiamine form thiamine allyl disulfide, identified as allithiamine in the original chemistry report.
primary_references
ALLITHIAMINE A NEWLY FOUND DERIVATIVE OF VITAMIN B1. I. DISCOVERY OF ALLITHIAMINE | 1954 | https://www.jstage.jst.go.jp/article/biochemistry1922/41/1/41_1_29/_article
source_locator
Reviewed reference lines 61-61; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 61–61
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Historical chemical identification; publisher abstract; full reaction conditions not extracted. · Recorded from source · Recorded from source
**Vitamin B1 chemistry.** The original allithiamine report identified thiamine allyl disulfide as a product of reaction between allicin and thiamine. This creates a real chemical connection to vitamin B1. It does not establish how much forms after eating garlic, clinical correction of thiamine deficiency, or superiority of garlic over thiamine treatment. Allithiamine is distinct from thiamine tetrahydrofurfuryl disulfide and other synthetic derivatives. [Fujiwara 1954](https://www.jstage.jst.go.jp/article/biochemistry1922/41/1/41_1_29/_article)
Complete structured claim and evidence
Allicin stability depends on the medium; vegetable oil had a 3.1-hour chemical half-life and a separate 0.8-hour antibacterial-activity half-life.
Allicin → Preparation-dependent chemical allicin loss Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Room-temperature preparation comparisons; aqueous/alcoholic extracts and vegetable oil.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not a universal body half-life. Full preparation-specific kinetic tables remain unextracted.
plain_language
Allicin stability depends on the medium; vegetable oil had a 3.1-hour chemical half-life and a separate 0.8-hour antibacterial-activity half-life.
primary_references
Biological and chemical stability of garlic-derived allicin. | 2008 | DOI 10.1021/jf8000907 | PMID 18489116 | https://pubmed.ncbi.nlm.nih.gov/18489116/ | https://doi.org/10.1021/jf8000907
source_locator
Reviewed reference lines 19-19; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 19–19
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Room-temperature preparation comparisons; aqueous/alcoholic extracts and vegetable oil. · Recorded from source · Recorded from source
**Stability depends on medium.** Chemical allicin loss and loss of antibacterial activity were different measurements in aqueous, alcoholic, and oil preparations. A room-temperature study reported persistence over days in some aqueous/alcoholic conditions; vegetable oil gave a chemical half-life of 3.1 hours and an activity half-life of 0.8 hours. These are preparation-specific measurements, not a universal half-life in crushed garlic, blood, or the human body. Thiol consumption in biological material is also distinct from spontaneous decomposition. [Fujisawa 2008](https://pubmed.ncbi.nlm.nih.gov/18489116/)
Complete structured claim and evidence
Previously crushed garlic retained some platelet-inhibitory activity after six-minute heating that abolished it in uncrushed samples.
Crushed and uncrushed heated garlic preparations in the 2007 platelet study → Inhibition of aggregation in human platelet assays with garlic extracts Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Garlic crushed before six-minute heating", "comparator": "Garlic heated uncrushed for the same time", "endpoint": "Previously crushed garlic retained some platelet-inhibitory activity after six-minute heating that abolished it in uncrushed samples.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human platelets exposed to extracts of heated garlic; in vitro.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Relative retained inhibitory activity, not increased bleeding or reduced human thrombosis after a meal.
plain_language
Previously crushed garlic retained some platelet-inhibitory activity after six-minute heating that abolished it in uncrushed samples.
primary_references
Effect of cooking on garlic (Allium sativum L.) antiplatelet activity and thiosulfinates content. | 2007 | DOI 10.1021/jf062587s | PMID 17256959 | https://pubmed.ncbi.nlm.nih.gov/17256959/ | https://doi.org/10.1021/jf062587s
source_locator
Reviewed reference lines 21-21; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 21–21
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human platelets exposed to extracts of heated garlic; in vitro. · Recorded from source · Recorded from source
**Crushing and cooking.** In the tested garlic-extract platelet assay, brief heating retained activity; six minutes of heating eliminated activity from uncrushed samples but left reduced activity in previously crushed samples. Heating longer than ten minutes eliminated the measured activity. These were extracts applied to human platelets in vitro, not a clinical comparison of meals or bleeding risk. Crushing first gives alliinase time to act but does not make its products heat-proof. [Cavagnaro 2007](https://pubmed.ncbi.nlm.nih.gov/17256959/)
Complete structured claim and evidence
Heating beyond ten minutes eliminated the tested garlic-extract platelet-inhibitory activity.
Crushed and uncrushed heated garlic preparations in the 2007 platelet study → Inhibition of aggregation in human platelet assays with garlic extracts Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Prolonged heating", "comparator": "Unheated garlic extract", "endpoint": "Heating beyond ten minutes eliminated the tested garlic-extract platelet-inhibitory activity.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
In vitro platelet assay after specified cooking conditions.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Heating beyond ten minutes eliminated the tested garlic-extract platelet-inhibitory activity.
primary_references
Effect of cooking on garlic (Allium sativum L.) antiplatelet activity and thiosulfinates content. | 2007 | DOI 10.1021/jf062587s | PMID 17256959 | https://pubmed.ncbi.nlm.nih.gov/17256959/ | https://doi.org/10.1021/jf062587s
source_locator
Reviewed reference lines 21-21; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 21–21
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · In vitro platelet assay after specified cooking conditions. · Recorded from source · Recorded from source
**Crushing and cooking.** In the tested garlic-extract platelet assay, brief heating retained activity; six minutes of heating eliminated activity from uncrushed samples but left reduced activity in previously crushed samples. Heating longer than ten minutes eliminated the measured activity. These were extracts applied to human platelets in vitro, not a clinical comparison of meals or bleeding risk. Crushing first gives alliinase time to act but does not make its products heat-proof. [Cavagnaro 2007](https://pubmed.ncbi.nlm.nih.gov/17256959/)
Complete structured claim and evidence
Resting crushed garlic before microwave heating preserved some inhibition of rat mammary carcinogen-DNA adduct formation.
Garlic preparations in the rat mammary DNA-adduct heating study → DMBA-metabolite DNA adducts in rat mammary epithelium Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Crushed garlic rested before heating", "comparator": "Garlic heated without the preheating rest", "endpoint": "Resting crushed garlic before microwave heating preserved some inhibition of rat mammary carcinogen-DNA adduct formation.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat mammary DMBA adduct endpoint; ten-minute rest before sixty-second microwave exposure.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific animal surrogate endpoint, not human cancer prevention.
plain_language
Resting crushed garlic before microwave heating preserved some inhibition of rat mammary carcinogen-DNA adduct formation.
primary_references
The influence of heating on the anticancer properties of garlic. | 2001 | DOI 10.1093/jn/131.3.1054s | PMID 11238815 | https://pubmed.ncbi.nlm.nih.gov/11238815/ | https://doi.org/10.1093/jn/131.3.1054s
source_locator
Reviewed reference lines 23-23; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 23–23
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat mammary DMBA adduct endpoint; ten-minute rest before sixty-second microwave exposure. · Recorded from source · Recorded from source
**The ten-minute rest.** A rat mammary DNA-adduct experiment found that letting crushed garlic stand ten minutes before a sixty-second microwave exposure prevented complete loss of the measured protective effect. The endpoint involved carcinogen-metabolite binding to DNA. It neither establishes a universal culinary optimum nor proves prevention of human cancer. [Song and Milner 2001](https://pubmed.ncbi.nlm.nih.gov/11238815/)
Complete structured claim and evidence
Six-to-ten-minute boiling increased measured linear allyl-polysulfide content relative to other tested preparation times.
Boiled crushed garlic preparations in the 2017 polysulfide study → Measured linear allyl-polysulfide content in garlic preparations Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Crushed-garlic preparation, chemical analyses and cell-based sulfide assay; 3-30-minute time series.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
The time dependence is nonmonotonic; 20-30 minutes reduced these measures. Not clinical superiority of a recipe.
plain_language
Six-to-ten-minute boiling increased measured linear allyl-polysulfide content relative to other tested preparation times.
primary_references
Boiling enriches the linear polysulfides and the hydrogen sulfide-releasing activity of garlic. | 2017 | DOI 10.1016/j.foodchem.2016.10.076 | PMID 27979174 | https://pubmed.ncbi.nlm.nih.gov/27979174/ | https://doi.org/10.1016/j.foodchem.2016.10.076
source_locator
Reviewed reference lines 25-25; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 25–25
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Crushed-garlic preparation, chemical analyses and cell-based sulfide assay; 3-30-minute time series. · Recorded from source · Recorded from source
**Heating changes the mixture.** In crushed garlic, boiling for six to ten minutes increased measured linear allyl polysulfides and sulfide-releasing activity in the study's assay; twenty to thirty minutes reduced these measures. This concerns transformation products and assay conditions, so it can coexist with loss of alliinase or intact allicin. Different chemical endpoints are not automatically contradictory. [Tocmo 2017](https://pubmed.ncbi.nlm.nih.gov/27979174/)
Complete structured claim and evidence
Six-to-ten-minute boiling increased measured sulfide-releasing assay activity relative to other tested preparation times.
Boiled crushed garlic preparations in the 2017 polysulfide study → Garlic preparation sulfide-releasing assay activity Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Crushed-garlic preparation, chemical analyses and cell-based sulfide assay; 3-30-minute time series.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
The time dependence is nonmonotonic; 20-30 minutes reduced these measures. Not clinical superiority of a recipe.
plain_language
Six-to-ten-minute boiling increased measured sulfide-releasing assay activity relative to other tested preparation times.
primary_references
Boiling enriches the linear polysulfides and the hydrogen sulfide-releasing activity of garlic. | 2017 | DOI 10.1016/j.foodchem.2016.10.076 | PMID 27979174 | https://pubmed.ncbi.nlm.nih.gov/27979174/ | https://doi.org/10.1016/j.foodchem.2016.10.076
source_locator
Reviewed reference lines 25-25; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 25–25
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Crushed-garlic preparation, chemical analyses and cell-based sulfide assay; 3-30-minute time series. · Recorded from source · Recorded from source
**Heating changes the mixture.** In crushed garlic, boiling for six to ten minutes increased measured linear allyl polysulfides and sulfide-releasing activity in the study's assay; twenty to thirty minutes reduced these measures. This concerns transformation products and assay conditions, so it can coexist with loss of alliinase or intact allicin. Different chemical endpoints are not automatically contradictory. [Tocmo 2017](https://pubmed.ncbi.nlm.nih.gov/27979174/)
Complete structured claim and evidence
Allicin permeated the tested membrane and reached thiols on the other side.
Allicin → Allicin permeation through model phospholipid bilayers Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Phospholipid vesicles loaded with hydrophilic thiols
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Allicin permeated the tested membrane and reached thiols on the other side.
primary_references
The mode of action of allicin: its ready permeability through phospholipid membranes may contribute to its biological activity. | 2000 | DOI 10.1016/s0005-2736(99)00174-1 | PMID 10631291 | https://pubmed.ncbi.nlm.nih.gov/10631291/ | https://doi.org/10.1016/s0005-2736(99)00174-1
source_locator
Reviewed reference lines 27-27; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 27–27
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Phospholipid vesicles loaded with hydrophilic thiols · Recorded from source · Recorded from source
**Membrane entry.** Allicin crossed phospholipid vesicles and human erythrocyte membranes and reacted with enclosed thiols. The investigators did not find membrane leakage, fusion, or aggregation in those assays. Permeation supports intracellular target access during direct exposure; it does not establish oral delivery to a distant tissue or make transport and resistance irrelevant in every organism. [Miron 2000](https://pubmed.ncbi.nlm.nih.gov/10631291/)
Complete structured claim and evidence
Allicin permeated the tested membrane and reached thiols on the other side.
Allicin → Allicin entry into isolated human erythrocytes Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Isolated human red blood cells
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Allicin permeated the tested membrane and reached thiols on the other side.
primary_references
The mode of action of allicin: its ready permeability through phospholipid membranes may contribute to its biological activity. | 2000 | DOI 10.1016/s0005-2736(99)00174-1 | PMID 10631291 | https://pubmed.ncbi.nlm.nih.gov/10631291/ | https://doi.org/10.1016/s0005-2736(99)00174-1
source_locator
Reviewed reference lines 27-27; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 27–27
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Isolated human red blood cells · Recorded from source · Recorded from source
**Membrane entry.** Allicin crossed phospholipid vesicles and human erythrocyte membranes and reacted with enclosed thiols. The investigators did not find membrane leakage, fusion, or aggregation in those assays. Permeation supports intracellular target access during direct exposure; it does not establish oral delivery to a distant tissue or make transport and resistance irrelevant in every organism. [Miron 2000](https://pubmed.ncbi.nlm.nih.gov/10631291/)
Complete structured claim and evidence
Allicin did not produce detected leakage, fusion or aggregation in the tested membrane assays.
Allicin → Leakage in allicin-exposed membrane assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Allicin exposure", "comparator": "Corresponding membrane assay control", "endpoint": "Allicin did not produce detected leakage, fusion or aggregation in the tested membrane assays.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Artificial membrane assays; primary abstract; exact exposure unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not proof of safety of all membranes, doses, or tissues.
plain_language
Allicin did not produce detected leakage, fusion or aggregation in the tested membrane assays.
primary_references
The mode of action of allicin: its ready permeability through phospholipid membranes may contribute to its biological activity. | 2000 | DOI 10.1016/s0005-2736(99)00174-1 | PMID 10631291 | https://pubmed.ncbi.nlm.nih.gov/10631291/ | https://doi.org/10.1016/s0005-2736(99)00174-1
source_locator
Reviewed reference lines 27-27; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 27–27
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Artificial membrane assays; primary abstract; exact exposure unextracted. · Recorded from source · Recorded from source
**Membrane entry.** Allicin crossed phospholipid vesicles and human erythrocyte membranes and reacted with enclosed thiols. The investigators did not find membrane leakage, fusion, or aggregation in those assays. Permeation supports intracellular target access during direct exposure; it does not establish oral delivery to a distant tissue or make transport and resistance irrelevant in every organism. [Miron 2000](https://pubmed.ncbi.nlm.nih.gov/10631291/)
Complete structured claim and evidence
The tested preparation gave 80-111% relative breath AMS exposure versus homogenized raw garlic.
Non-enteric garlic tablets in the 2018 breath study → Human breath allyl-methyl-sulfide exposure over 32 hours Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Thirteen participants across preparation comparisons; 32-hour breath metabolite AUC.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Indirect relative marker; not percent intact allicin entering blood or efficacy equivalence.
plain_language
The tested preparation gave 80-111% relative breath AMS exposure versus homogenized raw garlic.
primary_references
Allicin Bioavailability and Bioequivalence from Garlic Supplements and Garlic Foods. | 2018 | DOI 10.3390/nu10070812 | PMID 29937536 | https://pubmed.ncbi.nlm.nih.gov/29937536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/ | https://doi.org/10.3390/nu10070812
source_locator
Reviewed reference lines 29-29; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 29–29
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Thirteen participants across preparation comparisons; 32-hour breath metabolite AUC. · Recorded from source · Recorded from source
**Human breath measurements.** Lawson and Hunsaker compared preparations using thirty-two-hour breath allyl methyl sulfide (AMS) exposure in thirteen participants. Their relative results were 80–111% for tested non-enteric tablets, 36–104% for enteric tablets, and 22–57% for enteric products with high-protein meals, relative to homogenized raw garlic. These percentages are not absolute bioavailability of intact plasma allicin. The study also found contributions from SAC-related precursors to AMS, particularly relevant to preparations with inhibited alliinase. Thus AMS is a useful preparation-comparison marker with chemical-origin limitations. Enteric coating is not automatically superior. Meal effects, disintegration, enzyme activity, and the assay all matter. [Lawson and Hunsaker 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/)
Complete structured claim and evidence
The tested preparation gave 36-104% relative breath AMS exposure versus homogenized raw garlic.
Enteric garlic tablets in the 2018 breath study → Human breath allyl-methyl-sulfide exposure over 32 hours Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Thirteen participants across preparation comparisons; 32-hour breath metabolite AUC.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Indirect relative marker; not percent intact allicin entering blood or efficacy equivalence.
plain_language
The tested preparation gave 36-104% relative breath AMS exposure versus homogenized raw garlic.
primary_references
Allicin Bioavailability and Bioequivalence from Garlic Supplements and Garlic Foods. | 2018 | DOI 10.3390/nu10070812 | PMID 29937536 | https://pubmed.ncbi.nlm.nih.gov/29937536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/ | https://doi.org/10.3390/nu10070812
source_locator
Reviewed reference lines 29-29; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 29–29
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Thirteen participants across preparation comparisons; 32-hour breath metabolite AUC. · Recorded from source · Recorded from source
**Human breath measurements.** Lawson and Hunsaker compared preparations using thirty-two-hour breath allyl methyl sulfide (AMS) exposure in thirteen participants. Their relative results were 80–111% for tested non-enteric tablets, 36–104% for enteric tablets, and 22–57% for enteric products with high-protein meals, relative to homogenized raw garlic. These percentages are not absolute bioavailability of intact plasma allicin. The study also found contributions from SAC-related precursors to AMS, particularly relevant to preparations with inhibited alliinase. Thus AMS is a useful preparation-comparison marker with chemical-origin limitations. Enteric coating is not automatically superior. Meal effects, disintegration, enzyme activity, and the assay all matter. [Lawson and Hunsaker 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/)
Complete structured claim and evidence
A high-protein meal reduced relative breath AMS exposure from the tested enteric products to 22-57%.
Enteric garlic tablets in the 2018 breath study → Human breath allyl-methyl-sulfide exposure over 32 hours Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Same products with low-protein meal administered · Enteric garlic tablets in the 2018 breath study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same products with low-protein meal co-administered · High-protein meal used in the 2018 garlic tablet comparison Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Enteric tablets with high-protein meal", "comparator": "Same products with low-protein meal", "endpoint": "A high-protein meal reduced relative breath AMS exposure from the tested enteric products to 22-57%.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "garlic-enteric-lawson-2018", "state": "administered"}, {"entity_slug": "high-protein-meal-lawson-2018", "state": "co-administered"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human enteric-tablet/meal comparison; breath AMS AUC.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Joint formulation-meal exposure; not a general protein-induced inhibition of allicin or clinical benefit.
plain_language
A high-protein meal reduced relative breath AMS exposure from the tested enteric products to 22-57%.
primary_references
Allicin Bioavailability and Bioequivalence from Garlic Supplements and Garlic Foods. | 2018 | DOI 10.3390/nu10070812 | PMID 29937536 | https://pubmed.ncbi.nlm.nih.gov/29937536/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/ | https://doi.org/10.3390/nu10070812
source_locator
Reviewed reference lines 29-29; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 29–29
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human enteric-tablet/meal comparison; breath AMS AUC. · Recorded from source · Recorded from source
**Human breath measurements.** Lawson and Hunsaker compared preparations using thirty-two-hour breath allyl methyl sulfide (AMS) exposure in thirteen participants. Their relative results were 80–111% for tested non-enteric tablets, 36–104% for enteric tablets, and 22–57% for enteric products with high-protein meals, relative to homogenized raw garlic. These percentages are not absolute bioavailability of intact plasma allicin. The study also found contributions from SAC-related precursors to AMS, particularly relevant to preparations with inhibited alliinase. Thus AMS is a useful preparation-comparison marker with chemical-origin limitations. Enteric coating is not automatically superior. Meal effects, disintegration, enzyme activity, and the assay all matter. [Lawson and Hunsaker 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6073756/)
Complete structured claim and evidence
Thirty-three organosulfur analytes were characterized in urine after twenty grams of black garlic, including N-acetyl products.
Black garlic meal in the 2023 urine study → Urinary organosulfur analytes after human black-garlic intake Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Healthy-human acute feeding, 24-hour urine; UHPLC-HRMS.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Some pathway assignments tentative; not proof of systemic intact allicin or exact pathway flux.
plain_language
Thirty-three organosulfur analytes were characterized in urine after twenty grams of black garlic, including N-acetyl products.
primary_references
Bioavailability of Organosulfur Compounds after the Ingestion of Black Garlic by Healthy Humans. | 2023 | DOI 10.3390/antiox12040925 | PMID 37107300 | https://pubmed.ncbi.nlm.nih.gov/37107300/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10135770/ | https://doi.org/10.3390/antiox12040925
source_locator
Reviewed reference lines 33-33; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 33–33
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Healthy-human acute feeding, 24-hour urine; UHPLC-HRMS. · Recorded from source · Recorded from source
**Black garlic is a separate intervention.** After twenty grams of black garlic, a human urine study characterized thirty-three organosulfur analytes over twenty-four hours, including SAC-related and alliin-related N-acetyl products. Urinary detection supports exposure to constituents of that preparation; it is not evidence that intact allicin reached a tumor, artery, or brain. Some pathway assignments were tentative. [Moreno-Ortega 2023](https://pmc.ncbi.nlm.nih.gov/articles/PMC10135770/)
Complete structured claim and evidence
Reported SAC oral bioavailability was 98.2% in rats, 103.0% in mice, and 87.2% in dogs.
S-allyl-L-cysteine / SAC → SAC oral bioavailability in rat mouse and dog pharmacokinetic comparisons Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Species-separated pharmacokinetic estimates; original accessible abstract.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not human values; estimate above 100% is variability, not additional dose. Not allicin pharmacokinetics.
plain_language
Reported SAC oral bioavailability was 98.2% in rats, 103.0% in mice, and 87.2% in dogs.
primary_references
Pharmacokinetics of the garlic compound S-allylcysteine. | 1994 | DOI 10.1055/s-2006-959461 | PMID 8073085 | https://pubmed.ncbi.nlm.nih.gov/8073085/ | https://doi.org/10.1055/s-2006-959461
source_locator
Reviewed reference lines 35-35; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 35–35
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Species-separated pharmacokinetic estimates; original accessible abstract. · Recorded from source · Recorded from source
**SAC pharmacokinetics are species-specific.** The frequently quoted high oral SAC bioavailability came from rats, mice, and dogs: 98.2%, 103.0%, and 87.2%, respectively, in the cited experiment. An estimate above 100% reflects the pharmacokinetic comparison and experimental variability, not creation of additional dose. These values are not measured human allicin bioavailability. [Nagae 1994](https://pubmed.ncbi.nlm.nih.gov/8073085/)
Complete structured claim and evidence
S-thioallylated peptides were detected from 332 proteins after direct allicin exposure.
Allicin → Protein S-thioallylation in human Jurkat cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin for ten minutes, LC-MS/MS.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
The full supplemental list is not independently resolved into 332 canonical proteins here. Adduct detection is separate from function or human dietary target engagement.
plain_language
S-thioallylated peptides were detected from 332 proteins after direct allicin exposure.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin for ten minutes, LC-MS/MS. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human fructose-bisphosphate aldolase A / ALDOA in allicin-exposed Jurkat cells.
Allicin → Human fructose-bisphosphate aldolase A / ALDOA Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human fructose-bisphosphate aldolase A / ALDOA in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human glyceraldehyde-3-phosphate dehydrogenase / GAPDH in allicin-exposed Jurkat cells.
Allicin → Human glyceraldehyde-3-phosphate dehydrogenase / GAPDH Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human glyceraldehyde-3-phosphate dehydrogenase / GAPDH in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human pyruvate kinase PKM, splice isoform unresolved / PKM in allicin-exposed Jurkat cells.
Allicin → Human pyruvate kinase PKM, splice isoform unresolved / PKM Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human pyruvate kinase PKM, splice isoform unresolved / PKM in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human alpha-enolase / ENO1 in allicin-exposed Jurkat cells.
Allicin → Human alpha-enolase / ENO1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human alpha-enolase / ENO1 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human copper-zinc superoxide dismutase / SOD1 in allicin-exposed Jurkat cells.
Allicin → Human copper-zinc superoxide dismutase / SOD1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human copper-zinc superoxide dismutase / SOD1 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human peroxiredoxin 1 / PRDX1 in allicin-exposed Jurkat cells.
Allicin → Human peroxiredoxin 1 / PRDX1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human peroxiredoxin 1 / PRDX1 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human cofilin 1 / CFL1 in allicin-exposed Jurkat cells.
Allicin → Human cofilin 1 / CFL1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human cofilin 1 / CFL1 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human plastin 2 / LCP1 in allicin-exposed Jurkat cells.
Allicin → Human plastin 2 / LCP1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human plastin 2 / LCP1 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human filamin A / FLNA in allicin-exposed Jurkat cells.
Allicin → Human filamin A / FLNA Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human filamin A / FLNA in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human filamin B / FLNB in allicin-exposed Jurkat cells.
Allicin → Human filamin B / FLNB Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human filamin B / FLNB in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human heat shock protein family A member 4 / HSPA4 in allicin-exposed Jurkat cells.
Allicin → Human heat shock protein family A member 4 / HSPA4 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human heat shock protein family A member 4 / HSPA4 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human eukaryotic elongation factor 2 / EEF2 in allicin-exposed Jurkat cells.
Allicin → Human eukaryotic elongation factor 2 / EEF2 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human eukaryotic elongation factor 2 / EEF2 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
S-thioallylation was detected on Human high mobility group box 1 / HMGB1 in allicin-exposed Jurkat cells.
Allicin → Human high mobility group box 1 / HMGB1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Protein modification detected; no blanket inhibition, protein depletion, necessity for phenotype, or oral target engagement is asserted. Isoform is retained as unresolved where appropriate.
plain_language
S-thioallylation was detected on Human high mobility group box 1 / HMGB1 in allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells, 100 uM allicin, ten minutes; main-text proteomic target identification. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
Free cellular thiols fell approximately 50% after allicin treatment.
Allicin → Free cellular thiols measured in human Jurkat cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin exposure at the specified assay dose/time", "comparator": "Untreated matched cells", "endpoint": "Free cellular thiols fell approximately 50% after allicin treatment.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Jurkat cells; ten-minute 100 uM exposure for thiols/enolase, 24-hour MTT observation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
MTT, free thiols and specific enzyme activity measure different quantities. The lysate assay does not isolate every possible contribution to inhibition.
plain_language
Free cellular thiols fell approximately 50% after allicin treatment.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells; ten-minute 100 uM exposure for thiols/enolase, 24-hour MTT observation. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
Enolase activity decreased in lysates from allicin-exposed Jurkat cells.
Allicin → Enolase activity in human Jurkat cell lysates Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin exposure at the specified assay dose/time", "comparator": "Untreated matched cells", "endpoint": "Enolase activity decreased in lysates from allicin-exposed Jurkat cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Jurkat cells; ten-minute 100 uM exposure for thiols/enolase, 24-hour MTT observation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
MTT, free thiols and specific enzyme activity measure different quantities. The lysate assay does not isolate every possible contribution to inhibition.
plain_language
Enolase activity decreased in lysates from allicin-exposed Jurkat cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells; ten-minute 100 uM exposure for thiols/enolase, 24-hour MTT observation. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
MTT metabolic-activity readout did not significantly decrease after exposure up to 100 uM in the tested Jurkat system.
Allicin → MTT metabolic-activity readout in human Jurkat cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin exposure at the specified assay dose/time", "comparator": "Untreated matched cells", "endpoint": "MTT metabolic-activity readout did not significantly decrease after exposure up to 100 uM in the tested Jurkat system.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human Jurkat cells; ten-minute 100 uM exposure for thiols/enolase, 24-hour MTT observation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
MTT, free thiols and specific enzyme activity measure different quantities. The lysate assay does not isolate every possible contribution to inhibition.
plain_language
MTT metabolic-activity readout did not significantly decrease after exposure up to 100 uM in the tested Jurkat system.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human Jurkat cells; ten-minute 100 uM exposure for thiols/enolase, 24-hour MTT observation. · Recorded from source · Recorded from source
**The human protein experiment.** Direct exposure of Jurkat cells to 100 µM allicin for ten minutes produced S-thioallylated peptides from 332 proteins, detected by an approximately +72-Da cysteine modification. Total free thiols fell by about half. Targets reported in the main text include ALDOA, GAPDH, PKM, ENO1, SOD1, PRDX1, CFL1, LCP1, FLNA, FLNB, HSPA4, EEF2, and HMGB1, alongside actin, tubulin, and HSP90 groups. These are adduct records; individual isoforms are not invented where unresolved. ENO1-associated lysate activity decreased, while the twenty-four-hour MTT readout was unchanged at up to 100 µM. MTT preservation does not mean every cellular function was unaffected. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
Allicin disrupted filamentous-actin organization in mouse L929 fibroblasts.
Allicin → F-actin organization in mouse L929 fibroblasts Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin", "comparator": "Untreated mouse fibroblasts", "endpoint": "Allicin disrupted filamentous-actin organization in mouse L929 fibroblasts.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse L929, 25-100 uM, ten minutes; rhodamine-phalloidin imaging.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Exact individual protein mediation was not established; not a human Jurkat functional result.
plain_language
Allicin disrupted filamentous-actin organization in mouse L929 fibroblasts.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 45-45; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 45–45
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse L929, 25-100 uM, ten minutes; rhodamine-phalloidin imaging. · Recorded from source · Recorded from source
**Cytoskeleton and zinc.** In separate mouse-cell experiments in the same paper, 25–100 µM allicin disrupted L929 fibroblast actin organization after ten minutes. In EL-4 cells, 25 µM increased labile zinc at thirty minutes. For the IL-2 experiment, cells received 25 µM allicin for thirty minutes, were washed and supplied fresh medium, then received 0.5 ng/mL IL-1β for twenty-four hours; allicin pretreatment enhanced the stimulated IL-2 response. Detecting SOD1 modification in human Jurkat cells does not prove that SOD1 supplied the released zinc in mouse EL-4 cells. These outcomes do not establish improved human zinc nutrition or immune protection. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
Allicin increased labile zinc in mouse EL-4 cells.
Allicin → Labile zinc in mouse EL-4 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin 25 uM", "comparator": "Untreated cells", "endpoint": "Allicin increased labile zinc in mouse EL-4 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse EL-4, 25 uM, 30 minutes.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not additional total zinc or identification of SOD1 as the donor. Mouse functional assay and human proteomic adducts are separate.
plain_language
Allicin increased labile zinc in mouse EL-4 cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 45-45; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 45–45
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse EL-4, 25 uM, 30 minutes. · Recorded from source · Recorded from source
**Cytoskeleton and zinc.** In separate mouse-cell experiments in the same paper, 25–100 µM allicin disrupted L929 fibroblast actin organization after ten minutes. In EL-4 cells, 25 µM increased labile zinc at thirty minutes. For the IL-2 experiment, cells received 25 µM allicin for thirty minutes, were washed and supplied fresh medium, then received 0.5 ng/mL IL-1β for twenty-four hours; allicin pretreatment enhanced the stimulated IL-2 response. Detecting SOD1 modification in human Jurkat cells does not prove that SOD1 supplied the released zinc in mouse EL-4 cells. These outcomes do not establish improved human zinc nutrition or immune protection. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
Allicin pretreatment followed by washing enhanced subsequent IL-1beta-stimulated IL-2 production in mouse EL-4 cells.
Allicin → IL-1beta-stimulated IL-2 production in mouse EL-4 cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
IL-1beta stimulation without allicin pretreatment pretreatment followed by wash · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
IL-1beta stimulation without allicin pretreatment subsequent stimulation · Interleukin-1 beta / IL1B Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Allicin pretreatment, wash, then IL-1beta stimulation", "comparator": "IL-1beta stimulation without allicin pretreatment", "endpoint": "Allicin pretreatment followed by washing enhanced subsequent IL-1beta-stimulated IL-2 production in mouse EL-4 cells.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "allicin", "state": "pretreatment followed by wash"}, {"entity_slug": "il1b", "state": "subsequent stimulation"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse EL-4: allicin 25 uM for 30 minutes, wash and fresh medium, then IL-1beta 0.5 ng/mL for 24 hours.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Sequential joint condition; not simultaneous exposure, basal IL-2 enhancement or human immune protection.
plain_language
Allicin pretreatment followed by washing enhanced subsequent IL-1beta-stimulated IL-2 production in mouse EL-4 cells.
primary_references
The human allicin-proteome: S-thioallylation of proteins by the garlic defence substance allicin and its biological effects. | 2019 | DOI 10.1016/j.freeradbiomed.2018.11.022 | PMID 30500420 | https://pubmed.ncbi.nlm.nih.gov/30500420/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/ | https://doi.org/10.1016/j.freeradbiomed.2018.11.022
source_locator
Reviewed reference lines 45-45; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 45–45
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse EL-4: allicin 25 uM for 30 minutes, wash and fresh medium, then IL-1beta 0.5 ng/mL for 24 hours. · Recorded from source · Recorded from source
**Cytoskeleton and zinc.** In separate mouse-cell experiments in the same paper, 25–100 µM allicin disrupted L929 fibroblast actin organization after ten minutes. In EL-4 cells, 25 µM increased labile zinc at thirty minutes. For the IL-2 experiment, cells received 25 µM allicin for thirty minutes, were washed and supplied fresh medium, then received 0.5 ng/mL IL-1β for twenty-four hours; allicin pretreatment enhanced the stimulated IL-2 response. Detecting SOD1 modification in human Jurkat cells does not prove that SOD1 supplied the released zinc in mouse EL-4 cells. These outcomes do not establish improved human zinc nutrition or immune protection. [Gruhlke 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6342545/)
Complete structured claim and evidence
Allicin inhibited the tested purified papain.
Allicin → Carica papaya papain Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Allicin incubation", "comparator": "Enzyme without allicin", "endpoint": "Allicin inhibited the tested purified papain.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Purified enzyme chemical-inhibition assay; species encoded in target.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Exact dose/time unextracted from the accessible abstract; thiol-mediated reversal is target-dependent, not universal irreversibility.
plain_language
Allicin inhibited the tested purified papain.
primary_references
The mode of action of allicin: trapping of radicals and interaction with thiol containing proteins. | 1998 | DOI 10.1016/s0304-4165(97)00104-9 | PMID 9528659 | https://pubmed.ncbi.nlm.nih.gov/9528659/ | https://doi.org/10.1016/s0304-4165(97)00104-9
source_locator
Reviewed reference lines 41-41; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 41–41
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified enzyme chemical-inhibition assay; species encoded in target. · Recorded from source · Recorded from source
**Enzyme inhibition and reversal differ by target.** The early purified-enzyme study observed inhibition of papain, bacterial NADP-dependent alcohol dehydrogenase, and horse-liver NAD-dependent alcohol dehydrogenase. Thiols could reactivate the enzymes, but not interchangeably: glutathione restored papain activity, whereas it did not restore the tested bacterial dehydrogenase under those conditions. Dithiothreitol or mercaptoethanol had different reversal profiles. Covalent inhibition is therefore not equivalent to unrecoverable injury, and a general glutathione rescue cannot be assumed for every enzyme. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Allicin inhibited the tested purified bacterial NADP-dependent alcohol dehydrogenase.
Allicin → Thermoanaerobium brockii NADP-dependent alcohol dehydrogenase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Allicin incubation", "comparator": "Enzyme without allicin", "endpoint": "Allicin inhibited the tested purified bacterial NADP-dependent alcohol dehydrogenase.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Purified enzyme chemical-inhibition assay; species encoded in target.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Exact dose/time unextracted from the accessible abstract; thiol-mediated reversal is target-dependent, not universal irreversibility.
plain_language
Allicin inhibited the tested purified bacterial NADP-dependent alcohol dehydrogenase.
primary_references
The mode of action of allicin: trapping of radicals and interaction with thiol containing proteins. | 1998 | DOI 10.1016/s0304-4165(97)00104-9 | PMID 9528659 | https://pubmed.ncbi.nlm.nih.gov/9528659/ | https://doi.org/10.1016/s0304-4165(97)00104-9
source_locator
Reviewed reference lines 41-41; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 41–41
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified enzyme chemical-inhibition assay; species encoded in target. · Recorded from source · Recorded from source
**Enzyme inhibition and reversal differ by target.** The early purified-enzyme study observed inhibition of papain, bacterial NADP-dependent alcohol dehydrogenase, and horse-liver NAD-dependent alcohol dehydrogenase. Thiols could reactivate the enzymes, but not interchangeably: glutathione restored papain activity, whereas it did not restore the tested bacterial dehydrogenase under those conditions. Dithiothreitol or mercaptoethanol had different reversal profiles. Covalent inhibition is therefore not equivalent to unrecoverable injury, and a general glutathione rescue cannot be assumed for every enzyme. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Allicin inhibited the tested purified horse-liver alcohol dehydrogenase.
Allicin → Horse-liver NAD-dependent alcohol dehydrogenase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Allicin incubation", "comparator": "Enzyme without allicin", "endpoint": "Allicin inhibited the tested purified horse-liver alcohol dehydrogenase.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Purified enzyme chemical-inhibition assay; species encoded in target.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Exact dose/time unextracted from the accessible abstract; thiol-mediated reversal is target-dependent, not universal irreversibility.
plain_language
Allicin inhibited the tested purified horse-liver alcohol dehydrogenase.
primary_references
The mode of action of allicin: trapping of radicals and interaction with thiol containing proteins. | 1998 | DOI 10.1016/s0304-4165(97)00104-9 | PMID 9528659 | https://pubmed.ncbi.nlm.nih.gov/9528659/ | https://doi.org/10.1016/s0304-4165(97)00104-9
source_locator
Reviewed reference lines 41-41; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 41–41
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified enzyme chemical-inhibition assay; species encoded in target. · Recorded from source · Recorded from source
**Enzyme inhibition and reversal differ by target.** The early purified-enzyme study observed inhibition of papain, bacterial NADP-dependent alcohol dehydrogenase, and horse-liver NAD-dependent alcohol dehydrogenase. Thiols could reactivate the enzymes, but not interchangeably: glutathione restored papain activity, whereas it did not restore the tested bacterial dehydrogenase under those conditions. Dithiothreitol or mercaptoethanol had different reversal profiles. Covalent inhibition is therefore not equivalent to unrecoverable injury, and a general glutathione rescue cannot be assumed for every enzyme. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Glutathione restored activity of allicin-inhibited papain.
GSH → Carica papaya papain Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Allicin-inhibited enzyme without effective reductant prior inhibitory exposure · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Allicin-inhibited enzyme without effective reductant added · GSH Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "GSH addition after allicin inhibition", "comparator": "Allicin-inhibited enzyme without effective reductant", "endpoint": "Glutathione restored activity of allicin-inhibited papain.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "allicin", "state": "prior inhibitory exposure"}, {"entity_slug": "glutathione", "state": "added"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Purified enzyme, prior allicin inhibition, reductant comparison.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Glutathione restored activity of allicin-inhibited papain.
primary_references
The mode of action of allicin: trapping of radicals and interaction with thiol containing proteins. | 1998 | DOI 10.1016/s0304-4165(97)00104-9 | PMID 9528659 | https://pubmed.ncbi.nlm.nih.gov/9528659/ | https://doi.org/10.1016/s0304-4165(97)00104-9
source_locator
Reviewed reference lines 41-41; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 41–41
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified enzyme, prior allicin inhibition, reductant comparison. · Recorded from source · Recorded from source
**Enzyme inhibition and reversal differ by target.** The early purified-enzyme study observed inhibition of papain, bacterial NADP-dependent alcohol dehydrogenase, and horse-liver NAD-dependent alcohol dehydrogenase. Thiols could reactivate the enzymes, but not interchangeably: glutathione restored papain activity, whereas it did not restore the tested bacterial dehydrogenase under those conditions. Dithiothreitol or mercaptoethanol had different reversal profiles. Covalent inhibition is therefore not equivalent to unrecoverable injury, and a general glutathione rescue cannot be assumed for every enzyme. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Glutathione did not restore the allicin-inhibited bacterial dehydrogenase in the tested assay.
GSH → Thermoanaerobium brockii NADP-dependent alcohol dehydrogenase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Allicin-inhibited enzyme without effective reductant prior inhibitory exposure · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Allicin-inhibited enzyme without effective reductant added · GSH Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "GSH addition after allicin inhibition", "comparator": "Allicin-inhibited enzyme without effective reductant", "endpoint": "Glutathione did not restore the allicin-inhibited bacterial dehydrogenase in the tested assay.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "allicin", "state": "prior inhibitory exposure"}, {"entity_slug": "glutathione", "state": "added"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Purified enzyme, prior allicin inhibition, reductant comparison.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Glutathione did not restore the allicin-inhibited bacterial dehydrogenase in the tested assay.
primary_references
The mode of action of allicin: trapping of radicals and interaction with thiol containing proteins. | 1998 | DOI 10.1016/s0304-4165(97)00104-9 | PMID 9528659 | https://pubmed.ncbi.nlm.nih.gov/9528659/ | https://doi.org/10.1016/s0304-4165(97)00104-9
source_locator
Reviewed reference lines 41-41; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 41–41
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified enzyme, prior allicin inhibition, reductant comparison. · Recorded from source · Recorded from source
**Enzyme inhibition and reversal differ by target.** The early purified-enzyme study observed inhibition of papain, bacterial NADP-dependent alcohol dehydrogenase, and horse-liver NAD-dependent alcohol dehydrogenase. Thiols could reactivate the enzymes, but not interchangeably: glutathione restored papain activity, whereas it did not restore the tested bacterial dehydrogenase under those conditions. Dithiothreitol or mercaptoethanol had different reversal profiles. Covalent inhibition is therefore not equivalent to unrecoverable injury, and a general glutathione rescue cannot be assumed for every enzyme. [Rabinkov 1998](https://pubmed.ncbi.nlm.nih.gov/9528659/)
Complete structured claim and evidence
Purified yeast glutathione reductase used GSSA as a substrate with NADPH consumption; apparent Km was 0.50 mM.
Saccharomyces cerevisiae glutathione reductase / Glr1 → NADPH-dependent GSSA reduction by purified yeast glutathione reductase Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Purified commercial Saccharomyces cerevisiae enzyme; NADPH absorbance assay without DTNB.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not human GSR validation. GSSG comparator used a different assay, and Km alone does not measure catalytic efficiency.
plain_language
Purified yeast glutathione reductase used GSSA as a substrate with NADPH consumption; apparent Km was 0.50 mM.
primary_references
S-allylmercaptoglutathione Is a Substrate for Glutathione Reductase (E.C. 1.8.1.7) from Yeast (Saccharomyces cerevisiae). | 2018 | DOI 10.3390/antiox7070086 | PMID 29986384 | https://pubmed.ncbi.nlm.nih.gov/29986384/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6070820/ | https://doi.org/10.3390/antiox7070086
source_locator
Reviewed reference lines 47-47; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 47–47
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified commercial Saccharomyces cerevisiae enzyme; NADPH absorbance assay without DTNB. · Recorded from source · Recorded from source
**GSSA recycling and NADPH.** Purified yeast glutathione reductase reduced GSSA with NADPH consumption. Reported apparent Km values were 0.50 mM for GSSA and 0.07 mM for GSSG. They do not establish an eightfold difference in catalytic efficiency: turnover and assay differences matter, and the GSSA measurement deliberately omitted the DTNB cycling reagent used for GSSG. GSSA also supported growth of glutathione-synthesis-defective yeast. That rescue is consistent with recovery of usable glutathione, but it is not a human GSR experiment or proof that this enzyme was the exclusive route in living cells. [Horn 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6070820/)
Complete structured claim and evidence
GSSA supplementation supported growth of GSH1-deficient yeast on otherwise glutathione-unsupplemented medium.
S-Allylmercaptoglutathione / GSSA → Growth of yeast lacking GSH1 Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
GSH1-deficient yeast without exogenous glutathione source deleted · Saccharomyces cerevisiae glutamate-cysteine ligase Gsh1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
GSH1-deficient yeast without exogenous glutathione source supplied · S-Allylmercaptoglutathione / GSSA Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "GSSA supplied to GSH1-deficient yeast", "comparator": "GSH1-deficient yeast without exogenous glutathione source", "endpoint": "GSSA supplementation supported growth of GSH1-deficient yeast on otherwise glutathione-unsupplemented medium.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "yeast-gsh1", "state": "deleted"}, {"entity_slug": "s-allylmercaptoglutathione", "state": "supplied"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae GSH1 deletion; GSSA compared with unsupplemented growth medium.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Rescue supports usable GSH recovery but does not prove the exclusive in vivo reductase or human rescue.
plain_language
GSSA supplementation supported growth of GSH1-deficient yeast on otherwise glutathione-unsupplemented medium.
primary_references
S-allylmercaptoglutathione Is a Substrate for Glutathione Reductase (E.C. 1.8.1.7) from Yeast (Saccharomyces cerevisiae). | 2018 | DOI 10.3390/antiox7070086 | PMID 29986384 | https://pubmed.ncbi.nlm.nih.gov/29986384/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6070820/ | https://doi.org/10.3390/antiox7070086
source_locator
Reviewed reference lines 47-47; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 47–47
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae GSH1 deletion; GSSA compared with unsupplemented growth medium. · Recorded from source · Recorded from source
**GSSA recycling and NADPH.** Purified yeast glutathione reductase reduced GSSA with NADPH consumption. Reported apparent Km values were 0.50 mM for GSSA and 0.07 mM for GSSG. They do not establish an eightfold difference in catalytic efficiency: turnover and assay differences matter, and the GSSA measurement deliberately omitted the DTNB cycling reagent used for GSSG. GSSA also supported growth of glutathione-synthesis-defective yeast. That rescue is consistent with recovery of usable glutathione, but it is not a human GSR experiment or proof that this enzyme was the exclusive route in living cells. [Horn 2018](https://pmc.ncbi.nlm.nih.gov/articles/PMC6070820/)
Complete structured claim and evidence
Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
Saccharomyces cerevisiae glutathione reductase / Glr1 → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Wild-type yeast at the same allicin exposure deleted · Saccharomyces cerevisiae glutathione reductase / Glr1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Wild-type yeast at the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "yeast-glr1 deletion with allicin", "comparator": "Wild-type yeast at the same allicin exposure", "endpoint": "Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-glr1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Keep dose and compound distinctions: analogue effects cannot substitute for allicin. Not a human nutrient-deficiency phenotype.
plain_language
Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
primary_references
The Sulfilimine Analogue of Allicin, S-Allyl-S-(S-allyl)-N-Cyanosulfilimine, Is Antimicrobial and Reacts with Glutathione. | 2020 | DOI 10.3390/antiox9111086 | PMID 33158268 | https://pubmed.ncbi.nlm.nih.gov/33158268/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/ | https://doi.org/10.3390/antiox9111086
source_locator
Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3. · Recorded from source · Recorded from source
**Redox-defense impairment.** A study comparing allicin with a sulfilimine analogue included allicin-exposed Saccharomyces cerevisiae mutants. The GLR1, ZWF1, and YAP1 perturbations connect susceptibility to glutathione recycling, NADPH supply, and stress regulation; effects depended on concentration and compound. The analogue was more potent in some low-concentration comparisons, and its results must not be copied onto allicin. TRX2 loss had a much smaller effect in this system. Human B2 deficiency, G6PD deficiency, or selenium status cannot be assigned the yeast phenotype without direct evidence. [Horn 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/)
Complete structured claim and evidence
Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
Saccharomyces cerevisiae glucose-6-phosphate dehydrogenase / Zwf1 → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Wild-type yeast at the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Wild-type yeast at the same allicin exposure deleted · Saccharomyces cerevisiae glucose-6-phosphate dehydrogenase / Zwf1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "yeast-zwf1 deletion with allicin", "comparator": "Wild-type yeast at the same allicin exposure", "endpoint": "Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-zwf1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Keep dose and compound distinctions: analogue effects cannot substitute for allicin. Not a human nutrient-deficiency phenotype.
plain_language
Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
primary_references
The Sulfilimine Analogue of Allicin, S-Allyl-S-(S-allyl)-N-Cyanosulfilimine, Is Antimicrobial and Reacts with Glutathione. | 2020 | DOI 10.3390/antiox9111086 | PMID 33158268 | https://pubmed.ncbi.nlm.nih.gov/33158268/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/ | https://doi.org/10.3390/antiox9111086
source_locator
Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3. · Recorded from source · Recorded from source
**Redox-defense impairment.** A study comparing allicin with a sulfilimine analogue included allicin-exposed Saccharomyces cerevisiae mutants. The GLR1, ZWF1, and YAP1 perturbations connect susceptibility to glutathione recycling, NADPH supply, and stress regulation; effects depended on concentration and compound. The analogue was more potent in some low-concentration comparisons, and its results must not be copied onto allicin. TRX2 loss had a much smaller effect in this system. Human B2 deficiency, G6PD deficiency, or selenium status cannot be assigned the yeast phenotype without direct evidence. [Horn 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/)
Complete structured claim and evidence
Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
Saccharomyces cerevisiae oxidative-stress transcription factor / Yap1 → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Wild-type yeast at the same allicin exposure deleted · Saccharomyces cerevisiae oxidative-stress transcription factor / Yap1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Wild-type yeast at the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "yeast-yap1 deletion with allicin", "comparator": "Wild-type yeast at the same allicin exposure", "endpoint": "Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-yap1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Keep dose and compound distinctions: analogue effects cannot substitute for allicin. Not a human nutrient-deficiency phenotype.
plain_language
Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
primary_references
The Sulfilimine Analogue of Allicin, S-Allyl-S-(S-allyl)-N-Cyanosulfilimine, Is Antimicrobial and Reacts with Glutathione. | 2020 | DOI 10.3390/antiox9111086 | PMID 33158268 | https://pubmed.ncbi.nlm.nih.gov/33158268/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/ | https://doi.org/10.3390/antiox9111086
source_locator
Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3. · Recorded from source · Recorded from source
**Redox-defense impairment.** A study comparing allicin with a sulfilimine analogue included allicin-exposed Saccharomyces cerevisiae mutants. The GLR1, ZWF1, and YAP1 perturbations connect susceptibility to glutathione recycling, NADPH supply, and stress regulation; effects depended on concentration and compound. The analogue was more potent in some low-concentration comparisons, and its results must not be copied onto allicin. TRX2 loss had a much smaller effect in this system. Human B2 deficiency, G6PD deficiency, or selenium status cannot be assigned the yeast phenotype without direct evidence. [Horn 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/)
Complete structured claim and evidence
Allicin shifted the bacillithiol redox potential toward a more oxidized state in Staphylococcus aureus.
Allicin → Bacillithiol redox potential in Staphylococcus aureus Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Allicin stress", "comparator": "Matched unstressed bacterial cells", "endpoint": "Allicin shifted the bacillithiol redox potential toward a more oxidized state in Staphylococcus aureus.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Bacterial redox-biosensor study; primary abstract; exact dose/time unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Redox potential is not total bacillithiol depletion; no equivalence to human GSH physiology.
plain_language
Allicin shifted the bacillithiol redox potential toward a more oxidized state in Staphylococcus aureus.
primary_references
Staphylococcus aureus responds to allicin by global S-thioallylation - Role of the Brx/BSH/YpdA pathway and the disulfide reductase MerA to overcome allicin stress. | 2019 | DOI 10.1016/j.freeradbiomed.2019.05.018 | PMID 31121222 | https://pubmed.ncbi.nlm.nih.gov/31121222/ | https://doi.org/10.1016/j.freeradbiomed.2019.05.018
source_locator
Reviewed reference lines 51-51; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 51–51
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Bacterial redox-biosensor study; primary abstract; exact dose/time unextracted. · Recorded from source · Recorded from source
**Bacterial thiol systems differ.** Staphylococcus aureus uses bacillithiol rather than treating glutathione as its universal buffer. The 2019 study reported a bacillithiol redox shift, protein S-thioallylation, and reversal through bacilliredoxin/bacillithiol/YpdA chemistry; YpdA could use the allyl-bacillithiol adduct to regenerate bacillithiol. These are organism-specific repair findings, not evidence for the same proteins in humans. [Loi 2019](https://pubmed.ncbi.nlm.nih.gov/31121222/)
Complete structured claim and evidence
The bacilliredoxin/bacillithiol/YpdA pathway reversed protein S-thioallylation in the reported biochemical study.
Staphylococcus aureus bacilliredoxin/bacillithiol/YpdA repair system → Protein S-thioallylation in Staphylococcus aureus Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Staphylococcus aureus biochemical repair evidence; abstract-level access.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The bacilliredoxin/bacillithiol/YpdA pathway reversed protein S-thioallylation in the reported biochemical study.
primary_references
Staphylococcus aureus responds to allicin by global S-thioallylation - Role of the Brx/BSH/YpdA pathway and the disulfide reductase MerA to overcome allicin stress. | 2019 | DOI 10.1016/j.freeradbiomed.2019.05.018 | PMID 31121222 | https://pubmed.ncbi.nlm.nih.gov/31121222/ | https://doi.org/10.1016/j.freeradbiomed.2019.05.018
source_locator
Reviewed reference lines 51-51; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 51–51
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Staphylococcus aureus biochemical repair evidence; abstract-level access. · Recorded from source · Recorded from source
**Bacterial thiol systems differ.** Staphylococcus aureus uses bacillithiol rather than treating glutathione as its universal buffer. The 2019 study reported a bacillithiol redox shift, protein S-thioallylation, and reversal through bacilliredoxin/bacillithiol/YpdA chemistry; YpdA could use the allyl-bacillithiol adduct to regenerate bacillithiol. These are organism-specific repair findings, not evidence for the same proteins in humans. [Loi 2019](https://pubmed.ncbi.nlm.nih.gov/31121222/)
Complete structured claim and evidence
YpdA accepted the allyl-bacillithiol adduct BSSA as a substrate to regenerate bacillithiol.
Staphylococcus aureus bacillithiol-disulfide reductase / YpdA → Bacillithiol / BSH Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Purified bacterial reductase assay; abstract-level access.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
YpdA accepted the allyl-bacillithiol adduct BSSA as a substrate to regenerate bacillithiol.
primary_references
Staphylococcus aureus responds to allicin by global S-thioallylation - Role of the Brx/BSH/YpdA pathway and the disulfide reductase MerA to overcome allicin stress. | 2019 | DOI 10.1016/j.freeradbiomed.2019.05.018 | PMID 31121222 | https://pubmed.ncbi.nlm.nih.gov/31121222/ | https://doi.org/10.1016/j.freeradbiomed.2019.05.018
source_locator
Reviewed reference lines 51-51; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 51–51
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified bacterial reductase assay; abstract-level access. · Recorded from source · Recorded from source
**Bacterial thiol systems differ.** Staphylococcus aureus uses bacillithiol rather than treating glutathione as its universal buffer. The 2019 study reported a bacillithiol redox shift, protein S-thioallylation, and reversal through bacilliredoxin/bacillithiol/YpdA chemistry; YpdA could use the allyl-bacillithiol adduct to regenerate bacillithiol. These are organism-specific repair findings, not evidence for the same proteins in humans. [Loi 2019](https://pubmed.ncbi.nlm.nih.gov/31121222/)
Complete structured claim and evidence
Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.
Allicin → Viability of the 2017 mammalian allicin cell-line panel Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin concentration series", "comparator": "Matched untreated cells in each model", "endpoint": "Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.", "effect_direction": "mixed", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human A549/HUVEC/HT29/MCF7 and mouse 3T3; separate viability, proliferation and apoptosis assays.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Separate species and endpoints; no cancer-selective clinical efficacy or direct measurement of every GSH species.
plain_language
Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.
primary_references
The Effects of Allicin, a Reactive Sulfur Species from Garlic, on a Selection of Mammalian Cell Lines. | 2016 | DOI 10.3390/antiox6010001 | PMID 28035949 | https://pubmed.ncbi.nlm.nih.gov/28035949/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC5384165/ | https://doi.org/10.3390/antiox6010001
source_locator
Reviewed reference lines 53-53; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 53–53
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human A549/HUVEC/HT29/MCF7 and mouse 3T3; separate viability, proliferation and apoptosis assays. · Recorded from source · Recorded from source
**Mammalian injury is context-dependent.** Allicin reduced viability or proliferation and altered thiol-associated fluorescence in a panel including human A549, HUVEC, HT29, and MCF7 cells and mouse 3T3 cells. Sensitivity and apoptotic responses differed. Fluorescence changes are not a complete measurement of every glutathione species. Thiol reactivity does not guarantee selective toxicity to microbes or cancer cells. [Gruhlke 2017](https://pmc.ncbi.nlm.nih.gov/articles/PMC5384165/)
Complete structured claim and evidence
Deletion of yeast-ctr1 increased yeast sensitivity to allicin.
Saccharomyces cerevisiae high-affinity copper transporter / Ctr1 → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae high-affinity copper transporter / Ctr1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "yeast-ctr1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-ctr1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-ctr1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
plain_language
Deletion of yeast-ctr1 increased yeast sensitivity to allicin.
primary_references
A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · Recorded from source · Recorded from source
**Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
Complete structured claim and evidence
Deletion of yeast-mac1 increased yeast sensitivity to allicin.
Saccharomyces cerevisiae copper-responsive transcription factor / Mac1 → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae copper-responsive transcription factor / Mac1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "yeast-mac1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-mac1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-mac1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
plain_language
Deletion of yeast-mac1 increased yeast sensitivity to allicin.
primary_references
A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · Recorded from source · Recorded from source
**Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
Complete structured claim and evidence
Deletion of yeast-zap1 increased yeast sensitivity to allicin.
Saccharomyces cerevisiae zinc-responsive transcription factor / Zap1 → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae zinc-responsive transcription factor / Zap1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "yeast-zap1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-zap1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-zap1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
plain_language
Deletion of yeast-zap1 increased yeast sensitivity to allicin.
primary_references
A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · Recorded from source · Recorded from source
**Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
Complete structured claim and evidence
Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.
Copper(II) ion → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Same sensitized yeast with allicin without added metal added in relevant mutant background · Copper(II) ion Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same sensitized yeast with allicin without added metal present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Metal addition to the corresponding sensitized allicin-exposed yeast", "comparator": "Same sensitized yeast with allicin without added metal", "endpoint": "Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "copper-ii", "state": "added in relevant mutant background"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Abstract reports copper/zinc rescue but does not provide all strain-specific values. No human mineral-deficiency or supplementation claim.
plain_language
Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.
primary_references
A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted. · Recorded from source · Recorded from source
**Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
Complete structured claim and evidence
Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.
Zinc(II) ion → Saccharomyces cerevisiae growth during allicin exposure Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Same sensitized yeast with allicin without added metal added in relevant mutant background · Zinc(II) ion Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same sensitized yeast with allicin without added metal present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Metal addition to the corresponding sensitized allicin-exposed yeast", "comparator": "Same sensitized yeast with allicin without added metal", "endpoint": "Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "zinc-ion", "state": "added in relevant mutant background"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Abstract reports copper/zinc rescue but does not provide all strain-specific values. No human mineral-deficiency or supplementation claim.
plain_language
Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.
primary_references
A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted. · Recorded from source · Recorded from source
**Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
Complete structured claim and evidence
Allicin inhibited growth of tested bacterial isolates with substantial strain and assay variation.
Allicin → Growth of the tested bacterial isolates exposed to allicin Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin exposure", "comparator": "Matched bacterial assay control", "endpoint": "Allicin inhibited growth of tested bacterial isolates with substantial strain and assay variation.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
In vitro clinical-isolate panel; liquid/vapor observations; primary full-text results.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not an organism-independent MIC, clinical infection therapy, or safe inhaled exposure.
plain_language
Allicin inhibited growth of tested bacterial isolates with substantial strain and assay variation.
primary_references
Diallylthiosulfinate (Allicin), a Volatile Antimicrobial from Garlic (Allium sativum), Kills Human Lung Pathogenic Bacteria, Including MDR Strains, as a Vapor. | 2017 | DOI 10.3390/molecules22101711 | PMID 29023413 | https://pubmed.ncbi.nlm.nih.gov/29023413/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6151386/ | https://doi.org/10.3390/molecules22101711
source_locator
Reviewed reference lines 65-65; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 65–65
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · In vitro clinical-isolate panel; liquid/vapor observations; primary full-text results. · Recorded from source · Recorded from source
**Laboratory antimicrobial activity.** Purified allicin inhibited multiple tested respiratory bacterial isolates, including some resistant to clinical antibiotics; susceptibility varied by organism and assay. The same investigation measured mammalian-cell and rat-lung-slice toxicity. Added glutathione reduced toxicity in those models. The experimental 1-mM glutathione condition must not be presented as a validated normal plasma concentration or a safe inhalation regimen. Luminal or surface accessibility is a hypothesis about delivery, not a calculation proving efficacy from nominal dose divided by fluid volume. [Reiter 2017](https://pmc.ncbi.nlm.nih.gov/articles/PMC6151386/)
Complete structured claim and evidence
Added extracellular glutathione reduced injury from allicin in Human A549/Beas-2B epithelial cultures.
GSH → Allicin injury in human A549 and Beas-2B cultures Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Same allicin exposure without added GSH present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same allicin exposure without added GSH added extracellularly · GSH Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Allicin plus 1 mM extracellular GSH", "comparator": "Same allicin exposure without added GSH", "endpoint": "Added extracellular glutathione reduced injury from allicin in Human A549/Beas-2B epithelial cultures.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "glutathione", "state": "added extracellularly"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human A549/Beas-2B epithelial cultures; 1 mM extracellular GSH, direct allicin exposure; metabolic/LDH assays.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Quenching changes free exposure; it is not proof of intracellular repair or a validated physiological plasma GSH level.
plain_language
Added extracellular glutathione reduced injury from allicin in Human A549/Beas-2B epithelial cultures.
primary_references
Diallylthiosulfinate (Allicin), a Volatile Antimicrobial from Garlic (Allium sativum), Kills Human Lung Pathogenic Bacteria, Including MDR Strains, as a Vapor. | 2017 | DOI 10.3390/molecules22101711 | PMID 29023413 | https://pubmed.ncbi.nlm.nih.gov/29023413/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6151386/ | https://doi.org/10.3390/molecules22101711
source_locator
Reviewed reference lines 65-65; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 65–65
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human A549/Beas-2B epithelial cultures; 1 mM extracellular GSH, direct allicin exposure; metabolic/LDH assays. · Recorded from source · Recorded from source
**Laboratory antimicrobial activity.** Purified allicin inhibited multiple tested respiratory bacterial isolates, including some resistant to clinical antibiotics; susceptibility varied by organism and assay. The same investigation measured mammalian-cell and rat-lung-slice toxicity. Added glutathione reduced toxicity in those models. The experimental 1-mM glutathione condition must not be presented as a validated normal plasma concentration or a safe inhalation regimen. Luminal or surface accessibility is a hypothesis about delivery, not a calculation proving efficacy from nominal dose divided by fluid volume. [Reiter 2017](https://pmc.ncbi.nlm.nih.gov/articles/PMC6151386/)
Complete structured claim and evidence
Added extracellular glutathione reduced injury from allicin in Rat precision-cut lung slices.
GSH → Allicin injury in rat precision-cut lung slices Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Same allicin exposure without added GSH present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same allicin exposure without added GSH added extracellularly · GSH Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Allicin plus 1 mM extracellular GSH", "comparator": "Same allicin exposure without added GSH", "endpoint": "Added extracellular glutathione reduced injury from allicin in Rat precision-cut lung slices.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "glutathione", "state": "added extracellularly"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat precision-cut lung slices; 1 mM extracellular GSH, direct allicin exposure; metabolic/LDH assays.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Quenching changes free exposure; it is not proof of intracellular repair or a validated physiological plasma GSH level.
plain_language
Added extracellular glutathione reduced injury from allicin in Rat precision-cut lung slices.
primary_references
Diallylthiosulfinate (Allicin), a Volatile Antimicrobial from Garlic (Allium sativum), Kills Human Lung Pathogenic Bacteria, Including MDR Strains, as a Vapor. | 2017 | DOI 10.3390/molecules22101711 | PMID 29023413 | https://pubmed.ncbi.nlm.nih.gov/29023413/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6151386/ | https://doi.org/10.3390/molecules22101711
source_locator
Reviewed reference lines 65-65; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 65–65
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat precision-cut lung slices; 1 mM extracellular GSH, direct allicin exposure; metabolic/LDH assays. · Recorded from source · Recorded from source
**Laboratory antimicrobial activity.** Purified allicin inhibited multiple tested respiratory bacterial isolates, including some resistant to clinical antibiotics; susceptibility varied by organism and assay. The same investigation measured mammalian-cell and rat-lung-slice toxicity. Added glutathione reduced toxicity in those models. The experimental 1-mM glutathione condition must not be presented as a validated normal plasma concentration or a safe inhalation regimen. Luminal or surface accessibility is a hypothesis about delivery, not a calculation proving efficacy from nominal dose divided by fluid volume. [Reiter 2017](https://pmc.ncbi.nlm.nih.gov/articles/PMC6151386/)
Complete structured claim and evidence
Naturally adapted Pseudomonas isolates demonstrated resistance to allicin associated with multicomponent redox defenses.
Allicin → Observed allicin resistance in naturally adapted Pseudomonas isolates Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Naturally isolated bacteria and laboratory characterization; no clinical resistance prevalence estimate.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Broad targeting does not make resistance impossible. This is an observed resistance limitation, not an increase in resistance caused by oral garlic.
plain_language
Naturally adapted Pseudomonas isolates demonstrated resistance to allicin associated with multicomponent redox defenses.
primary_references
Genetic and molecular characterization of multicomponent resistance of Pseudomonas against allicin. | 2020 | DOI 10.26508/lsa.202000670 | PMID 32234751 | https://pubmed.ncbi.nlm.nih.gov/32234751/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7119367/ | https://doi.org/10.26508/lsa.202000670
source_locator
Reviewed reference lines 67-67; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 67–67
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Naturally isolated bacteria and laboratory characterization; no clinical resistance prevalence estimate. · Recorded from source · Recorded from source
**Resistance exists.** Naturally allicin-resistant Pseudomonas isolates and multicomponent redox defenses were characterized. Broad thiol targeting does not require an organism to replace every susceptible cysteine before resistance can occur. Resistance and variation between strains limit generalization from susceptibility assays. Laboratory findings also do not establish allicin as a clinical treatment for H. pylori, parasites, or an altered microbiome. [Borlinghaus 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7119367/)
Complete structured claim and evidence
Allicin engaged the mouse-trpa1-dependent sensory response in mouse channel-loss and neuronal experiments.
Allicin → Mouse Trpa1 ion channel Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Mouse DRG neurons and pain-related behavior; separate single-channel knockout comparisons.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Participation supported by converging comparisons; the other channel still contributes. Not direct chemical adduct identification in vivo.
plain_language
Allicin engaged the mouse-trpa1-dependent sensory response in mouse channel-loss and neuronal experiments.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse DRG neurons and pain-related behavior; separate single-channel knockout comparisons. · Recorded from source · Recorded from source
**Sensory activation.** Experiments identified allicin-dependent activation of TRPA1 and TRPV1. In the later mouse study, allicin stimulated dorsal-root-ganglion neurons and pain-related behavior. Removing either Trpa1 or Trpv1 reduced, but did not abolish, the behavioral response. The channels provide overlapping sensory routes rather than one exclusive receptor. Irritation, chemical burns, and allergic dermatitis are different outcomes. [Macpherson 2005](https://pubmed.ncbi.nlm.nih.gov/15916949/) [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.
Mouse Trpa1 ion channel → Mouse pain-related behavior after allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Wild-type with the same allicin exposure deleted · Mouse Trpa1 ion channel Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Wild-type with the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "mouse-trpa1 deletion with allicin", "comparator": "Wild-type with the same allicin exposure", "endpoint": "Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "mouse-trpa1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse single-gene knockout compared with its wild-type littermate background.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No double-knockout inference; behavioral assay, not proof of human allergy or burns.
plain_language
Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse single-gene knockout compared with its wild-type littermate background. · Recorded from source · Recorded from source
**Sensory activation.** Experiments identified allicin-dependent activation of TRPA1 and TRPV1. In the later mouse study, allicin stimulated dorsal-root-ganglion neurons and pain-related behavior. Removing either Trpa1 or Trpv1 reduced, but did not abolish, the behavioral response. The channels provide overlapping sensory routes rather than one exclusive receptor. Irritation, chemical burns, and allergic dermatitis are different outcomes. [Macpherson 2005](https://pubmed.ncbi.nlm.nih.gov/15916949/) [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
Allicin engaged the mouse-trpv1-dependent sensory response in mouse channel-loss and neuronal experiments.
Allicin → Mouse transient receptor potential vanilloid 1 / Trpv1 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Mouse DRG neurons and pain-related behavior; separate single-channel knockout comparisons.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Participation supported by converging comparisons; the other channel still contributes. Not direct chemical adduct identification in vivo.
plain_language
Allicin engaged the mouse-trpv1-dependent sensory response in mouse channel-loss and neuronal experiments.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse DRG neurons and pain-related behavior; separate single-channel knockout comparisons. · Recorded from source · Recorded from source
**Sensory activation.** Experiments identified allicin-dependent activation of TRPA1 and TRPV1. In the later mouse study, allicin stimulated dorsal-root-ganglion neurons and pain-related behavior. Removing either Trpa1 or Trpv1 reduced, but did not abolish, the behavioral response. The channels provide overlapping sensory routes rather than one exclusive receptor. Irritation, chemical burns, and allergic dermatitis are different outcomes. [Macpherson 2005](https://pubmed.ncbi.nlm.nih.gov/15916949/) [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.
Mouse transient receptor potential vanilloid 1 / Trpv1 → Mouse pain-related behavior after allicin exposure Recorded from sourceungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Wild-type with the same allicin exposure deleted · Mouse transient receptor potential vanilloid 1 / Trpv1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Wild-type with the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "mouse-trpv1 deletion with allicin", "comparator": "Wild-type with the same allicin exposure", "endpoint": "Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "mouse-trpv1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse single-gene knockout compared with its wild-type littermate background.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No double-knockout inference; behavioral assay, not proof of human allergy or burns.
plain_language
Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse single-gene knockout compared with its wild-type littermate background. · Recorded from source · Recorded from source
**Sensory activation.** Experiments identified allicin-dependent activation of TRPA1 and TRPV1. In the later mouse study, allicin stimulated dorsal-root-ganglion neurons and pain-related behavior. Removing either Trpa1 or Trpv1 reduced, but did not abolish, the behavioral response. The channels provide overlapping sensory routes rather than one exclusive receptor. Irritation, chemical burns, and allergic dermatitis are different outcomes. [Macpherson 2005](https://pubmed.ncbi.nlm.nih.gov/15916949/) [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
Allicin activated rat TRPV1 expressed in HEK293 membrane patches.
Allicin → Allicin-evoked current through rat TRPV1 in HEK293 patches Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Allicin exposure", "comparator": "Patch before allicin", "endpoint": "Allicin activated rat TRPV1 expressed in HEK293 membrane patches.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat TRPV1 construct in human HEK293 host cells; inside-out patch recordings.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Allicin activated rat TRPV1 expressed in HEK293 membrane patches.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat TRPV1 construct in human HEK293 host cells; inside-out patch recordings. · Recorded from source · Recorded from source
**A tested TRPV1 cysteine.** In rat TRPV1 expressed in HEK293 cells, the C157A substitution eliminated allicin responsiveness; reinserting C157 into a cysteine-less construct restored it. Capsaicin responsiveness persisted in the relevant mutant controls. A reducing agent reversed activation. This is direct functional evidence for a cysteine-dependent activation mechanism in that construct, not proof that every electrophile makes the same adduct or that the cell line makes the protein human. [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
The rat-trpv1-c157a construct did not show allicin responsiveness while relevant capsaicin responses persisted.
Allicin → Allicin-evoked current through rat TRPV1 in HEK293 patches Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Same mutant patch before allicin expressed · Rat TRPV1 C157A experimental construct Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same mutant patch before allicin applied · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Allicin applied to rat-trpv1-c157a", "comparator": "Same mutant patch before allicin", "endpoint": "The rat-trpv1-c157a construct did not show allicin responsiveness while relevant capsaicin responses persisted.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "rat-trpv1-c157a", "state": "expressed"}, {"entity_slug": "allicin", "state": "applied"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat channel variant expressed in HEK293; Figure 8 functional comparison.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No response to allicin, not nonfunctional protein. Human homolog residue numbers are not silently assigned.
plain_language
The rat-trpv1-c157a construct did not show allicin responsiveness while relevant capsaicin responses persisted.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat channel variant expressed in HEK293; Figure 8 functional comparison. · Recorded from source · Recorded from source
**A tested TRPV1 cysteine.** In rat TRPV1 expressed in HEK293 cells, the C157A substitution eliminated allicin responsiveness; reinserting C157 into a cysteine-less construct restored it. Capsaicin responsiveness persisted in the relevant mutant controls. A reducing agent reversed activation. This is direct functional evidence for a cysteine-dependent activation mechanism in that construct, not proof that every electrophile makes the same adduct or that the cell line makes the protein human. [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
The rat-trpv1-cysteine-less construct did not show allicin responsiveness while relevant capsaicin responses persisted.
Allicin → Allicin-evoked current through rat TRPV1 in HEK293 patches Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Same mutant patch before allicin applied · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same mutant patch before allicin expressed · Rat TRPV1 cysteine-less experimental construct Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Allicin applied to rat-trpv1-cysteine-less", "comparator": "Same mutant patch before allicin", "endpoint": "The rat-trpv1-cysteine-less construct did not show allicin responsiveness while relevant capsaicin responses persisted.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "rat-trpv1-cysteine-less", "state": "expressed"}, {"entity_slug": "allicin", "state": "applied"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat channel variant expressed in HEK293; Figure 8 functional comparison.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No response to allicin, not nonfunctional protein. Human homolog residue numbers are not silently assigned.
plain_language
The rat-trpv1-cysteine-less construct did not show allicin responsiveness while relevant capsaicin responses persisted.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat channel variant expressed in HEK293; Figure 8 functional comparison. · Recorded from source · Recorded from source
**A tested TRPV1 cysteine.** In rat TRPV1 expressed in HEK293 cells, the C157A substitution eliminated allicin responsiveness; reinserting C157 into a cysteine-less construct restored it. Capsaicin responsiveness persisted in the relevant mutant controls. A reducing agent reversed activation. This is direct functional evidence for a cysteine-dependent activation mechanism in that construct, not proof that every electrophile makes the same adduct or that the cell line makes the protein human. [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
Restoring C157 to the cysteine-less rat TRPV1 construct restored responsiveness to allicin.
Allicin → Allicin-evoked current through rat TRPV1 in HEK293 patches Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Cysteine-less construct at corresponding allicin exposure applied · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Cysteine-less construct at corresponding allicin exposure expressed · Rat TRPV1 cysteine-less construct with C157 restored Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Allicin applied to C157-restored construct", "comparator": "Cysteine-less construct at corresponding allicin exposure", "endpoint": "Restoring C157 to the cysteine-less rat TRPV1 construct restored responsiveness to allicin.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "rat-trpv1-c157-only", "state": "expressed"}, {"entity_slug": "allicin", "state": "applied"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat TRPV1 C157-only construct in HEK293; Figure 8.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Restoring C157 to the cysteine-less rat TRPV1 construct restored responsiveness to allicin.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat TRPV1 C157-only construct in HEK293; Figure 8. · Recorded from source · Recorded from source
**A tested TRPV1 cysteine.** In rat TRPV1 expressed in HEK293 cells, the C157A substitution eliminated allicin responsiveness; reinserting C157 into a cysteine-less construct restored it. Capsaicin responsiveness persisted in the relevant mutant controls. A reducing agent reversed activation. This is direct functional evidence for a cysteine-dependent activation mechanism in that construct, not proof that every electrophile makes the same adduct or that the cell line makes the protein human. [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
A reducing agent reversed allicin-evoked TRPV1 activation in the patch assay.
Dithiothreitol / DTT → Allicin-evoked current through rat TRPV1 in HEK293 patches Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Allicin-activated channel before DTT prior exposure · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Allicin-activated channel before DTT added · Dithiothreitol / DTT Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "DTT after allicin", "comparator": "Allicin-activated channel before DTT", "endpoint": "A reducing agent reversed allicin-evoked TRPV1 activation in the patch assay.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "dithiothreitol", "state": "added"}, {"entity_slug": "allicin", "state": "prior exposure"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat TRPV1 in HEK293; DTT addition after allicin exposure.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Experimental reducing agent, not an oral treatment recommendation.
plain_language
A reducing agent reversed allicin-evoked TRPV1 activation in the patch assay.
primary_references
A single N-terminal cysteine in TRPV1 determines activation by pungent compounds from onion and garlic. | 2008 | DOI 10.1038/nn2056 | PMID 18297068 | https://pubmed.ncbi.nlm.nih.gov/18297068/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/ | https://doi.org/10.1038/nn2056
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat TRPV1 in HEK293; DTT addition after allicin exposure. · Recorded from source · Recorded from source
**A tested TRPV1 cysteine.** In rat TRPV1 expressed in HEK293 cells, the C157A substitution eliminated allicin responsiveness; reinserting C157 into a cysteine-less construct restored it. Capsaicin responsiveness persisted in the relevant mutant controls. A reducing agent reversed activation. This is direct functional evidence for a cysteine-dependent activation mechanism in that construct, not proof that every electrophile makes the same adduct or that the cell line makes the protein human. [Salazar 2008](https://pmc.ncbi.nlm.nih.gov/articles/PMC4370189/)
Complete structured claim and evidence
The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.
Allyl isothiocyanate / AITC → GLP-1 secretion in mouse intestinal cultures Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "allyl-isothiocyanate", "comparator": "Matched culture vehicle", "endpoint": "The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
This experiment did not test allicin. Shared receptor identity is a research connection, not transferred efficacy.
plain_language
The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.
primary_references
Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay. · Recorded from source · Recorded from source
**The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
Complete structured claim and evidence
The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.
Carvacrol → GLP-1 secretion in mouse intestinal cultures Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "carvacrol", "comparator": "Matched culture vehicle", "endpoint": "The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
This experiment did not test allicin. Shared receptor identity is a research connection, not transferred efficacy.
plain_language
The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.
primary_references
Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay. · Recorded from source · Recorded from source
**The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
Complete structured claim and evidence
Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.
D-glucose → Calcium signaling in mouse intestinal L cells Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Glucose response without antagonist pharmacologically blocked · Mouse Trpa1 ion channel Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Glucose response without antagonist stimulus · D-glucose Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Glucose response with TRPA1 antagonist", "comparator": "Glucose response without antagonist", "endpoint": "Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "glucose", "state": "stimulus"}, {"entity_slug": "mouse-trpa1", "state": "pharmacologically blocked"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse primary L cells; 10 mM glucose with or without A-967079.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No loss of glucose response in this assay; not a general role for allicin in glycemic control.
plain_language
Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.
primary_references
Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse primary L cells; 10 mM glucose with or without A-967079. · Recorded from source · Recorded from source
**The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
Complete structured claim and evidence
Oral AITC raised GLP-1 in both wild-type and Trpa1-null mice; the response was not reduced by Trpa1 loss.
Allyl isothiocyanate / AITC → Mouse plasma GLP-1 response Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
AITC in wild-type mice deleted · Mouse Trpa1 ion channel Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
AITC in wild-type mice administered · Allyl isothiocyanate / AITC Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "AITC in Trpa1-null mice", "comparator": "AITC in wild-type mice", "endpoint": "Oral AITC raised GLP-1 in both wild-type and Trpa1-null mice; the response was not reduced by Trpa1 loss.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "allyl-isothiocyanate", "state": "administered"}, {"entity_slug": "mouse-trpa1", "state": "deleted"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse oral AITC 15 mg/kg; plasma measurement at five minutes.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
The null concerns genotype effect; AITC increased GLP-1 versus vehicle. Does not prove TRPA1 mediation in vivo.
plain_language
Oral AITC raised GLP-1 in both wild-type and Trpa1-null mice; the response was not reduced by Trpa1 loss.
primary_references
Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse oral AITC 15 mg/kg; plasma measurement at five minutes. · Recorded from source · Recorded from source
**The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
Complete structured claim and evidence
Lower oral AITC doses did not significantly increase plasma GLP-1 in the tested mice.
Allyl isothiocyanate / AITC → Mouse plasma GLP-1 response Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Lower-dose AITC", "comparator": "Vehicle", "endpoint": "Lower oral AITC doses did not significantly increase plasma GLP-1 in the tested mice.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse oral 0.15 and 1.5 mg/kg AITC; five-minute measurement.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
AITC-specific short-term null; no allicin conclusion.
plain_language
Lower oral AITC doses did not significantly increase plasma GLP-1 in the tested mice.
primary_references
Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse oral 0.15 and 1.5 mg/kg AITC; five-minute measurement. · Recorded from source · Recorded from source
**The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
Complete structured claim and evidence
Capsaicin did not increase GLP-1 secretion in the tested mouse intestinal and GLUTag cultures.
Capsaicin → GLP-1 secretion in mouse intestinal cultures Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Capsaicin", "comparator": "Matched basal culture", "endpoint": "Capsaicin did not increase GLP-1 secretion in the tested mouse intestinal and GLUTag cultures.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Capsaicin 100 nM, two-hour secretion assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No generic TRPV1-to-GLP-1 effect inferred; no allicin exposure in this experiment.
plain_language
Capsaicin did not increase GLP-1 secretion in the tested mouse intestinal and GLUTag cultures.
primary_references
Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Capsaicin 100 nM, two-hour secretion assay. · Recorded from source · Recorded from source
**The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
Complete structured claim and evidence
Glucose sustained sulfide production during repeated garlic-juice exposures in isolated human erythrocytes.
D-glucose → Garlic-dependent sulfide production by isolated human erythrocytes Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Garlic juice without glucose present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Garlic juice without glucose present · D-glucose Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Garlic juice with glucose", "comparator": "Garlic juice without glucose", "endpoint": "Glucose sustained sulfide production during repeated garlic-juice exposures in isolated human erythrocytes.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "glucose", "state": "present"}, {"entity_slug": "garlic-juice-benavides-2007", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Isolated human RBCs, oxygen-controlled/anoxic assay, repeated garlic additions with or without 10 mM glucose.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Ex vivo resource dependence; not a glucose-intake recommendation or selective G6PD/B2 experiment.
plain_language
Glucose sustained sulfide production during repeated garlic-juice exposures in isolated human erythrocytes.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 79-79; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 79–79
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Isolated human RBCs, oxygen-controlled/anoxic assay, repeated garlic additions with or without 10 mM glucose. · Recorded from source · Recorded from source
**Glucose and erythrocyte redox state.** In isolated human erythrocytes, glucose sustained sulfide production during repeated garlic-juice exposures. Without glucose, production capacity declined and the GSH/GSSG balance shifted despite conserved total glutathione equivalents. This is a resource-dependent ex vivo observation. NADPH production through the pentose-phosphate pathway was a proposed explanation, not a selective G6PD perturbation or proof of a B2-dependent clinical response. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
Without glucose, garlic exposure decreased the reduced-to-oxidized GSH balance while conserving total glutathione equivalents.
Garlic juice tested in the 2007 erythrocyte and vessel study → Erythrocyte GSH/GSSG balance during garlic-juice exposure Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Garlic exposure with glucose present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Garlic exposure with glucose absent · D-glucose Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Garlic exposure without glucose", "comparator": "Garlic exposure with glucose", "endpoint": "Without glucose, garlic exposure decreased the reduced-to-oxidized GSH balance while conserving total glutathione equivalents.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "garlic-juice-benavides-2007", "state": "present"}, {"entity_slug": "glucose", "state": "absent"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human RBC biochemical measurements; matched glucose conditions.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Redox balance change, not disappearance of all sulfur or proven nutrient deficiency in a patient.
plain_language
Without glucose, garlic exposure decreased the reduced-to-oxidized GSH balance while conserving total glutathione equivalents.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 79-79; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 79–79
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human RBC biochemical measurements; matched glucose conditions. · Recorded from source · Recorded from source
**Glucose and erythrocyte redox state.** In isolated human erythrocytes, glucose sustained sulfide production during repeated garlic-juice exposures. Without glucose, production capacity declined and the GSH/GSSG balance shifted despite conserved total glutathione equivalents. This is a resource-dependent ex vivo observation. NADPH production through the pentose-phosphate pathway was a proposed explanation, not a selective G6PD perturbation or proof of a B2-dependent clinical response. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
The tested thiol glutathione supported sulfide generation with garlic juice in a cell-free assay.
GSH → Garlic-associated sulfide generation in cell-free thiol assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Garlic juice in buffer without reducing thiol present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Garlic juice in buffer without reducing thiol present · GSH Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "glutathione plus garlic juice", "comparator": "Garlic juice in buffer without reducing thiol", "endpoint": "The tested thiol glutathione supported sulfide generation with garlic juice in a cell-free assay.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "glutathione", "state": "present"}, {"entity_slug": "garlic-juice-benavides-2007", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Alternative thiols are not equivalent in rate/yield. NAC directly participates, so it is not a selective intracellular-GSH manipulation.
plain_language
The tested thiol glutathione supported sulfide generation with garlic juice in a cell-free assay.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay. · Recorded from source · Recorded from source
**Alternative thiols and the vascular null.** GSH, cysteine, homocysteine, and NAC each supported garlic-associated sulfide generation in cell-free assays. In rat aortic rings, added GSH aided detectable sulfide production, but its omission did not significantly alter the tested polysulfide-induced relaxation. Membrane and intracellular thiols therefore matter alongside the added reagent. NAC is a direct participant in this chemistry, not a selective way to raise cellular GSH. Results in deoxygenated red-cell assays and oxygen-controlled rat vessels are not human oral pharmacokinetics. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
The tested thiol l-cysteine supported sulfide generation with garlic juice in a cell-free assay.
L-Cysteine → Garlic-associated sulfide generation in cell-free thiol assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Garlic juice in buffer without reducing thiol present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Garlic juice in buffer without reducing thiol present · L-Cysteine Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "l-cysteine plus garlic juice", "comparator": "Garlic juice in buffer without reducing thiol", "endpoint": "The tested thiol l-cysteine supported sulfide generation with garlic juice in a cell-free assay.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "l-cysteine", "state": "present"}, {"entity_slug": "garlic-juice-benavides-2007", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Alternative thiols are not equivalent in rate/yield. NAC directly participates, so it is not a selective intracellular-GSH manipulation.
plain_language
The tested thiol l-cysteine supported sulfide generation with garlic juice in a cell-free assay.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay. · Recorded from source · Recorded from source
**Alternative thiols and the vascular null.** GSH, cysteine, homocysteine, and NAC each supported garlic-associated sulfide generation in cell-free assays. In rat aortic rings, added GSH aided detectable sulfide production, but its omission did not significantly alter the tested polysulfide-induced relaxation. Membrane and intracellular thiols therefore matter alongside the added reagent. NAC is a direct participant in this chemistry, not a selective way to raise cellular GSH. Results in deoxygenated red-cell assays and oxygen-controlled rat vessels are not human oral pharmacokinetics. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
The tested thiol homocysteine supported sulfide generation with garlic juice in a cell-free assay.
Homocysteine → Garlic-associated sulfide generation in cell-free thiol assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Garlic juice in buffer without reducing thiol present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Garlic juice in buffer without reducing thiol present · Homocysteine Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "homocysteine plus garlic juice", "comparator": "Garlic juice in buffer without reducing thiol", "endpoint": "The tested thiol homocysteine supported sulfide generation with garlic juice in a cell-free assay.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "homocysteine", "state": "present"}, {"entity_slug": "garlic-juice-benavides-2007", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Alternative thiols are not equivalent in rate/yield. NAC directly participates, so it is not a selective intracellular-GSH manipulation.
plain_language
The tested thiol homocysteine supported sulfide generation with garlic juice in a cell-free assay.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay. · Recorded from source · Recorded from source
**Alternative thiols and the vascular null.** GSH, cysteine, homocysteine, and NAC each supported garlic-associated sulfide generation in cell-free assays. In rat aortic rings, added GSH aided detectable sulfide production, but its omission did not significantly alter the tested polysulfide-induced relaxation. Membrane and intracellular thiols therefore matter alongside the added reagent. NAC is a direct participant in this chemistry, not a selective way to raise cellular GSH. Results in deoxygenated red-cell assays and oxygen-controlled rat vessels are not human oral pharmacokinetics. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
The tested thiol n-acetylcysteine supported sulfide generation with garlic juice in a cell-free assay.
N-Acetyl-L-cysteine → Garlic-associated sulfide generation in cell-free thiol assays Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Garlic juice in buffer without reducing thiol present · Garlic juice tested in the 2007 erythrocyte and vessel study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Garlic juice in buffer without reducing thiol present · N-Acetyl-L-cysteine Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "n-acetylcysteine plus garlic juice", "comparator": "Garlic juice in buffer without reducing thiol", "endpoint": "The tested thiol n-acetylcysteine supported sulfide generation with garlic juice in a cell-free assay.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "n-acetylcysteine", "state": "present"}, {"entity_slug": "garlic-juice-benavides-2007", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Alternative thiols are not equivalent in rate/yield. NAC directly participates, so it is not a selective intracellular-GSH manipulation.
plain_language
The tested thiol n-acetylcysteine supported sulfide generation with garlic juice in a cell-free assay.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Cell-free 2 mM thiol with garlic juice; pH 7.35, 37 C, low-oxygen assay. · Recorded from source · Recorded from source
**Alternative thiols and the vascular null.** GSH, cysteine, homocysteine, and NAC each supported garlic-associated sulfide generation in cell-free assays. In rat aortic rings, added GSH aided detectable sulfide production, but its omission did not significantly alter the tested polysulfide-induced relaxation. Membrane and intracellular thiols therefore matter alongside the added reagent. NAC is a direct participant in this chemistry, not a selective way to raise cellular GSH. Results in deoxygenated red-cell assays and oxygen-controlled rat vessels are not human oral pharmacokinetics. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
Omission of added GSH did not significantly alter the tested polysulfide-induced rat aortic relaxation.
GSH → Rat aortic-ring relaxation in the garlic-polysulfide study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_condition
Same tested polysulfide with added GSH one tested donor · Diallyl trisulfide / DATS Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Same tested polysulfide with added GSH no exogenous addition · GSH Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Polysulfide exposure without added GSH", "comparator": "Same tested polysulfide with added GSH", "endpoint": "Omission of added GSH did not significantly alter the tested polysulfide-induced rat aortic relaxation.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "glutathione", "state": "no exogenous addition"}, {"entity_slug": "diallyl-trisulfide", "state": "one tested donor"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat aortic rings; Figure 3E, DATS/DPDS comparisons with and without 1 mM added GSH.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Omitting added GSH does not remove endogenous vascular thiols. Null is relaxation, not sulfide generation; no clinical glutathione gate.
plain_language
Omission of added GSH did not significantly alter the tested polysulfide-induced rat aortic relaxation.
primary_references
Hydrogen sulfide mediates the vasoactivity of garlic. | 2007 | DOI 10.1073/pnas.0705710104 | PMID 17951430 | https://pubmed.ncbi.nlm.nih.gov/17951430/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/ | https://doi.org/10.1073/pnas.0705710104
source_locator
Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat aortic rings; Figure 3E, DATS/DPDS comparisons with and without 1 mM added GSH. · Recorded from source · Recorded from source
**Alternative thiols and the vascular null.** GSH, cysteine, homocysteine, and NAC each supported garlic-associated sulfide generation in cell-free assays. In rat aortic rings, added GSH aided detectable sulfide production, but its omission did not significantly alter the tested polysulfide-induced relaxation. Membrane and intracellular thiols therefore matter alongside the added reagent. NAC is a direct participant in this chemistry, not a selective way to raise cellular GSH. Results in deoxygenated red-cell assays and oxygen-controlled rat vessels are not human oral pharmacokinetics. [Benavides 2007](https://pmc.ncbi.nlm.nih.gov/articles/PMC2084282/)
Complete structured claim and evidence
DATS reacted rapidly with GSH to release sulfide through the reported exchange and perthiol-reduction chemistry.
Diallyl trisulfide / DATS → Sulfide generation in the DATS plus GSH chemical assay Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Purified-compound chemical study; abstract-level access.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
DATS-specific; no automatic transfer to allicin, DADS, aged extract, or human blood-pressure response.
plain_language
DATS reacted rapidly with GSH to release sulfide through the reported exchange and perthiol-reduction chemistry.
primary_references
Diallyl Trisulfide Is a Fast H2S Donor, but Diallyl Disulfide Is a Slow One: The Reaction Pathways and Intermediates of Glutathione with Polysulfides. | 2015 | DOI 10.1021/acs.orglett.5b01962 | PMID 26301500 | https://pubmed.ncbi.nlm.nih.gov/26301500/ | https://doi.org/10.1021/acs.orglett.5b01962
source_locator
Reviewed reference lines 83-83; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 83–83
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified-compound chemical study; abstract-level access. · Recorded from source · Recorded from source
**DATS and DADS differ.** A later chemical study found rapid GSH-dependent sulfide release from DATS, involving an allyl-perthiol intermediate, but very little and slow release from DADS. DATS contamination could account for fast release attributed to DADS. Sulfur-chain length, purity, and reaction conditions belong in the record. This qualifies older attribution without deleting either observation; it does not establish that allicin or aged garlic extract has the same behavior. [Liang 2015](https://pubmed.ncbi.nlm.nih.gov/26301500/)
Complete structured claim and evidence
Purified DADS released only a small amount of sulfide slowly with GSH; DATS impurity can explain apparent rapid DADS release.
Diallyl disulfide / DADS → Sulfide generation in the DADS plus GSH chemical assay Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Purified-compound comparison; source-specific purity interpretation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Slow/minute is not zero. Historical observations remain preserved with purity qualification, not erased as fictional experiments.
plain_language
Purified DADS released only a small amount of sulfide slowly with GSH; DATS impurity can explain apparent rapid DADS release.
primary_references
Diallyl Trisulfide Is a Fast H2S Donor, but Diallyl Disulfide Is a Slow One: The Reaction Pathways and Intermediates of Glutathione with Polysulfides. | 2015 | DOI 10.1021/acs.orglett.5b01962 | PMID 26301500 | https://pubmed.ncbi.nlm.nih.gov/26301500/ | https://doi.org/10.1021/acs.orglett.5b01962
source_locator
Reviewed reference lines 83-83; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 83–83
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Purified-compound comparison; source-specific purity interpretation. · Recorded from source · Recorded from source
**DATS and DADS differ.** A later chemical study found rapid GSH-dependent sulfide release from DATS, involving an allyl-perthiol intermediate, but very little and slow release from DADS. DATS contamination could account for fast release attributed to DADS. Sulfur-chain length, purity, and reaction conditions belong in the record. This qualifies older attribution without deleting either observation; it does not establish that allicin or aged garlic extract has the same behavior. [Liang 2015](https://pubmed.ncbi.nlm.nih.gov/26301500/)
Complete structured claim and evidence
AGE at Heart reported an approximately 5.0 +/- 2.1 mmHg placebo-adjusted systolic reduction in the full analysis group.
Aged garlic extract in AGE at Heart 2016 → Systolic blood pressure Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Specified aged garlic extract", "comparator": "Placebo", "endpoint": "AGE at Heart reported an approximately 5.0 +/- 2.1 mmHg placebo-adjusted systolic reduction in the full analysis group.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
1.2 g/day AGE containing 1.2 mg SAC, 12 weeks; 88 analyzed after seven completer exclusions.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not purified allicin; selected responders are not the overall randomized comparison; no established sulfide mediator.
plain_language
AGE at Heart reported an approximately 5.0 +/- 2.1 mmHg placebo-adjusted systolic reduction in the full analysis group.
primary_references
The effect of aged garlic extract on blood pressure and other cardiovascular risk factors in uncontrolled hypertensives: the AGE at Heart trial. | 2016 | DOI 10.2147/ibpc.s93335 | PMID 26869811 | https://pubmed.ncbi.nlm.nih.gov/26869811/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4734812/ | https://doi.org/10.2147/ibpc.s93335
source_locator
Reviewed reference lines 89-89; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 89–89
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 1.2 g/day AGE containing 1.2 mg SAC, 12 weeks; 88 analyzed after seven completer exclusions. · Recorded from source · Recorded from source
**Blood pressure.** AGE at Heart tested 1.2 g/day aged garlic extract containing 1.2 mg SAC for twelve weeks. Ninety-five participants completed the trial; seven were excluded for protocol deviations, leaving eighty-eight in the full analysis. Mean placebo-adjusted systolic change was about −5.0 ± 2.1 mmHg. The overall diastolic difference was not significant (−1.9 ± 1.2 mmHg, P=0.12). Larger reductions in retrospectively defined responders do not replace the overall comparison. This was an extract trial, not purified allicin or proof of sulfide mediation. Manufacturer involvement and the analysis exclusions limit interpretation. [Ried 2016](https://pmc.ncbi.nlm.nih.gov/articles/PMC4734812/)
Complete structured claim and evidence
The overall diastolic difference in AGE at Heart was not significant: -1.9 +/- 1.2 mmHg, P=0.12.
Aged garlic extract in AGE at Heart 2016 → Diastolic blood pressure in the garlic trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Specified aged garlic extract", "comparator": "Placebo", "endpoint": "The overall diastolic difference in AGE at Heart was not significant: -1.9 +/- 1.2 mmHg, P=0.12.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Same 12-week trial and analysis group.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preserve alongside the systolic result; not universal lack of BP effect.
plain_language
The overall diastolic difference in AGE at Heart was not significant: -1.9 +/- 1.2 mmHg, P=0.12.
primary_references
The effect of aged garlic extract on blood pressure and other cardiovascular risk factors in uncontrolled hypertensives: the AGE at Heart trial. | 2016 | DOI 10.2147/ibpc.s93335 | PMID 26869811 | https://pubmed.ncbi.nlm.nih.gov/26869811/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4734812/ | https://doi.org/10.2147/ibpc.s93335
source_locator
Reviewed reference lines 89-89; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 89–89
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same 12-week trial and analysis group. · Recorded from source · Recorded from source
**Blood pressure.** AGE at Heart tested 1.2 g/day aged garlic extract containing 1.2 mg SAC for twelve weeks. Ninety-five participants completed the trial; seven were excluded for protocol deviations, leaving eighty-eight in the full analysis. Mean placebo-adjusted systolic change was about −5.0 ± 2.1 mmHg. The overall diastolic difference was not significant (−1.9 ± 1.2 mmHg, P=0.12). Larger reductions in retrospectively defined responders do not replace the overall comparison. This was an extract trial, not purified allicin or proof of sulfide mediation. Manufacturer involvement and the analysis exclusions limit interpretation. [Ried 2016](https://pmc.ncbi.nlm.nih.gov/articles/PMC4734812/)
Complete structured claim and evidence
The raw-garlic-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.
Raw garlic intervention in Gardner 2007 → LDL cholesterol in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "raw-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The raw-garlic-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The raw-garlic-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The raw-garlic-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.
Raw garlic intervention in Gardner 2007 → HDL cholesterol in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "raw-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The raw-garlic-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The raw-garlic-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The raw-garlic-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.
Raw garlic intervention in Gardner 2007 → Triglycerides in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "raw-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The raw-garlic-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The raw-garlic-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The raw-garlic-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.
Raw garlic intervention in Gardner 2007 → Total cholesterol to HDL ratio in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "raw-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The raw-garlic-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The raw-garlic-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The garlic-powder-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.
Garlic powder intervention in Gardner 2007 → LDL cholesterol in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "garlic-powder-gardner-2007", "comparator": "Placebo", "endpoint": "The garlic-powder-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The garlic-powder-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The garlic-powder-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.
Garlic powder intervention in Gardner 2007 → HDL cholesterol in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "garlic-powder-gardner-2007", "comparator": "Placebo", "endpoint": "The garlic-powder-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The garlic-powder-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The garlic-powder-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.
Garlic powder intervention in Gardner 2007 → Triglycerides in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "garlic-powder-gardner-2007", "comparator": "Placebo", "endpoint": "The garlic-powder-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The garlic-powder-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The garlic-powder-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.
Garlic powder intervention in Gardner 2007 → Total cholesterol to HDL ratio in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "garlic-powder-gardner-2007", "comparator": "Placebo", "endpoint": "The garlic-powder-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The garlic-powder-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The aged-garlic-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.
Aged garlic extract intervention in Gardner 2007 → LDL cholesterol in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "aged-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The aged-garlic-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The aged-garlic-gardner-2007 intervention did not significantly improve LDL cholesterol in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The aged-garlic-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.
Aged garlic extract intervention in Gardner 2007 → HDL cholesterol in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "aged-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The aged-garlic-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The aged-garlic-gardner-2007 intervention did not significantly improve HDL cholesterol in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The aged-garlic-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.
Aged garlic extract intervention in Gardner 2007 → Triglycerides in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "aged-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The aged-garlic-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The aged-garlic-gardner-2007 intervention did not significantly improve triglycerides in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The aged-garlic-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.
Aged garlic extract intervention in Gardner 2007 → Total cholesterol to HDL ratio in garlic intervention trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "aged-garlic-gardner-2007", "comparator": "Placebo", "endpoint": "The aged-garlic-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
192 adults randomized across four arms; clove-equivalent products six days/week for six months.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Preparation-specific human null; not an inference that isolated allicin inhibits or fails to inhibit every cholesterol enzyme.
plain_language
The aged-garlic-gardner-2007 intervention did not significantly improve total cholesterol/HDL ratio in the six-month randomized trial.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 192 adults randomized across four arms; clove-equivalent products six days/week for six months. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The European AGE trial reported lower coronary calcium-score progression than placebo over one year.
Aged garlic extract in the European 2020 coronary-calcium trial → Coronary calcium-score progression in the aged garlic trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Specified aged garlic extract", "comparator": "Placebo", "endpoint": "The European AGE trial reported lower coronary calcium-score progression than placebo over one year.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
104 randomized, 93 analyzed; 2.4 g/day AGE; baseline-adjusted analyses of imaging progression.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Retrospective trial registration, baseline imbalances and manufacturer support; surrogate imaging outcome, not plaque reversal or fewer cardiovascular events.
plain_language
The European AGE trial reported lower coronary calcium-score progression than placebo over one year.
primary_references
The effect of aged garlic extract on the atherosclerotic process - a randomized double-blind placebo-controlled trial. | 2020 | DOI 10.1186/s12906-020-02932-5 | PMID 32349742 | https://pubmed.ncbi.nlm.nih.gov/32349742/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7191741/ | https://doi.org/10.1186/s12906-020-02932-5
source_locator
Reviewed reference lines 93-93; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 93–93
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 104 randomized, 93 analyzed; 2.4 g/day AGE; baseline-adjusted analyses of imaging progression. · Recorded from source · Recorded from source
**Coronary imaging.** A European trial randomized 104 participants to 2.4 g/day aged garlic extract or placebo for one year; ninety-three were analyzed. It reported lower coronary-calcium progression with the extract. It was retrospectively registered and received manufacturer funding and product support alongside other funding. Coronary calcium progression is an imaging outcome, not proof of plaque reversal, fewer infarctions, or allicin target engagement. It must remain distinct from low-attenuation plaque and total plaque-volume measurements. [Wlosinska 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7191741/)
Complete structured claim and evidence
The allicin-containing supplement trial recorded 24 cold episodes versus 65 with placebo.
Allicin-containing supplement in Josling 2001 → Recorded cold or flu incidence in garlic trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Tested allicin-containing supplement", "comparator": "Placebo", "endpoint": "The allicin-containing supplement trial recorded 24 cold episodes versus 65 with placebo.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
146 volunteers randomized, one capsule/day for 12 weeks; self-reported diaries.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Episodes are not numbers of infected participants; not pure allicin target engagement or proof of mechanism.
plain_language
The allicin-containing supplement trial recorded 24 cold episodes versus 65 with placebo.
primary_references
Preventing the common cold with a garlic supplement: a double-blind, placebo-controlled survey. | 2001 | DOI 10.1007/bf02850113 | PMID 11697022 | https://pubmed.ncbi.nlm.nih.gov/11697022/ | https://doi.org/10.1007/bf02850113
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 146 volunteers randomized, one capsule/day for 12 weeks; self-reported diaries. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
Cold/flu incidence did not differ significantly after 90 days of aged garlic extract in Nantz 2012.
Aged garlic extract in Nantz 2012 → Recorded cold or flu incidence in garlic trials Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Aged garlic extract", "comparator": "Placebo", "endpoint": "Cold/flu incidence did not differ significantly after 90 days of aged garlic extract in Nantz 2012.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
120 participants randomized; 2.56 g/day AGE; secondary diary endpoint.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Different preparation from Josling; not a same-intervention replication.
plain_language
Cold/flu incidence did not differ significantly after 90 days of aged garlic extract in Nantz 2012.
primary_references
Supplementation with aged garlic extract improves both NK and γδ-T cell function and reduces the severity of cold and flu symptoms: a randomized, double-blind, placebo-controlled nutrition intervention. | 2012 | DOI 10.1016/j.clnu.2011.11.019 | PMID 22280901 | https://pubmed.ncbi.nlm.nih.gov/22280901/ | https://doi.org/10.1016/j.clnu.2011.11.019
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 120 participants randomized; 2.56 g/day AGE; secondary diary endpoint. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
Some symptom and activity-impact measures improved with aged garlic extract despite the null incidence comparison.
Aged garlic extract in Nantz 2012 → Symptom and activity-impact outcomes in the aged garlic trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Aged garlic extract", "comparator": "Placebo", "endpoint": "Some symptom and activity-impact measures improved with aged garlic extract despite the null incidence comparison.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Same 90-day randomized trial; symptom diary outcomes.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Multiple secondary symptom endpoints; not confirmed antiviral mechanism or allicin efficacy.
plain_language
Some symptom and activity-impact measures improved with aged garlic extract despite the null incidence comparison.
primary_references
Supplementation with aged garlic extract improves both NK and γδ-T cell function and reduces the severity of cold and flu symptoms: a randomized, double-blind, placebo-controlled nutrition intervention. | 2012 | DOI 10.1016/j.clnu.2011.11.019 | PMID 22280901 | https://pubmed.ncbi.nlm.nih.gov/22280901/ | https://doi.org/10.1016/j.clnu.2011.11.019
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Same 90-day randomized trial; symptom diary outcomes. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
Aged garlic extract increased the reported ex vivo immune-cell proliferation readout after 45 days.
Aged garlic extract in Nantz 2012 → Ex vivo gamma-delta T-cell proliferation in Nantz 2012 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Aged garlic extract 2.56 g/day", "comparator": "Placebo", "endpoint": "Aged garlic extract increased the reported ex vivo immune-cell proliferation readout after 45 days.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human randomized AGE study; separate gamma-delta T-cell and NK-cell proliferation assays.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Measured cell-function endpoint; not proof it mediated the illness outcomes or was caused by allicin.
plain_language
Aged garlic extract increased the reported ex vivo immune-cell proliferation readout after 45 days.
primary_references
Supplementation with aged garlic extract improves both NK and γδ-T cell function and reduces the severity of cold and flu symptoms: a randomized, double-blind, placebo-controlled nutrition intervention. | 2012 | DOI 10.1016/j.clnu.2011.11.019 | PMID 22280901 | https://pubmed.ncbi.nlm.nih.gov/22280901/ | https://doi.org/10.1016/j.clnu.2011.11.019
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human randomized AGE study; separate gamma-delta T-cell and NK-cell proliferation assays. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
Aged garlic extract increased the reported ex vivo immune-cell proliferation readout after 45 days.
Aged garlic extract in Nantz 2012 → Ex vivo NK-cell proliferation in Nantz 2012 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_contrast
{"intervention": "Aged garlic extract 2.56 g/day", "comparator": "Placebo", "endpoint": "Aged garlic extract increased the reported ex vivo immune-cell proliferation readout after 45 days.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human randomized AGE study; separate gamma-delta T-cell and NK-cell proliferation assays.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Measured cell-function endpoint; not proof it mediated the illness outcomes or was caused by allicin.
plain_language
Aged garlic extract increased the reported ex vivo immune-cell proliferation readout after 45 days.
primary_references
Supplementation with aged garlic extract improves both NK and γδ-T cell function and reduces the severity of cold and flu symptoms: a randomized, double-blind, placebo-controlled nutrition intervention. | 2012 | DOI 10.1016/j.clnu.2011.11.019 | PMID 22280901 | https://pubmed.ncbi.nlm.nih.gov/22280901/ | https://doi.org/10.1016/j.clnu.2011.11.019
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human randomized AGE study; separate gamma-delta T-cell and NK-cell proliferation assays. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
Garlic supplementation did not significantly reduce gastric cancer incidence: adjusted OR 0.81, 95% CI 0.57-1.13.
Aged garlic extract plus steam-distilled oil in the Shandong trial → Gastric cancer incidence in the Shandong trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Assigned aged garlic extract plus distilled oil regimen", "comparator": "Assigned garlic placebo, separately randomized other interventions", "endpoint": "Garlic supplementation did not significantly reduce gastric cancer incidence: adjusted OR 0.81, 95% CI 0.57-1.13.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
3365 participants in factorial trial; extract plus oil for 7.3 years, 22.3-year follow-up.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High-risk population, long-term endpoint-specific inference; mortality boundary is sensitive to rounding. Vitamins C/E/selenium were a separate intervention, not demonstrated synergy or allicin cancer therapy.
plain_language
Garlic supplementation did not significantly reduce gastric cancer incidence: adjusted OR 0.81, 95% CI 0.57-1.13.
primary_references
Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. | 2019 | DOI 10.1136/bmj.l5016 | PMID 31511230 | https://pubmed.ncbi.nlm.nih.gov/31511230/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/ | https://doi.org/10.1136/bmj.l5016
source_locator
Reviewed reference lines 97-97; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 97–97
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 3365 participants in factorial trial; extract plus oil for 7.3 years, 22.3-year follow-up. · Recorded from source · Recorded from source
**Shandong outcomes and formulation.** The factorial trial included 3,365 residents of a high-risk Chinese region. The garlic regimen was two capsules, each containing 200 mg aged garlic extract and 1 mg steam-distilled garlic oil, twice daily for 7.3 years. Over 22.3 years, gastric-cancer incidence was not significantly reduced (adjusted odds ratio 0.81, 95% CI 0.57–1.13), while gastric-cancer mortality was lower (hazard ratio 0.66, 95% CI 0.43–1.00 after rounding). The secondary analysis reports the upper bound as 0.999. Other cancer and cardiovascular-mortality results were not significant. This endpoint-specific, borderline mortality signal must not be replaced with either a blanket null or a cancer-treatment claim. The independently assigned vitamin intervention contained C, E, and selenium; its effects are not garlic effects or proof of garlic–vitamin synergy. [Li 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/) [Guo 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7320300/)
Complete structured claim and evidence
Garlic supplementation was associated with lower gastric cancer mortality: HR 0.66, 95% CI 0.43-1.00 rounded; secondary analysis reports 0.999.
Aged garlic extract plus steam-distilled oil in the Shandong trial → Gastric cancer mortality in the Shandong trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Assigned aged garlic extract plus distilled oil regimen", "comparator": "Assigned garlic placebo, separately randomized other interventions", "endpoint": "Garlic supplementation was associated with lower gastric cancer mortality: HR 0.66, 95% CI 0.43-1.00 rounded; secondary analysis reports 0.999.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
3365 participants in factorial trial; extract plus oil for 7.3 years, 22.3-year follow-up.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High-risk population, long-term endpoint-specific inference; mortality boundary is sensitive to rounding. Vitamins C/E/selenium were a separate intervention, not demonstrated synergy or allicin cancer therapy.
plain_language
Garlic supplementation was associated with lower gastric cancer mortality: HR 0.66, 95% CI 0.43-1.00 rounded; secondary analysis reports 0.999.
primary_references
Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. | 2019 | DOI 10.1136/bmj.l5016 | PMID 31511230 | https://pubmed.ncbi.nlm.nih.gov/31511230/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/ | https://doi.org/10.1136/bmj.l5016
source_locator
Reviewed reference lines 97-97; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 97–97
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 3365 participants in factorial trial; extract plus oil for 7.3 years, 22.3-year follow-up. · Recorded from source · Recorded from source
**Shandong outcomes and formulation.** The factorial trial included 3,365 residents of a high-risk Chinese region. The garlic regimen was two capsules, each containing 200 mg aged garlic extract and 1 mg steam-distilled garlic oil, twice daily for 7.3 years. Over 22.3 years, gastric-cancer incidence was not significantly reduced (adjusted odds ratio 0.81, 95% CI 0.57–1.13), while gastric-cancer mortality was lower (hazard ratio 0.66, 95% CI 0.43–1.00 after rounding). The secondary analysis reports the upper bound as 0.999. Other cancer and cardiovascular-mortality results were not significant. This endpoint-specific, borderline mortality signal must not be replaced with either a blanket null or a cancer-treatment claim. The independently assigned vitamin intervention contained C, E, and selenium; its effects are not garlic effects or proof of garlic–vitamin synergy. [Li 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/) [Guo 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7320300/)
Complete structured claim and evidence
Garlic supplementation did not significantly change cardiovascular mortality in the long-term Shandong analysis.
Aged garlic extract plus steam-distilled oil in the Shandong trial → Cardiovascular mortality in the Shandong trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_contrast
{"intervention": "Assigned aged garlic extract plus distilled oil regimen", "comparator": "Assigned garlic placebo, separately randomized other interventions", "endpoint": "Garlic supplementation did not significantly change cardiovascular mortality in the long-term Shandong analysis.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
3365 participants in factorial trial; extract plus oil for 7.3 years, 22.3-year follow-up.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
High-risk population, long-term endpoint-specific inference; mortality boundary is sensitive to rounding. Vitamins C/E/selenium were a separate intervention, not demonstrated synergy or allicin cancer therapy.
plain_language
Garlic supplementation did not significantly change cardiovascular mortality in the long-term Shandong analysis.
primary_references
Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. | 2019 | DOI 10.1136/bmj.l5016 | PMID 31511230 | https://pubmed.ncbi.nlm.nih.gov/31511230/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/ | https://doi.org/10.1136/bmj.l5016
source_locator
Reviewed reference lines 97-97; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 97–97
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · 3365 participants in factorial trial; extract plus oil for 7.3 years, 22.3-year follow-up. · Recorded from source · Recorded from source
**Shandong outcomes and formulation.** The factorial trial included 3,365 residents of a high-risk Chinese region. The garlic regimen was two capsules, each containing 200 mg aged garlic extract and 1 mg steam-distilled garlic oil, twice daily for 7.3 years. Over 22.3 years, gastric-cancer incidence was not significantly reduced (adjusted odds ratio 0.81, 95% CI 0.57–1.13), while gastric-cancer mortality was lower (hazard ratio 0.66, 95% CI 0.43–1.00 after rounding). The secondary analysis reports the upper bound as 0.999. Other cancer and cardiovascular-mortality results were not significant. This endpoint-specific, borderline mortality signal must not be replaced with either a blanket null or a cancer-treatment claim. The independently assigned vitamin intervention contained C, E, and selenium; its effects are not garlic effects or proof of garlic–vitamin synergy. [Li 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/) [Guo 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7320300/)
Complete structured claim and evidence
The garlic-caplet regimen lowered the reported saquinavir auc by approximately 51% versus baseline.
Garlic caplets in the saquinavir interaction study → Human plasma saquinavir AUC Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Saquinavir before garlic supplementation administered · Saquinavir Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Saquinavir before garlic supplementation administered · Garlic caplets in the saquinavir interaction study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Saquinavir during tested garlic regimen", "comparator": "Saquinavir before garlic supplementation", "endpoint": "The garlic-caplet regimen lowered the reported saquinavir auc by approximately 51% versus baseline.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "saquinavir", "state": "administered"}, {"entity_slug": "garlic-caplets-piscitelli-2002", "state": "administered"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Ten healthy volunteers; sequential saquinavir pharmacokinetic measurements before and during garlic supplementation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
CYP3A4/P-glycoprotein mechanism not established; no class-wide 51% interaction assigned to all garlic or all substrates.
plain_language
The garlic-caplet regimen lowered the reported saquinavir auc by approximately 51% versus baseline.
primary_references
The effect of garlic supplements on the pharmacokinetics of saquinavir. | 2002 | DOI 10.1086/324351 | PMID 11740713 | https://pubmed.ncbi.nlm.nih.gov/11740713/ | https://doi.org/10.1086/324351
source_locator
Reviewed reference lines 101-101; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 101–101
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Ten healthy volunteers; sequential saquinavir pharmacokinetic measurements before and during garlic supplementation. · Recorded from source · Recorded from source
**Saquinavir exposure.** In ten healthy volunteers, a garlic-supplement regimen reduced saquinavir AUC by about 51%, trough concentration by 49%, and peak concentration by 54%. After washout, values had not fully returned to baseline. This is a measured pharmacokinetic interaction with that preparation; combined CYP3A4 and P-glycoprotein induction was not established as its causal mechanism. The magnitude should not be assigned to all garlic foods, purified allicin, or every CYP3A4 substrate. [Piscitelli 2002](https://pubmed.ncbi.nlm.nih.gov/11740713/)
Complete structured claim and evidence
The garlic-caplet regimen lowered the reported saquinavir trough by approximately 49% versus baseline.
Garlic caplets in the saquinavir interaction study → Human plasma saquinavir trough concentration Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Saquinavir before garlic supplementation administered · Saquinavir Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Saquinavir before garlic supplementation administered · Garlic caplets in the saquinavir interaction study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Saquinavir during tested garlic regimen", "comparator": "Saquinavir before garlic supplementation", "endpoint": "The garlic-caplet regimen lowered the reported saquinavir trough by approximately 49% versus baseline.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "saquinavir", "state": "administered"}, {"entity_slug": "garlic-caplets-piscitelli-2002", "state": "administered"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Ten healthy volunteers; sequential saquinavir pharmacokinetic measurements before and during garlic supplementation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
CYP3A4/P-glycoprotein mechanism not established; no class-wide 51% interaction assigned to all garlic or all substrates.
plain_language
The garlic-caplet regimen lowered the reported saquinavir trough by approximately 49% versus baseline.
primary_references
The effect of garlic supplements on the pharmacokinetics of saquinavir. | 2002 | DOI 10.1086/324351 | PMID 11740713 | https://pubmed.ncbi.nlm.nih.gov/11740713/ | https://doi.org/10.1086/324351
source_locator
Reviewed reference lines 101-101; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 101–101
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Ten healthy volunteers; sequential saquinavir pharmacokinetic measurements before and during garlic supplementation. · Recorded from source · Recorded from source
**Saquinavir exposure.** In ten healthy volunteers, a garlic-supplement regimen reduced saquinavir AUC by about 51%, trough concentration by 49%, and peak concentration by 54%. After washout, values had not fully returned to baseline. This is a measured pharmacokinetic interaction with that preparation; combined CYP3A4 and P-glycoprotein induction was not established as its causal mechanism. The magnitude should not be assigned to all garlic foods, purified allicin, or every CYP3A4 substrate. [Piscitelli 2002](https://pubmed.ncbi.nlm.nih.gov/11740713/)
Complete structured claim and evidence
The garlic-caplet regimen lowered the reported saquinavir cmax by approximately 54% versus baseline.
Garlic caplets in the saquinavir interaction study → Human plasma saquinavir peak concentration Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_condition
Saquinavir before garlic supplementation administered · Saquinavir Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Saquinavir before garlic supplementation administered · Garlic caplets in the saquinavir interaction study Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "Saquinavir during tested garlic regimen", "comparator": "Saquinavir before garlic supplementation", "endpoint": "The garlic-caplet regimen lowered the reported saquinavir cmax by approximately 54% versus baseline.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "saquinavir", "state": "administered"}, {"entity_slug": "garlic-caplets-piscitelli-2002", "state": "administered"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Ten healthy volunteers; sequential saquinavir pharmacokinetic measurements before and during garlic supplementation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
CYP3A4/P-glycoprotein mechanism not established; no class-wide 51% interaction assigned to all garlic or all substrates.
plain_language
The garlic-caplet regimen lowered the reported saquinavir cmax by approximately 54% versus baseline.
primary_references
The effect of garlic supplements on the pharmacokinetics of saquinavir. | 2002 | DOI 10.1086/324351 | PMID 11740713 | https://pubmed.ncbi.nlm.nih.gov/11740713/ | https://doi.org/10.1086/324351
source_locator
Reviewed reference lines 101-101; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 101–101
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Ten healthy volunteers; sequential saquinavir pharmacokinetic measurements before and during garlic supplementation. · Recorded from source · Recorded from source
**Saquinavir exposure.** In ten healthy volunteers, a garlic-supplement regimen reduced saquinavir AUC by about 51%, trough concentration by 49%, and peak concentration by 54%. After washout, values had not fully returned to baseline. This is a measured pharmacokinetic interaction with that preparation; combined CYP3A4 and P-glycoprotein induction was not established as its causal mechanism. The magnitude should not be assigned to all garlic foods, purified allicin, or every CYP3A4 substrate. [Piscitelli 2002](https://pubmed.ncbi.nlm.nih.gov/11740713/)
Complete structured claim and evidence
The aged-garlic-ried-2016 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Aged garlic extract in AGE at Heart 2016 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The aged-garlic-ried-2016 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
The effect of aged garlic extract on blood pressure and other cardiovascular risk factors in uncontrolled hypertensives: the AGE at Heart trial. | 2016 | DOI 10.2147/ibpc.s93335 | PMID 26869811 | https://pubmed.ncbi.nlm.nih.gov/26869811/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4734812/ | https://doi.org/10.2147/ibpc.s93335
source_locator
Reviewed reference lines 89-89; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 89–89
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Blood pressure.** AGE at Heart tested 1.2 g/day aged garlic extract containing 1.2 mg SAC for twelve weeks. Ninety-five participants completed the trial; seven were excluded for protocol deviations, leaving eighty-eight in the full analysis. Mean placebo-adjusted systolic change was about −5.0 ± 2.1 mmHg. The overall diastolic difference was not significant (−1.9 ± 1.2 mmHg, P=0.12). Larger reductions in retrospectively defined responders do not replace the overall comparison. This was an extract trial, not purified allicin or proof of sulfide mediation. Manufacturer involvement and the analysis exclusions limit interpretation. [Ried 2016](https://pmc.ncbi.nlm.nih.gov/articles/PMC4734812/)
Complete structured claim and evidence
The raw-garlic-gardner-2007 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Raw garlic intervention in Gardner 2007 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The raw-garlic-gardner-2007 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The garlic-powder-gardner-2007 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Garlic powder intervention in Gardner 2007 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The garlic-powder-gardner-2007 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The aged-garlic-gardner-2007 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Aged garlic extract intervention in Gardner 2007 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The aged-garlic-gardner-2007 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
Effect of raw garlic vs commercial garlic supplements on plasma lipid concentrations in adults with moderate hypercholesterolemia: a randomized clinical trial. | 2007 | DOI 10.1001/archinte.167.4.346 | PMID 17325296 | https://pubmed.ncbi.nlm.nih.gov/17325296/ | https://doi.org/10.1001/archinte.167.4.346
source_locator
Reviewed reference lines 91-91; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 91–91
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Cholesterol null.** Gardner randomized 192 adults with moderately elevated LDL cholesterol to raw garlic, garlic powder, aged garlic extract, or placebo for six months. Products equivalent to roughly a four-gram clove were used six days per week and chemically monitored. None significantly improved LDL, HDL, triglycerides, or the total-cholesterol/HDL ratio. This substantial null result should remain visible beside biochemical enzyme findings. It neither disproves every possible formulation nor proves that all positive trials were publication bias. [Gardner 2007](https://pubmed.ncbi.nlm.nih.gov/17325296/)
Complete structured claim and evidence
The aged-garlic-wlosinska-2020 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Aged garlic extract in the European 2020 coronary-calcium trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The aged-garlic-wlosinska-2020 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
The effect of aged garlic extract on the atherosclerotic process - a randomized double-blind placebo-controlled trial. | 2020 | DOI 10.1186/s12906-020-02932-5 | PMID 32349742 | https://pubmed.ncbi.nlm.nih.gov/32349742/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7191741/ | https://doi.org/10.1186/s12906-020-02932-5
source_locator
Reviewed reference lines 93-93; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 93–93
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Coronary imaging.** A European trial randomized 104 participants to 2.4 g/day aged garlic extract or placebo for one year; ninety-three were analyzed. It reported lower coronary-calcium progression with the extract. It was retrospectively registered and received manufacturer funding and product support alongside other funding. Coronary calcium progression is an imaging outcome, not proof of plaque reversal, fewer infarctions, or allicin target engagement. It must remain distinct from low-attenuation plaque and total plaque-volume measurements. [Wlosinska 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7191741/)
Complete structured claim and evidence
The garlic-supplement-josling-2001 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Allicin-containing supplement in Josling 2001 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The garlic-supplement-josling-2001 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
Preventing the common cold with a garlic supplement: a double-blind, placebo-controlled survey. | 2001 | DOI 10.1007/bf02850113 | PMID 11697022 | https://pubmed.ncbi.nlm.nih.gov/11697022/ | https://doi.org/10.1007/bf02850113
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
The aged-garlic-nantz-2012 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Aged garlic extract in Nantz 2012 Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The aged-garlic-nantz-2012 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
Supplementation with aged garlic extract improves both NK and γδ-T cell function and reduces the severity of cold and flu symptoms: a randomized, double-blind, placebo-controlled nutrition intervention. | 2012 | DOI 10.1016/j.clnu.2011.11.019 | PMID 22280901 | https://pubmed.ncbi.nlm.nih.gov/22280901/ | https://doi.org/10.1016/j.clnu.2011.11.019
source_locator
Reviewed reference lines 95-95; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 95–95
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Cold outcomes differ by preparation.** Josling's trial randomized 146 volunteers for twelve weeks and reported fewer diary-recorded colds with an allicin-containing supplement (24 versus 65 episodes). Nantz tested 2.56 g/day aged garlic extract in 120 participants: the ninety-day cold/flu incidence difference was not significant, although some symptom and activity-impact measures improved. At forty-five days, ex vivo γδ-T-cell and NK-cell proliferation also increased. These are different interventions and endpoints, not a replication of purified allicin efficacy. Neither proves that one specific compound caused the clinical effect. [Josling 2001](https://pubmed.ncbi.nlm.nih.gov/11697022/) [Nantz 2012](https://pubmed.ncbi.nlm.nih.gov/22280901/)
Complete structured claim and evidence
The garlic-extract-oil-shandong study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Aged garlic extract plus steam-distilled oil in the Shandong trial Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The garlic-extract-oil-shandong study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
Effects of Helicobacter pylori treatment and vitamin and garlic supplementation on gastric cancer incidence and mortality: follow-up of a randomized intervention trial. | 2019 | DOI 10.1136/bmj.l5016 | PMID 31511230 | https://pubmed.ncbi.nlm.nih.gov/31511230/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/ | https://doi.org/10.1136/bmj.l5016
source_locator
Reviewed reference lines 97-97; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 97–97
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Shandong outcomes and formulation.** The factorial trial included 3,365 residents of a high-risk Chinese region. The garlic regimen was two capsules, each containing 200 mg aged garlic extract and 1 mg steam-distilled garlic oil, twice daily for 7.3 years. Over 22.3 years, gastric-cancer incidence was not significantly reduced (adjusted odds ratio 0.81, 95% CI 0.57–1.13), while gastric-cancer mortality was lower (hazard ratio 0.66, 95% CI 0.43–1.00 after rounding). The secondary analysis reports the upper bound as 0.999. Other cancer and cardiovascular-mortality results were not significant. This endpoint-specific, borderline mortality signal must not be replaced with either a blanket null or a cancer-treatment claim. The independently assigned vitamin intervention contained C, E, and selenium; its effects are not garlic effects or proof of garlic–vitamin synergy. [Li 2019](https://pmc.ncbi.nlm.nih.gov/articles/PMC6737461/) [Guo 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7320300/)
Complete structured claim and evidence
The garlic-caplets-piscitelli-2002 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
Allicin → Garlic caplets in the saquinavir interaction study Recorded from sourceungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
experimental_model
Editorial study-scope relationship, not experimental causation or chemical composition.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation only. Does not assert allicin content, metabolic conversion, causation or intervention equivalence.
plain_language
The garlic-caplets-piscitelli-2002 study is a preparation-specific translation comparison; its outcomes are not assigned to purified allicin.
primary_references
The effect of garlic supplements on the pharmacokinetics of saquinavir. | 2002 | DOI 10.1086/324351 | PMID 11740713 | https://pubmed.ncbi.nlm.nih.gov/11740713/ | https://doi.org/10.1086/324351
source_locator
Reviewed reference lines 101-101; exact primary location described in quoted passage where extracted.
Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 101–101
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial study-scope relationship, not experimental causation or chemical composition. · Recorded from source · Recorded from source
**Saquinavir exposure.** In ten healthy volunteers, a garlic-supplement regimen reduced saquinavir AUC by about 51%, trough concentration by 49%, and peak concentration by 54%. After washout, values had not fully returned to baseline. This is a measured pharmacokinetic interaction with that preparation; combined CYP3A4 and P-glycoprotein induction was not established as its causal mechanism. The magnitude should not be assigned to all garlic foods, purified allicin, or every CYP3A4 substrate. [Piscitelli 2002](https://pubmed.ncbi.nlm.nih.gov/11740713/)
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

GSH1-deficient yeast can use GSSA as an exogenous glutathione source

Condition: machinery_impairment · Loss of yeast GSH1 with no exogenous GSH source.

Normal role: Intact machinery supports the context-specific response or buffering function described in the linked experiments.

Recorded consequence: GSSA supplementation supported growth in the tested background.

Scope: Experimental machinery perturbation, grouped under the allicin research chapter.

Allicin susceptibility with impaired yeast redox machinery

Condition: machinery_impairment · Separate GLR1, ZWF1 or YAP1 deletions during allicin exposure.

Normal role: Intact machinery supports the context-specific response or buffering function described in the linked experiments.

Recorded consequence: Increased susceptibility, with concentration and compound dependence.

Scope: Experimental machinery perturbation, grouped under the allicin research chapter.

Allicin susceptibility with impaired yeast metal acquisition or regulation

Condition: machinery_impairment · Separate CTR1, MAC1 or ZAP1 deletions during allicin exposure.

Normal role: Intact machinery supports the context-specific response or buffering function described in the linked experiments.

Recorded consequence: Greater allicin susceptibility in the identified mutant backgrounds.

Scope: Experimental machinery perturbation, grouped under the allicin research chapter.

Partial loss of allicin sensory response after single-channel knockout

Condition: machinery_impairment · Separate Trpa1 or Trpv1 knockout in mice.

Normal role: Intact machinery supports the context-specific response or buffering function described in the linked experiments.

Recorded consequence: Reduced but persistent pain-related response to allicin.

Scope: Experimental machinery perturbation, grouped under the allicin research chapter.

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Allicin: detailed mechanisms of action (reviewed 5 October 2026)Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · Recorded from sourceRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

1. **Human adduct repair.** Does purified human GSR reduce GSSA at relevant concentrations, and which repair routes dominate in intact human cells?Open research question from the reviewed reference; not an established causal claim.
2. **Exposure before efficacy.** Which chemically verified products produce measurable parent allicin or specific thioallylated proteins in a defined human tissue?Open research question from the reviewed reference; not an established causal claim.
3. **Thiol location.** Can extracellular quenching, intracellular protein protection, and reductase-dependent recovery be separated experimentally?Open research question from the reviewed reference; not an established causal claim.
4. **Metal redistribution.** Which proteins release zinc in the mouse-cell experiment, and does this occur at any measured dietary tissue exposure?Open research question from the reviewed reference; not an established causal claim.
5. **Yeast metal phenotype.** Does allicin limit metal uptake, perturb metalloprotein function, or both, and which results translate to human cells?Open research question from the reviewed reference; not an established causal claim.
6. **Vitamin dependencies.** Do B2/FAD supply or NADPH-producing pathways alter allicin-adduct repair in human cells, independently of broad changes in viability?Open research question from the reviewed reference; not an established causal claim.
7. **Vitamin B1 product formation.** How much allithiamine, if any, forms under actual gastrointestinal conditions after relevant garlic and thiamine exposures?Open research question from the reviewed reference; not an established causal claim.
8. **Intestinal signaling.** Does allicin itself alter GLP-1 release at measured luminal exposures, and is the response TRPA1-dependent in vivo?Open research question from the reviewed reference; not an established causal claim.
9. **Sulfide speciation.** How do validated free-sulfide and bound-sulfur measurements compare across pure DATS, pure DADS, garlic juice, and aged extract?Open research question from the reviewed reference; not an established causal claim.
10. **Clinical effect modification.** Does a prespecified redox or nutrient biomarker modify the randomized response to a chemically characterized preparation?Open research question from the reviewed reference; not an established causal claim.
11. **Target necessity.** Which of the detected protein adducts are necessary for a phenotype, rather than abundant bystanders, and what do unmodified or rescued controls show?Open research question from the reviewed reference; not an established causal claim.
12. **Selenium evidence gap.** Is there a direct allicin-specific thioredoxin-reductase/SecTRAP study that establishes the proposed chemical species and causal sequence?Open research question from the reviewed reference; not an established causal claim.

Chapters contain source-recorded findings and curated literature summaries. Read each finding's evidence grade, experimental context and review qualifications. The ledger is not medical advice.

Allicin

The mechanisms

Garlic alliinase is a PLP-dependent plant enzyme; its structural cofactor requirement is not a human B6 supplementation experiment.

PLP-dependent garlic alliinase cleaves alliin to the sulfenic-acid precursor; aminoacrylate formation leads to pyruvate and ammonia.

Two allylsulfenic-acid molecules condense to allicin with water loss.

Alliinase localization to garlic bundle-sheath cells qualifies where precursor-enzyme mixing occurs after tissue damage.

Allicin transformation and garlic processing involve chemically distinct e-ajoene; this provenance does not transfer the product's effects to allicin.

Allicin transformation and garlic processing involve chemically distinct z-ajoene; this provenance does not transfer the product's effects to allicin.

Allicin reacted with L-cysteine to form the identified mixed-disulfide product SAMC.

Allicin reacts with glutathione to form GSSA, distinct from GSSG.

Allicin and thiamine form thiamine allyl disulfide, identified as allithiamine in the original chemistry report.

Allicin stability depends on the medium; vegetable oil had a 3.1-hour chemical half-life and a separate 0.8-hour antibacterial-activity half-life.

Previously crushed garlic retained some platelet-inhibitory activity after six-minute heating that abolished it in uncrushed samples.

Heating beyond ten minutes eliminated the tested garlic-extract platelet-inhibitory activity.

Resting crushed garlic before microwave heating preserved some inhibition of rat mammary carcinogen-DNA adduct formation.

Six-to-ten-minute boiling increased measured linear allyl-polysulfide content relative to other tested preparation times.

Six-to-ten-minute boiling increased measured sulfide-releasing assay activity relative to other tested preparation times.

Allicin permeated the tested membrane and reached thiols on the other side.

Allicin permeated the tested membrane and reached thiols on the other side.

Allicin did not produce detected leakage, fusion or aggregation in the tested membrane assays.

The tested preparation gave 80-111% relative breath AMS exposure versus homogenized raw garlic.

The tested preparation gave 36-104% relative breath AMS exposure versus homogenized raw garlic.

A high-protein meal reduced relative breath AMS exposure from the tested enteric products to 22-57%.

Thirty-three organosulfur analytes were characterized in urine after twenty grams of black garlic, including N-acetyl products.

Reported SAC oral bioavailability was 98.2% in rats, 103.0% in mice, and 87.2% in dogs.

S-thioallylated peptides were detected from 332 proteins after direct allicin exposure.

S-thioallylation was detected on Human fructose-bisphosphate aldolase A / ALDOA in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human glyceraldehyde-3-phosphate dehydrogenase / GAPDH in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human pyruvate kinase PKM, splice isoform unresolved / PKM in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human alpha-enolase / ENO1 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human copper-zinc superoxide dismutase / SOD1 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human peroxiredoxin 1 / PRDX1 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human cofilin 1 / CFL1 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human plastin 2 / LCP1 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human filamin A / FLNA in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human filamin B / FLNB in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human heat shock protein family A member 4 / HSPA4 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human eukaryotic elongation factor 2 / EEF2 in allicin-exposed Jurkat cells.

S-thioallylation was detected on Human high mobility group box 1 / HMGB1 in allicin-exposed Jurkat cells.

Free cellular thiols fell approximately 50% after allicin treatment.

Enolase activity decreased in lysates from allicin-exposed Jurkat cells.

MTT metabolic-activity readout did not significantly decrease after exposure up to 100 uM in the tested Jurkat system.

Allicin disrupted filamentous-actin organization in mouse L929 fibroblasts.

Allicin increased labile zinc in mouse EL-4 cells.

Allicin pretreatment followed by washing enhanced subsequent IL-1beta-stimulated IL-2 production in mouse EL-4 cells.

Allicin inhibited the tested purified papain.

Allicin inhibited the tested purified bacterial NADP-dependent alcohol dehydrogenase.

Allicin inhibited the tested purified horse-liver alcohol dehydrogenase.

Glutathione restored activity of allicin-inhibited papain.

Glutathione did not restore the allicin-inhibited bacterial dehydrogenase in the tested assay.

Purified yeast glutathione reductase used GSSA as a substrate with NADPH consumption; apparent Km was 0.50 mM.

GSSA supplementation supported growth of GSH1-deficient yeast on otherwise glutathione-unsupplemented medium.

Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.

Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.

Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.

Allicin shifted the bacillithiol redox potential toward a more oxidized state in Staphylococcus aureus.

The bacilliredoxin/bacillithiol/YpdA pathway reversed protein S-thioallylation in the reported biochemical study.

YpdA accepted the allyl-bacillithiol adduct BSSA as a substrate to regenerate bacillithiol.

Direct allicin exposure reduced mammalian-cell viability or proliferation in a concentration- and cell-type-dependent manner.

Deletion of yeast-ctr1 increased yeast sensitivity to allicin.

Deletion of yeast-mac1 increased yeast sensitivity to allicin.

Deletion of yeast-zap1 increased yeast sensitivity to allicin.

Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.

Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.

Allicin inhibited growth of tested bacterial isolates with substantial strain and assay variation.

Added extracellular glutathione reduced injury from allicin in Human A549/Beas-2B epithelial cultures.

Added extracellular glutathione reduced injury from allicin in Rat precision-cut lung slices.

Naturally adapted Pseudomonas isolates demonstrated resistance to allicin associated with multicomponent redox defenses.

Allicin engaged the mouse-trpa1-dependent sensory response in mouse channel-loss and neuronal experiments.

Loss of mouse-trpa1 reduced but did not abolish allicin-evoked pain-related behavior.

Allicin engaged the mouse-trpv1-dependent sensory response in mouse channel-loss and neuronal experiments.

Loss of mouse-trpv1 reduced but did not abolish allicin-evoked pain-related behavior.

Allicin activated rat TRPV1 expressed in HEK293 membrane patches.

The rat-trpv1-c157a construct did not show allicin responsiveness while relevant capsaicin responses persisted.

The rat-trpv1-cysteine-less construct did not show allicin responsiveness while relevant capsaicin responses persisted.

Restoring C157 to the cysteine-less rat TRPV1 construct restored responsiveness to allicin.

A reducing agent reversed allicin-evoked TRPV1 activation in the patch assay.

The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.

The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.

Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.