Lipid peroxidation

evidence_span

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experimental_model

Spectroscopy, ESR, NMR and iron-driven lipid-oxidation experiments

exposure

CGA concentration series; iron-EDTA and iron-ADP comparisons

limitations

Chemical prevention of radical formation is distinct from radical scavenging. These assays do not measure human mineral stores, oral chelation therapy or clinical disease prevention.

nutrient_topic

Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

organism

Cell-free chemistry and bovine liver microsomes

plain_language

Protection in a tissue preparation is retained with its experimental scope.

primary_references

[chlorogenic_acid-p9501514] Iron chelation by chlorogenic acid as a natural antioxidant. (1998). https://pubmed.ncbi.nlm.nih.gov/9501514/ DOI: 10.1271/bbb.62.22

tissue_or_cell_type

Ferric complexes, Fenton-type chemistry and microsomal lipids

Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 724–735

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Spectroscopy, ESR, NMR and iron-driven lipid-oxidation experiments · source_derived_draft · unverified_draft

### chlorogenic_acid-microsomal-oxidation CGA reduced iron-induced bovine microsomal lipid peroxidation in a concentration-dependent manner. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Protection in a tissue preparation is retained with its experimental scope. organism: Cell-free chemistry and bovine liver microsomes tissue_or_cell_type: Ferric complexes, Fenton-type chemistry and microsomal lipids experimental_model: Spectroscopy, ESR, NMR and iron-driven lipid-oxidation experiments limitations: Chemical prevention of radical formation is distinct from radical scavenging. These assays do not measure human mineral stores, oral chelation therapy or clinical disease prevention. exposure: CGA concentration series; iron-EDTA and iron-ADP comparisons evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/9501514.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb573ad7da5b27974eff1c3a31d52becf53a72ffe3216703743aab82eacef1b7", "start_char": 0, "end_char": 797, "text_sha256": "eb573ad7da5b27974eff1c3a31d52becf53a72ffe3216703743aab82eacef1b7"} [chlorogenic_acid-p9501514] Iron chelation by chlorogenic acid as a natural antioxidant. (1998). https://pubmed.ncbi.nlm.nih.gov/9501514/ DOI: 10.1271/bbb.62.22

evidence_span

{"source_cache": "artifacts/k2-research/35922516.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a", "start_char": 0, "end_char": 1403, "text_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a"}

experimental_model

Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice

exposure

MK-4/K1, NAD(P)H, FSP1 loss and inhibitors

limitations

Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human recombinant FSP1, mammalian cells and mice

plain_language

The antioxidant action belongs to the reduced chemical form, not just the name on a supplement bottle.

primary_references

[k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3

tissue_or_cell_type

Lipid peroxidation and vitamin K reduction

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 786–797

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

### k2-kh2-lipid-protection Reduced vitamin K forms trapped radicals and inhibited phospholipid peroxidation in the tested systems. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The antioxidant action belongs to the reduced chemical form, not just the name on a supplement bottle. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a", "start_char": 0, "end_char": 1403, "text_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3

evidence_access

Primary abstract

experimental_model

Cell-free iron-loaded liposomes.

limitations

Ascorbate participated in the oxidation-initiating system; this is not evidence that vitamin C regenerates astaxanthin or that astaxanthin removes body iron.

nutrient_topic

Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin

plain_language

Its effect depended on the surrounding iron and oxidant chemistry.

primary_references

Astaxanthin and peridinin inhibit oxidative damage in Fe(2+)-loaded liposomes: scavenging oxyradicals or changing membrane permeability? · 2001 · https://pubmed.ncbi.nlm.nih.gov/11594777/ · DOI 10.1006/bbrc.2001.5765

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 174–180

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free iron-loaded liposomes. · source_derived_draft · unverified_draft

## astaxanthin-iron-ascorbate Its effect depended on the surrounding iron and oxidant chemistry. Astaxanthin reduced lipid damage in iron-loaded liposomes challenged using peroxide or ascorbate-dependent initiating systems. Model: Cell-free iron-loaded liposomes. Limitations: Ascorbate participated in the oxidation-initiating system; this is not evidence that vitamin C regenerates astaxanthin or that astaxanthin removes body iron. Evidence access: Primary abstract Astaxanthin and peridinin inhibit oxidative damage in Fe(2+)-loaded liposomes: scavenging oxyradicals or changing membrane permeability? · 2001 · https://pubmed.ncbi.nlm.nih.gov/11594777/ · DOI 10.1006/bbrc.2001.5765

evidence_access

Primary abstract

experimental_model

Cell-free phospholipid liposomes.

limitations

Regional chemistry was inferred from oxidation products, not direct proof of a permanently membrane-spanning orientation.

nutrient_topic

Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin

plain_language

Different regions of the molecule may participate in radical trapping.

primary_references

Efficient radical trapping at the surface and inside the phospholipid membrane is responsible for highly potent antiperoxidative activity of the carotenoid astaxanthin. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11406102/ · DOI 10.1016/s0005-2736(01)00326-1

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 158–164

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free phospholipid liposomes. · source_derived_draft · unverified_draft

## astaxanthin-iron-liposome Different regions of the molecule may participate in radical trapping. Astaxanthin inhibited ADP/Fe2+-initiated liposome peroxidation more strongly than beta-carotene in this assay; chemical degradation patterns suggested contributions from both its polyene and terminal rings. Model: Cell-free phospholipid liposomes. Limitations: Regional chemistry was inferred from oxidation products, not direct proof of a permanently membrane-spanning orientation. Evidence access: Primary abstract Efficient radical trapping at the surface and inside the phospholipid membrane is responsible for highly potent antiperoxidative activity of the carotenoid astaxanthin. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11406102/ · DOI 10.1016/s0005-2736(01)00326-1

evidence_access

Primary abstract

experimental_model

Rat liver microsomal oxidation assay under air.

limitations

This does not support a universal potency multiplier over vitamin E or human clinical efficacy.

nutrient_topic

Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin

plain_language

It interrupted oxidation in an experimental membrane preparation.

primary_references

Astaxanthin and canthaxanthin are potent antioxidants in a membrane model. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1497349/ · DOI 10.1016/0003-9861(92)90675-m

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 150–156

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat liver microsomal oxidation assay under air. · source_derived_draft · unverified_draft

## astaxanthin-microsome-oxidation It interrupted oxidation in an experimental membrane preparation. Astaxanthin inhibited radical-induced lipid peroxidation in rat liver microsomes, with activity comparable to alpha-tocopherol under the tested conditions. Model: Rat liver microsomal oxidation assay under air. Limitations: This does not support a universal potency multiplier over vitamin E or human clinical efficacy. Evidence access: Primary abstract Astaxanthin and canthaxanthin are potent antioxidants in a membrane model. · 1992 · https://pubmed.ncbi.nlm.nih.gov/1497349/ · DOI 10.1016/0003-9861(92)90675-m

evidence_access

Primary abstract

experimental_model

Photosensitized model lipid bilayers.

limitations

Oxidant source and position differ from other assays; this is context dependence, not an error requiring a universal ranking.

nutrient_topic

Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin

plain_language

Greater chemical stability did not guarantee greater protection.

primary_references

Inhibitory effect of beta-carotene and astaxanthin on photosensitized oxidation of phospholipid bilayers. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8006717/ · DOI 10.3177/jnsv.39.607

Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 166–172

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Photosensitized model lipid bilayers. · source_derived_draft · unverified_draft

## astaxanthin-photosensitizer-context Greater chemical stability did not guarantee greater protection. With a lipid-soluble photosensitizer in bilayers, astaxanthin was more stable yet less inhibitory than beta-carotene. Model: Photosensitized model lipid bilayers. Limitations: Oxidant source and position differ from other assays; this is context dependence, not an error requiring a universal ranking. Evidence access: Primary abstract Inhibitory effect of beta-carotene and astaxanthin on photosensitized oxidation of phospholipid bilayers. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8006717/ · DOI 10.3177/jnsv.39.607

availability_state

Selenium restriction becomes severe enough to compromise GPX4 function in a susceptible context.

experimental_scope

Cell and cancer-model evidence for parallel defenses; GPX4 may be relatively preserved during nutritional restriction.

limitations

The source does not establish a nutritional dose or plasma value that disables GPX4. GPX4 deletion or drug inhibition is not equivalent to ordinary dietary deficiency; parallel protection is not guaranteed in every cell.

trigger_kind

nutrient_deficiency

Selenium deficiency: a mechanism-first reference · lines 123–123

Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

But GPX4 is not the only barrier between a cell and ferroptosis. The FSP1–CoQ10 system provides a parallel, glutathione-independent defense by regenerating reduced CoQ, which can trap lipid radicals. Other systems also contribute. Evidence: cell and cancer-model experiments. [8,9]

access_level

abstract_only

compartment

Mitochondrial GSH versus intracellular GSH distinguished by authors

dose

Unknown: full methods unavailable

duration

Unknown: full methods unavailable

endpoint

lipid-peroxidation

evidence_location

Primary indexed abstract; experiment-specific methods unavailable

experimental_model

Protein interaction/stability, knockdown and compound experiments reported in abstract

exposure

human-crc-dlat-knockdown

limitations

ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.

nutrient_topic

Topical cross-reference only; no inheritance of another actor's effects. · GSH

organism

Human colorectal cancer models; individual experiments require full-text confirmation

plain_language

DLAT knockdown reportedly increased lipid peroxidation.

primary_locator

[{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]

primary_references

https://doi.org/10.1016/j.freeradbiomed.2026.04.133

tissue_or_cell_type

Colorectal cancer models; claim-specific cell line not established from abstract

DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 784–798

AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

DLAT knockdown reportedly increased lipid peroxidation. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: lipid-peroxidation exposure: human-crc-dlat-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: DLAT knockdown reportedly increased lipid peroxidation.

access_level

abstract_only

compartment

Mitochondrial GSH versus intracellular GSH distinguished by authors

dose

Unknown: full methods unavailable

duration

Unknown: full methods unavailable

endpoint

lipid-peroxidation

evidence_location

Primary indexed abstract; experiment-specific methods unavailable

experimental_model

Protein interaction/stability, knockdown and compound experiments reported in abstract

exposure

human-crc-slc25a39-knockdown

limitations

ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.

nutrient_topic

Topical cross-reference only; no inheritance of another actor's effects. · GSH

organism

Human colorectal cancer models; individual experiments require full-text confirmation

plain_language

SLC25A39 knockdown reportedly increased lipid peroxidation.

primary_locator

[{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]

primary_references

https://doi.org/10.1016/j.freeradbiomed.2026.04.133

tissue_or_cell_type

Colorectal cancer models; claim-specific cell line not established from abstract

DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 835–849

AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

SLC25A39 knockdown reportedly increased lipid peroxidation. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: lipid-peroxidation exposure: human-crc-slc25a39-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: SLC25A39 knockdown reportedly increased lipid peroxidation.

dose

Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin

duration

Kinetic assays; urine collected 2-4 h after ingestion

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Cell-free biochemical systems and four human volunteers

limitations

Chemical activity does not establish clinical efficacy or a dietary iron interaction.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Cell-free biochemical systems and four human volunteers

plain_language

Betanidin inhibited cytochrome-c-driven linoleate peroxidation, with an assay IC50 of 0.8 micromolar.

primary_references

Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f

route

In vitro addition; separate oral juice arm

tissue

Lipid emulsions, membranes, LDL; urine arm separate

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 37–45

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Cell-free biochemical systems and four human volunteers · source_derived_draft · unverified_draft

## betalains-betanidin-linoleate Betanidin inhibited cytochrome-c-driven linoleate peroxidation, with an assay IC50 of 0.8 micromolar. Model/species: Cell-free biochemical systems and four human volunteers Tissue: Lipid emulsions, membranes, LDL; urine arm separate Exposure: Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin Route: In vitro addition; separate oral juice arm Duration: Kinetic assays; urine collected 2-4 h after ingestion Limits: Chemical activity does not establish clinical efficacy or a dietary iron interaction. Primary reference: Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f

dose

Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin

duration

Kinetic assays; urine collected 2-4 h after ingestion

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Cell-free biochemical systems and four human volunteers

limitations

Chemical activity does not establish clinical efficacy or a dietary iron interaction.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Cell-free biochemical systems and four human volunteers

plain_language

Added betanin inhibited iron-redox-driven lipid peroxidation in cell-free lipid preparations.

primary_references

Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f

route

In vitro addition; separate oral juice arm

tissue

Lipid emulsions, membranes, LDL; urine arm separate

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 27–35

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Cell-free biochemical systems and four human volunteers · source_derived_draft · unverified_draft

## betalains-betanin-iron-oxidation Added betanin inhibited iron-redox-driven lipid peroxidation in cell-free lipid preparations. Model/species: Cell-free biochemical systems and four human volunteers Tissue: Lipid emulsions, membranes, LDL; urine arm separate Exposure: Assay-specific submicromolar to micromolar concentrations; oral arm 300 mL beet juice with 120 mg betanin Route: In vitro addition; separate oral juice arm Duration: Kinetic assays; urine collected 2-4 h after ingestion Limits: Chemical activity does not establish clinical efficacy or a dietary iron interaction. Primary reference: Betalains--a new class of dietary cationized antioxidants. (2001). https://pubmed.ncbi.nlm.nih.gov/11714300/ DOI: 10.1021/jf010456f

dose

Experimental betanin addition; concentration not specified in accessed abstract

duration

Oxidation time courses; duration not specified in accessed abstract

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Isolated human LDL and MPO/nitrite biochemical system

limitations

Oxidation products were not chemically identified; clinical LDL lowering was not tested.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Isolated human LDL and MPO/nitrite biochemical system

plain_language

Betanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL.

primary_references

Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783

route

In vitro addition

tissue

LDL lipid compartment

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 187–195

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Isolated human LDL and MPO/nitrite biochemical system · source_derived_draft · unverified_draft

## betalains-mpo-ldl Betanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL. Model/species: Isolated human LDL and MPO/nitrite biochemical system Tissue: LDL lipid compartment Exposure: Experimental betanin addition; concentration not specified in accessed abstract Route: In vitro addition Duration: Oxidation time courses; duration not specified in accessed abstract Limits: Oxidation products were not chemically identified; clinical LDL lowering was not tested. Primary reference: Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783

dose

Experimental betanin addition; concentration not specified in accessed abstract

duration

Oxidation time courses; duration not specified in accessed abstract

evidence_access

Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.

evidence_scope

literature_reviewed; source-derived curation, not universally established human effects

experimental_model

Isolated human LDL and MPO/nitrite biochemical system

limitations

Oxidation products were not chemically identified; clinical LDL lowering was not tested.

nutrient_topic

Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains

organism

Isolated human LDL and MPO/nitrite biochemical system

plain_language

Unidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay.

primary_references

Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783

route

In vitro addition

tissue

LDL lipid compartment

Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 197–205

Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Isolated human LDL and MPO/nitrite biochemical system · source_derived_draft · unverified_draft

## betalains-oxidation-products Unidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay. Model/species: Isolated human LDL and MPO/nitrite biochemical system Tissue: LDL lipid compartment Exposure: Experimental betanin addition; concentration not specified in accessed abstract Route: In vitro addition Duration: Oxidation time courses; duration not specified in accessed abstract Limits: Oxidation products were not chemically identified; clinical LDL lowering was not tested. Primary reference: Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783

cross_nutrient

true

evidence_location

Primary abstract final result

experimental_model

Soybean L-alpha-phosphatidylcholine liposomes undergoing Fe(III)-triethylenetetramine-initiated peroxidation; EPR, optical and polarographic measurements

exposure

Aqueous ascorbic acid described as physiological concentration in abstract (exact dose unavailable); bilayer alpha-tocopheroxyl radical detected at 10^-8–10^-7 M.

limitations

This persistence endpoint is separate from the radical-reduction reaction and does not establish a supplementation effect in people.

nutrient_topic

Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C

organism

Glycine max lipid preparation; cell-free

plain_language

Vitamin C prolonged vitamin E’s protection against oxidation in the liposome experiment.

primary_references

[c-reg-scarpa] Formation of alpha-tocopherol radical and recycling of alpha-tocopherol by ascorbate during peroxidation of phosphatidylcholine liposomes. An electron paramagnetic resonance study. (1984). https://pubmed.ncbi.nlm.nih.gov/6089911/ DOI: 10.1016/0304-4165(84)90070-9

tissue_or_cell_type

Artificial liposomes

Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1215–1227

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Soybean L-alpha-phosphatidylcholine liposomes undergoing Fe(III)-triethylenetetramine-initiated peroxidation; EPR, optical and polarographic measurements · source_derived_draft · unverified_draft

### c-reg-tocopherol-antiperoxidation-persistence The inhibitory effect of alpha-tocopherol on liposome lipid peroxidation persisted while aqueous ascorbic acid remained available, consistent with continued tocopherol-radical recycling. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C prolonged vitamin E’s protection against oxidation in the liposome experiment. organism: Glycine max lipid preparation; cell-free tissue_or_cell_type: Artificial liposomes experimental_model: Soybean L-alpha-phosphatidylcholine liposomes undergoing Fe(III)-triethylenetetramine-initiated peroxidation; EPR, optical and polarographic measurements limitations: This persistence endpoint is separate from the radical-reduction reaction and does not establish a supplementation effect in people. exposure: Aqueous ascorbic acid described as physiological concentration in abstract (exact dose unavailable); bilayer alpha-tocopheroxyl radical detected at 10^-8–10^-7 M. cross_nutrient: true evidence_location: Primary abstract final result [c-reg-scarpa] Formation of alpha-tocopherol radical and recycling of alpha-tocopherol by ascorbate during peroxidation of phosphatidylcholine liposomes. An electron paramagnetic resonance study. (1984). https://pubmed.ncbi.nlm.nih.gov/6089911/ DOI: 10.1016/0304-4165(84)90070-9

evidence_span

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experimental_model

Lipid-peroxyl radical challenge in liposomes

exposure

AAPH or AMVN challenge; dietary and meso zeaxanthin

limitations

Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.

nutrient_topic

Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin

organism

Cell-free system with human GSTP1

plain_language

This binding-related effect persisted without glutathione.

primary_references

[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002

tissue_or_cell_type

Egg-yolk phosphatidylcholine liposomes

Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 288–299

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft

### zeaxanthin-gsh-independent The GSTP1–zeaxanthin protective effect did not require glutathione in this liposome experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This binding-related effect persisted without glutathione. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002

evidence_span

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experimental_model

Lipid-peroxyl radical challenge in liposomes

exposure

AAPH or AMVN challenge; dietary and meso zeaxanthin

limitations

Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.

nutrient_topic

Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin

organism

Cell-free system with human GSTP1

plain_language

Binding enhanced protection of the test membrane.

primary_references

[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002

tissue_or_cell_type

Egg-yolk phosphatidylcholine liposomes

Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 262–273

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft

### zeaxanthin-gstp1-synergy GSTP1-bound dietary zeaxanthin synergistically inhibited peroxidation induced by either radical generator. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Binding enhanced protection of the test membrane. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002

evidence_span

{"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"}

experimental_model

Lipid-peroxyl radical challenge in liposomes

exposure

AAPH or AMVN challenge; dietary and meso zeaxanthin

limitations

Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination.

nutrient_topic

Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin

organism

Cell-free system with human GSTP1

plain_language

The two stereoisomers were not identical in this comparison.

primary_references

[zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002

tissue_or_cell_type

Egg-yolk phosphatidylcholine liposomes

Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 301–312

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipid-peroxyl radical challenge in liposomes · source_derived_draft · unverified_draft

### zeaxanthin-meso-bound-protection GSTP1-bound meso-zeaxanthin was more protective than bound dietary zeaxanthin in this assay. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two stereoisomers were not identical in this comparison. organism: Cell-free system with human GSTP1 tissue_or_cell_type: Egg-yolk phosphatidylcholine liposomes experimental_model: Lipid-peroxyl radical challenge in liposomes limitations: Protein-associated antioxidant synergy is demonstrated in this assay, not a clinical supplement combination. exposure: AAPH or AMVN challenge; dietary and meso zeaxanthin evidence_span: {"source_cache": "artifacts/zeaxanthin-research/15949677.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194", "start_char": 0, "end_char": 1404, "text_sha256": "4ed175c0b5cf937df5a37c94739b40d713261c3a99e2bebc02b3b6a37ea3f194"} [zeaxanthin-p15949677] Synergistic effects of zeaxanthin and its binding protein in the prevention of lipid membrane oxidation. (2005). https://pubmed.ncbi.nlm.nih.gov/15949677/ DOI: 10.1016/j.bbadis.2005.02.002

cross_nutrient

true

evidence_location

Figure 4B

experimental_model

RSL3 challenge and flow-cytometric C11-BODIPY assay

exposure

E forms at 1 and 30 µM for 1 h before 0.5 µM RSL3 for 2 h.

limitations

Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. Probe oxidation is not a chemically resolved inventory of endogenous phospholipid products.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Homo sapiens

plain_language

Alpha-tocotrienol more effectively limited the lipid-oxidation reporter in this cancer-cell assay.

primary_references

[ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1

tissue_or_cell_type

HT-1080 fibrosarcoma cells

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 802–814

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RSL3 challenge and flow-cytometric C11-BODIPY assay · source_derived_draft · unverified_draft

### ver-alpha-t3-cellular-oxidation In HT-1080 cells challenged with the GPX4 inhibitor RSL3, alpha-tocotrienol suppressed the oxidized C11-BODIPY signal at lower tested concentrations than alpha-tocopherol. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Alpha-tocotrienol more effectively limited the lipid-oxidation reporter in this cancer-cell assay. organism: Homo sapiens tissue_or_cell_type: HT-1080 fibrosarcoma cells experimental_model: RSL3 challenge and flow-cytometric C11-BODIPY assay limitations: Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. Probe oxidation is not a chemically resolved inventory of endogenous phospholipid products. exposure: E forms at 1 and 30 µM for 1 h before 0.5 µM RSL3 for 2 h. cross_nutrient: true evidence_location: Figure 4B [ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1

cross_nutrient

false

evidence_location

Figure 4A; FENIX Methods

experimental_model

Cell-free fluorescence-enabled inhibited autoxidation

exposure

Vitamin E forms tested at 1, 10 and 100 µM; 1 mM lipid, 1 mM AAPH, 37 °C.

limitations

Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. Fluorescent reporter kinetics are not a universal radical-trapping rate constant.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Cell-free

plain_language

The two alpha forms differed in protection of artificial lipid membranes.

primary_references

[ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1

tissue_or_cell_type

Phosphatidylcholine liposomes

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 788–800

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free fluorescence-enabled inhibited autoxidation · source_derived_draft · unverified_draft

### ver-alpha-t3-liposomal-oxidation Alpha-tocotrienol suppressed AAPH-initiated liposomal oxidation more strongly than alpha-tocopherol in the study’s FENIX assay, which tracked competitive oxidation of a fluorescent reporter. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two alpha forms differed in protection of artificial lipid membranes. organism: Cell-free tissue_or_cell_type: Phosphatidylcholine liposomes experimental_model: Cell-free fluorescence-enabled inhibited autoxidation limitations: Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. Fluorescent reporter kinetics are not a universal radical-trapping rate constant. exposure: Vitamin E forms tested at 1, 10 and 100 µM; 1 mM lipid, 1 mM AAPH, 37 °C. cross_nutrient: false evidence_location: Figure 4A; FENIX Methods [ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1

cross_nutrient

true

evidence_location

Primary abstract

experimental_model

Microsomes and Triton-dispersed lipid micelles

exposure

Iron-dependent peroxidation; physiological vitamin E:phospholipid ratio as reported in abstract.

limitations

Exact concentrations are not available in the inspected abstract. Model-specific dependence does not imply every membrane requires added GPX4 to show E protection.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Rattus norvegicus

plain_language

Vitamin E protection depended on peroxide removal by the GPX4/glutathione system in these preparations.

primary_references

[ver-maiorino1989] Microsomal lipid peroxidation: effect of vitamin E and its functional interaction with phospholipid hydroperoxide glutathione peroxidase. (1989). https://pubmed.ncbi.nlm.nih.gov/2586229/ DOI: 10.1007/bf02535211

tissue_or_cell_type

Liver microsomal lipids

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 592–604

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microsomes and Triton-dispersed lipid micelles · source_derived_draft · unverified_draft

### ver-gpx4-gsh-tocopherol-cooperation At a physiological vitamin E-to-phospholipid ratio, inhibition of iron-dependent lipid peroxidation in rat liver microsomes and dispersed microsomal lipids was observed only when PHGPX (GPX4) and glutathione were also present. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E protection depended on peroxide removal by the GPX4/glutathione system in these preparations. organism: Rattus norvegicus tissue_or_cell_type: Liver microsomal lipids experimental_model: Microsomes and Triton-dispersed lipid micelles limitations: Exact concentrations are not available in the inspected abstract. Model-specific dependence does not imply every membrane requires added GPX4 to show E protection. exposure: Iron-dependent peroxidation; physiological vitamin E:phospholipid ratio as reported in abstract. cross_nutrient: true evidence_location: Primary abstract [ver-maiorino1989] Microsomal lipid peroxidation: effect of vitamin E and its functional interaction with phospholipid hydroperoxide glutathione peroxidase. (1989). https://pubmed.ncbi.nlm.nih.gov/2586229/ DOI: 10.1007/bf02535211

cross_nutrient

true

evidence_location

Primary abstract

experimental_model

Sequential peroxide reduction and iron challenge

exposure

Photoperoxidation → GSH/PHGPX → iron-dependent challenge.

limitations

Ascorbate participates in this deliberately pro-oxidizing assay; this is not evidence that normal vitamin C intake damages membranes.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Human-derived cell-free membranes

plain_language

Removing membrane hydroperoxides prevented an iron-driven burst of further oxidation.

primary_references

[ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4

tissue_or_cell_type

Erythrocyte ghosts

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 578–590

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sequential peroxide reduction and iron challenge · source_derived_draft · unverified_draft

### ver-peroxide-removal-iron-burst GSH/PHGPX pretreatment completely suppressed the subsequent radical-peroxidation burst when photooxidized erythrocyte ghosts were challenged with ascorbate/iron or xanthine/xanthine-oxidase/iron. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing membrane hydroperoxides prevented an iron-driven burst of further oxidation. organism: Human-derived cell-free membranes tissue_or_cell_type: Erythrocyte ghosts experimental_model: Sequential peroxide reduction and iron challenge limitations: Ascorbate participates in this deliberately pro-oxidizing assay; this is not evidence that normal vitamin C intake damages membranes. exposure: Photoperoxidation → GSH/PHGPX → iron-dependent challenge. cross_nutrient: true evidence_location: Primary abstract [ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4

evidence_span

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experimental_model

ESR spin trapping, spectrophotometry and tissue-homogenate oxidation

exposure

Nasunin isolated from Chouja eggplant; 1 micromolar homogenate experiment

limitations

Homogenates do not establish brain entry or neuronal protection after oral intake. SOD-equivalent units are assay calibration, not SOD induction.

nutrient_topic

Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin

organism

Cell-free chemistry and rat brain homogenates

plain_language

The tested tissue preparation suffered less lipid oxidation.

primary_references

[nasunin-p10100509] Antioxidant activity of nasunin, an anthocyanin in eggplant. (1998). https://pubmed.ncbi.nlm.nih.gov/10100509/

tissue_or_cell_type

Iron complex formation and lipid oxidation

Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 562–573

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ESR spin trapping, spectrophotometry and tissue-homogenate oxidation · source_derived_draft · unverified_draft

### nasunin-brain-lipid-oxidation Nasunin at 1 micromolar reduced lipid-peroxidation products in rat brain homogenates (P<0.001). Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The tested tissue preparation suffered less lipid oxidation. organism: Cell-free chemistry and rat brain homogenates tissue_or_cell_type: Iron complex formation and lipid oxidation experimental_model: ESR spin trapping, spectrophotometry and tissue-homogenate oxidation limitations: Homogenates do not establish brain entry or neuronal protection after oral intake. SOD-equivalent units are assay calibration, not SOD induction. exposure: Nasunin isolated from Chouja eggplant; 1 micromolar homogenate experiment evidence_span: {"source_cache": "artifacts/nasunin-research/10100509.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c9b0aa305d8c03dd6b8fe8c1fae505dc50b3347a43c00387e01d4e36ecd04c09", "start_char": 0, "end_char": 1400, "text_sha256": "c9b0aa305d8c03dd6b8fe8c1fae505dc50b3347a43c00387e01d4e36ecd04c09"} [nasunin-p10100509] Antioxidant activity of nasunin, an anthocyanin in eggplant. (1998). https://pubmed.ncbi.nlm.nih.gov/10100509/

evidence_span

{"source_cache": "artifacts/nasunin-research/10962130.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61b195a6eff14c25cfc341069c7cafb8fe4d0b374aa294b3d28e0e48bbed7c16", "start_char": 0, "end_char": 1706, "text_sha256": "61b195a6eff14c25cfc341069c7cafb8fe4d0b374aa294b3d28e0e48bbed7c16"}

experimental_model

DMPO-competition ESR assay and peroxide challenge

exposure

Variable DMPO concentrations; nasunin below 50 micromolar in homogenate experiments

limitations

Related investigators and overlapping numerical results with the 1998 report; not independent replication. Ferrous-chelation interpretation is distinct from the earlier Fe(III) stoichiometry experiment.

nutrient_topic

Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin

organism

Cell-free reaction and rat brain homogenate

plain_language

This is a biochemical protection result, not a brain-treatment trial.

primary_references

[nasunin-p10962130] Antioxidant activity of nasunin, an anthocyanin in eggplant peels. (2000). https://pubmed.ncbi.nlm.nih.gov/10962130/ DOI: 10.1016/s0300-483x(00)00202-x

tissue_or_cell_type

Fenton chemistry and lipid-peroxidation markers

Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 588–599

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · DMPO-competition ESR assay and peroxide challenge · source_derived_draft · unverified_draft

### nasunin-peroxide-lipid-protection Nasunin below 50 micromolar reduced peroxide-induced lipid-peroxidation readouts in rat brain homogenates. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This is a biochemical protection result, not a brain-treatment trial. organism: Cell-free reaction and rat brain homogenate tissue_or_cell_type: Fenton chemistry and lipid-peroxidation markers experimental_model: DMPO-competition ESR assay and peroxide challenge limitations: Related investigators and overlapping numerical results with the 1998 report; not independent replication. Ferrous-chelation interpretation is distinct from the earlier Fe(III) stoichiometry experiment. exposure: Variable DMPO concentrations; nasunin below 50 micromolar in homogenate experiments evidence_span: {"source_cache": "artifacts/nasunin-research/10962130.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61b195a6eff14c25cfc341069c7cafb8fe4d0b374aa294b3d28e0e48bbed7c16", "start_char": 0, "end_char": 1706, "text_sha256": "61b195a6eff14c25cfc341069c7cafb8fe4d0b374aa294b3d28e0e48bbed7c16"} [nasunin-p10962130] Antioxidant activity of nasunin, an anthocyanin in eggplant peels. (2000). https://pubmed.ncbi.nlm.nih.gov/10962130/ DOI: 10.1016/s0300-483x(00)00202-x

cell_type

neural lineage

experimental_model

Conditional knockout

limitations

Indirect redox consequence does not establish SELENOI peroxidase activity.

organism

mouse

Selenium: literature corrections and mechanism additions · lines 774–784

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Conditional knockout · secondary_verified · secondary_verified

## neural-selenoi-loss-increases-lipid-peroxidation Loss of SELENOI increased lipid damage in this neural model. Neural Selenoi deletion increased lipid-peroxidation readouts. Organism: mouse Cell type: neural lineage Experimental model: Conditional knockout Limitations: Indirect redox consequence does not establish SELENOI peroxidase activity. Primary reference: [Selenoprotein I is indispensable for ether lipid homeostasis and proper myelination](https://pubmed.ncbi.nlm.nih.gov/38582453/)

evidence_span

{"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"}

experimental_model

Twelve patients sampled at the first and fifteenth hyperbaric session

exposure

Fifteen hyperbaric oxygen treatments without antioxidant supplementation

limitations

A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Repeated treatment leaves measurable marks of oxidation in the blood.

primary_references

[hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

tissue_or_cell_type

Plasma and erythrocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 231–242

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve patients sampled at the first and fifteenth hyperbaric session · source_derived_draft · unverified_draft

### hbot-rom-accumulation Repeated exposures led to significant accumulation of plasma reactive oxygen metabolites and malondialdehyde across fifteen sessions. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Repeated treatment leaves measurable marks of oxidation in the blood. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Twelve patients sampled at the first and fifteenth hyperbaric session limitations: A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation. exposure: Fifteen hyperbaric oxygen treatments without antioxidant supplementation evidence_span: {"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"} [hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Thirty female guinea pig offspring, control/deficient/repleted diets, postnatal day 70

exposure

Prenatal/postnatal 100/100 mg vitamin C/kg diet versus 900/750 mg/kg controls; female offspring at day 70

limitations

An oxidative marker does not measure every developmental or neurological outcome.

nutrient_topic

Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C

organism

Cavia porcellus

plain_language

Low vitamin C increased a marker of brain lipid oxidation.

primary_references

[brain2014] Chronic vitamin C deficiency promotes redox imbalance in the brain but does not alter sodium-dependent vitamin C transporter 2 expression. (2014). https://pubmed.ncbi.nlm.nih.gov/24787032/ DOI: 10.3390/nu6051809

tissue_or_cell_type

Brain

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 494–505

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Thirty female guinea pig offspring, control/deficient/repleted diets, postnatal day 70 · source_derived_draft · unverified_draft

### vc-transport-diet-brain-mda Chronically vitamin-C-restricted guinea pigs had higher brain malondialdehyde than vitamin-C-sufficient controls at day 70. Condition category: nutrient_deficiency nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low vitamin C increased a marker of brain lipid oxidation. organism: Cavia porcellus tissue_or_cell_type: Brain experimental_model: Thirty female guinea pig offspring, control/deficient/repleted diets, postnatal day 70 limitations: An oxidative marker does not measure every developmental or neurological outcome. exposure: Prenatal/postnatal 100/100 mg vitamin C/kg diet versus 900/750 mg/kg controls; female offspring at day 70 cross_nutrient: false [brain2014] Chronic vitamin C deficiency promotes redox imbalance in the brain but does not alter sodium-dependent vitamin C transporter 2 expression. (2014). https://pubmed.ncbi.nlm.nih.gov/24787032/ DOI: 10.3390/nu6051809