Nutrient chapter

Taurine

Taurine. Species, exposure and limitations are retained in each linked claim.

84 recorded mechanisms · 8 availability situations · 8 preserved sources. Draft and verified records 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.

Purified human CSAD decarboxylated L-cysteine sulfinic acid to hypotaurine in PLP-containing enzyme assays.
Human cysteine sulfinic acid decarboxylase / CSAD → Hypotaurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, introduction and enzyme-assay results
experimental_model
Recombinant human enzyme; substrate kinetics and circular-dichroism assays.
limitations
Hypotaurine still needs oxidation to become taurine; this is not a human supplementation experiment.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Vitamin B6-dependent CSAD performs a step between cysteine and taurine.
primary_references
A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 33–39
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme; substrate kinetics and circular-dichroism assays. · source_derived_draft · unverified_draft
## taurine-csad-cysteinesulfinate Vitamin B6-dependent CSAD performs a step between cysteine and taurine. Purified human CSAD decarboxylated L-cysteine sulfinic acid to hypotaurine in PLP-containing enzyme assays. Model: Recombinant human enzyme; substrate kinetics and circular-dichroism assays. Limitations: Hypotaurine still needs oxidation to become taurine; this is not a human supplementation experiment. Evidence access: Primary full text, introduction and enzyme-assay results A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Complete structured claim and evidence
The purified human CSAD characterized in this study was a PLP-dependent enzyme, linking its decarboxylation chemistry to the active cofactor form of vitamin B6.
PLP → Human cysteine sulfinic acid decarboxylase / CSAD source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, enzyme characterization
experimental_model
Human recombinant CSAD biochemical characterization.
limitations
Cofactor dependence does not establish that extra B6 increases taurine in a replete person.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
CSAD needs the active B6 cofactor, not just its cysteine-derived substrate.
primary_references
A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 41–47
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant CSAD biochemical characterization. · source_derived_draft · unverified_draft
## taurine-csad-plp CSAD needs the active B6 cofactor, not just its cysteine-derived substrate. The purified human CSAD characterized in this study was a PLP-dependent enzyme, linking its decarboxylation chemistry to the active cofactor form of vitamin B6. Model: Human recombinant CSAD biochemical characterization. Limitations: Cofactor dependence does not establish that extra B6 increases taurine in a replete person. Evidence access: Primary full text, enzyme characterization A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Complete structured claim and evidence
Human CSAD also catalyzed L-cysteic-acid decarboxylation to taurine in vitro.
Human cysteine sulfinic acid decarboxylase / CSAD → Taurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, substrate comparison
experimental_model
Recombinant human enzyme; L-cysteic-acid substrate assays.
limitations
This alternative reaction does not quantify its contribution to human whole-body synthesis.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The same enzyme can use a more oxidized substrate to make taurine directly.
primary_references
A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 49–55
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme; L-cysteic-acid substrate assays. · source_derived_draft · unverified_draft
## taurine-csad-cysteic-acid The same enzyme can use a more oxidized substrate to make taurine directly. Human CSAD also catalyzed L-cysteic-acid decarboxylation to taurine in vitro. Model: Recombinant human enzyme; L-cysteic-acid substrate assays. Limitations: This alternative reaction does not quantify its contribution to human whole-body synthesis. Evidence access: Primary full text, substrate comparison A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Complete structured claim and evidence
Recombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay.
Mouse cysteamine dioxygenase / Ado → Hypotaurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified recombinant murine protein.
limitations
Do not assign the mouse enzyme kinetics directly to human ADO.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A separate enzyme provides a route from cysteamine.
primary_references
Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 57–63
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified recombinant murine protein. · source_derived_draft · unverified_draft
## taurine-ado-mouse-enzyme A separate enzyme provides a route from cysteamine. Recombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay. Model: Purified recombinant murine protein. Limitations: Do not assign the mouse enzyme kinetics directly to human ADO. Evidence access: Primary abstract Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Complete structured claim and evidence
RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine.
Human 2-aminoethanethiol dioxygenase / ADO → Hypotaurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human liver-derived cultured cells.
limitations
Cysteamine can arise through CoA breakdown; this experiment does not show that B5 supplementation raises taurine.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Human-cell gene silencing supports the cysteamine pathway.
primary_references
Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 65–71
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver-derived cultured cells. · source_derived_draft · unverified_draft
## taurine-ado-human-knockdown Human-cell gene silencing supports the cysteamine pathway. RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine. Model: Human liver-derived cultured cells. Limitations: Cysteamine can arise through CoA breakdown; this experiment does not show that B5 supplementation raises taurine. Evidence access: Primary abstract Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Complete structured claim and evidence
Recombinant human FMO1 catalyzed oxygenation of hypotaurine to taurine in vitro.
Human flavin-containing monooxygenase 1 / FMO1 → Taurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human FMO1 enzyme assays.
limitations
This identifies an enzyme activity; it does not establish FMO1 as the only possible route in every tissue.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
FMO1 completes the hypotaurine-to-taurine step.
primary_references
Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 73–79
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human FMO1 enzyme assays. · source_derived_draft · unverified_draft
## taurine-fmo1-oxidation FMO1 completes the hypotaurine-to-taurine step. Recombinant human FMO1 catalyzed oxygenation of hypotaurine to taurine in vitro. Model: Human FMO1 enzyme assays. Limitations: This identifies an enzyme activity; it does not establish FMO1 as the only possible route in every tissue. Evidence access: Primary abstract Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Complete structured claim and evidence
Human FMO1 converted hypotaurine to taurine with either NADPH or NADH as the reducing cofactor in the reported assays.
NADPH → Human flavin-containing monooxygenase 1 / FMO1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant human FMO1 biochemistry.
limitations
NAD(P)H availability, FMO1 abundance and substrate availability are separate variables; no niacin repletion effect was tested.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Niacin-derived electron carriers support this synthetic reaction.
primary_references
Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 81–87
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human FMO1 biochemistry. · source_derived_draft · unverified_draft
## taurine-fmo1-reducing-cofactors Niacin-derived electron carriers support this synthetic reaction. Human FMO1 converted hypotaurine to taurine with either NADPH or NADH as the reducing cofactor in the reported assays. Model: Recombinant human FMO1 biochemistry. Limitations: NAD(P)H availability, FMO1 abundance and substrate availability are separate variables; no niacin repletion effect was tested. Evidence access: Primary abstract Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Complete structured claim and evidence
Fmo1-null mice accumulated urinary hypotaurine and had less urinary taurine than wild-type mice.
Mouse flavin-containing monooxygenase 1 / Fmo1 → Urinary hypotaurine and taurine in Fmo1-null mice source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse knockout; urinary proton NMR metabolomics.
limitations
Urine metabolites do not directly measure every tissue pool or prove human dietary deficiency.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Disabling the final enzyme changed the precursor/product pattern.
primary_references
Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 89–95
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout; urinary proton NMR metabolomics. · source_derived_draft · unverified_draft
## taurine-fmo1-deletion Disabling the final enzyme changed the precursor/product pattern. Fmo1-null mice accumulated urinary hypotaurine and had less urinary taurine than wild-type mice. Model: Mouse knockout; urinary proton NMR metabolomics. Limitations: Urine metabolites do not directly measure every tissue pool or prove human dietary deficiency. Evidence access: Primary abstract Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Complete structured claim and evidence
Liver-specific Cdo1 deletion increased extrahepatic CDO abundance and hypotaurine; mice maintained taurine, glutathione and sulfate despite a taurine-free diet.
Mouse cysteine dioxygenase / Cdo1 → Extrahepatic compensation for hepatic Cdo1 loss in mice source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Conditional mouse liver knockout; kidney, adipose and pancreatic measurements.
limitations
This tissue-restricted deletion differs from complete pathway loss and from human deficiency.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Other tissues compensated when liver synthesis was impaired.
primary_references
Extrahepatic tissues compensate for loss of hepatic taurine synthesis in mice with liver-specific knockout of cysteine dioxygenase. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22414809/ · DOI 10.1152/ajpendo.00589.2011
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 97–103
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse liver knockout; kidney, adipose and pancreatic measurements. · source_derived_draft · unverified_draft
## taurine-hepatic-compensation Other tissues compensated when liver synthesis was impaired. Liver-specific Cdo1 deletion increased extrahepatic CDO abundance and hypotaurine; mice maintained taurine, glutathione and sulfate despite a taurine-free diet. Model: Conditional mouse liver knockout; kidney, adipose and pancreatic measurements. Limitations: This tissue-restricted deletion differs from complete pathway loss and from human deficiency. Evidence access: Primary abstract Extrahepatic tissues compensate for loss of hepatic taurine synthesis in mice with liver-specific knockout of cysteine dioxygenase. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22414809/ · DOI 10.1152/ajpendo.00589.2011
Complete structured claim and evidence
Human TauT structures and uptake assays characterized sodium- and chloride-dependent taurine transport and substrate recognition.
Human taurine transporter / SLC6A6 → Taurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human SLC6A6 cryo-EM structures plus biochemical transport assays.
limitations
Transport activity is distinct from oral absorption, blood concentration and tissue sufficiency.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Cells need a transporter to accumulate taurine.
primary_references
Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
transport_effect
raises Uptake assays characterised sodium- and chloride-dependent taurine transport.
transport_pool
the expressing cell Uptake assays characterised sodium- and chloride-dependent taurine transport.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 105–111
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human SLC6A6 cryo-EM structures plus biochemical transport assays. · source_derived_draft · unverified_draft
## taurine-taut-uptake Cells need a transporter to accumulate taurine. Human TauT structures and uptake assays characterized sodium- and chloride-dependent taurine transport and substrate recognition. Model: Human SLC6A6 cryo-EM structures plus biochemical transport assays. Limitations: Transport activity is distinct from oral absorption, blood concentration and tissue sufficiency. Evidence access: Primary abstract Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Complete structured claim and evidence
Replacing sodium strongly reduced taurine uptake in reconstituted human placental membranes; uptake kinetics supported two sodium ions per taurine.
Sodium ion → Human SLC6A6-mediated cellular taurine uptake source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human placental brush-border proteins reconstituted in proteoliposomes.
limitations
This was not purified SLC6A6 alone; the coupling estimate is assay-specific, not a reason to consume more sodium.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The sodium gradient helps power taurine entry.
primary_references
Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 113–119
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human placental brush-border proteins reconstituted in proteoliposomes. · source_derived_draft · unverified_draft
## taurine-placental-sodium The sodium gradient helps power taurine entry. Replacing sodium strongly reduced taurine uptake in reconstituted human placental membranes; uptake kinetics supported two sodium ions per taurine. Model: Human placental brush-border proteins reconstituted in proteoliposomes. Limitations: This was not purified SLC6A6 alone; the coupling estimate is assay-specific, not a reason to consume more sodium. Evidence access: Primary abstract Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Complete structured claim and evidence
Taurine uptake by reconstituted human placental membranes required chloride; chloride kinetics supported one chloride per taurine.
Chloride ion → Human SLC6A6-mediated cellular taurine uptake source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human placental membrane proteoliposomes.
limitations
Alternative anions supported at most 30% of control uptake; this does not define a dietary chloride threshold.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Chloride is part of the transport cycle.
primary_references
Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 121–127
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human placental membrane proteoliposomes. · source_derived_draft · unverified_draft
## taurine-placental-chloride Chloride is part of the transport cycle. Taurine uptake by reconstituted human placental membranes required chloride; chloride kinetics supported one chloride per taurine. Model: Human placental membrane proteoliposomes. Limitations: Alternative anions supported at most 30% of control uptake; this does not define a dietary chloride threshold. Evidence access: Primary abstract Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Complete structured claim and evidence
Human TauT structures captured beta-alanine and taurine as separately bound substrate analogues at the transporter binding site.
Beta-alanine → Taurine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human SLC6A6 cryo-EM structures and biochemical analysis.
limitations
Shared binding does not prove taurine depletion at typical beta-alanine supplement exposure.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Beta-alanine and taurine interact with the same molecular doorway.
primary_references
Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 129–135
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human SLC6A6 cryo-EM structures and biochemical analysis. · source_derived_draft · unverified_draft
## taurine-taut-beta-alanine Beta-alanine and taurine interact with the same molecular doorway. Human TauT structures captured beta-alanine and taurine as separately bound substrate analogues at the transporter binding site. Model: Human SLC6A6 cryo-EM structures and biochemical analysis. Limitations: Shared binding does not prove taurine depletion at typical beta-alanine supplement exposure. Evidence access: Primary abstract Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Complete structured claim and evidence
The human TauT study captured guanidinoacetate-bound transporter structures as part of its substrate-recognition analysis.
Guanidinoacetate → Human taurine transporter / SLC6A6 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human SLC6A6 structural study.
limitations
Binding structures alone do not quantify net transport or competition in a living human.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A creatine precursor also connects to this transporter.
primary_references
Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 137–143
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human SLC6A6 structural study. · source_derived_draft · unverified_draft
## taurine-taut-guanidinoacetate A creatine precursor also connects to this transporter. The human TauT study captured guanidinoacetate-bound transporter structures as part of its substrate-recognition analysis. Model: Human SLC6A6 structural study. Limitations: Binding structures alone do not quantify net transport or competition in a living human. Evidence access: Primary abstract Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Complete structured claim and evidence
The homozygous SLC6A6 p.Ala78Glu variant was associated with approximately 95% lower taurine uptake in patient peripheral blood mononuclear cells despite membrane localization of the variant protein.
Human taurine transporter / SLC6A6 → Human SLC6A6-mediated cellular taurine uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Two affected brothers; human genetic, cell and spectroscopy studies.
limitations
Variant-specific inherited disease, not a universal threshold for dietary taurine insufficiency.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A transporter can reach the membrane yet function poorly.
primary_references
Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 145–151
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Two affected brothers; human genetic, cell and spectroscopy studies. · source_derived_draft · unverified_draft
## taurine-taut-a78e A transporter can reach the membrane yet function poorly. The homozygous SLC6A6 p.Ala78Glu variant was associated with approximately 95% lower taurine uptake in patient peripheral blood mononuclear cells despite membrane localization of the variant protein. Model: Two affected brothers; human genetic, cell and spectroscopy studies. Limitations: Variant-specific inherited disease, not a universal threshold for dietary taurine insufficiency. Evidence access: Primary abstract Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
Complete structured claim and evidence
The two brothers carrying homozygous SLC6A6 p.Ala78Glu had panretinal degeneration and markedly reduced taurine in plasma, muscle and brain.
Human taurine transporter / SLC6A6 → Retinal degeneration in human SLC6A6 deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rare human family; retinal examinations and in-vivo spectroscopy.
limitations
Absence of extraocular clinical signs at that time does not mean every organ was unaffected.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Transport failure affected taurine availability in multiple compartments.
primary_references
Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 153–159
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rare human family; retinal examinations and in-vivo spectroscopy. · source_derived_draft · unverified_draft
## taurine-taut-retina Transport failure affected taurine availability in multiple compartments. The two brothers carrying homozygous SLC6A6 p.Ala78Glu had panretinal degeneration and markedly reduced taurine in plasma, muscle and brain. Model: Rare human family; retinal examinations and in-vivo spectroscopy. Limitations: Absence of extraocular clinical signs at that time does not mean every organ was unaffected. Evidence access: Primary abstract Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
Complete structured claim and evidence
In two siblings with SLC6A6 p.Gly399Val and about 15% residual transport, supervised taurine treatment at 100 mg/kg/day normalized blood taurine and corrected cardiomyopathy after 24 months.
Taurine → Cardiomyopathy in human SLC6A6 deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Uncontrolled two-sibling longitudinal treatment report.
limitations
Not a dosing recommendation or evidence that all SLC6A6 variants respond; residual transport and timing matter.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A partially working transporter permitted a clinical treatment response in this family.
primary_references
Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 161–167
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Uncontrolled two-sibling longitudinal treatment report. · source_derived_draft · unverified_draft
## taurine-taut-heart-treatment A partially working transporter permitted a clinical treatment response in this family. In two siblings with SLC6A6 p.Gly399Val and about 15% residual transport, supervised taurine treatment at 100 mg/kg/day normalized blood taurine and corrected cardiomyopathy after 24 months. Model: Uncontrolled two-sibling longitudinal treatment report. Limitations: Not a dosing recommendation or evidence that all SLC6A6 variants respond; residual transport and timing matter. Evidence access: Primary abstract Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
Complete structured claim and evidence
In the younger, six-year-old sibling in the p.Gly399Val family, taurine treatment was associated with arrested retinal degeneration and clinically improved vision over follow-up.
Taurine → Retinal degeneration in human SLC6A6 deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Same two-sibling report; retinal response documented in the younger child.
limitations
Not proof that established retinal loss is generally reversible or that treatment works with complete transport loss.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Early retinal disease stabilized in one treated child.
primary_references
Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 169–175
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same two-sibling report; retinal response documented in the younger child. · source_derived_draft · unverified_draft
## taurine-taut-retinal-treatment Early retinal disease stabilized in one treated child. In the younger, six-year-old sibling in the p.Gly399Val family, taurine treatment was associated with arrested retinal degeneration and clinically improved vision over follow-up. Model: Same two-sibling report; retinal response documented in the younger child. Limitations: Not proof that established retinal loss is generally reversible or that treatment works with complete transport loss. Evidence access: Primary abstract Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
Complete structured claim and evidence
SLC6A6 p.Thr249Ile and p.Ala294Thr missense variants showed complete loss of taurine transport in HEK293 cells and patient fibroblasts in the four-family study of seven affected individuals.
Human taurine transporter / SLC6A6 → Human SLC6A6-mediated cellular taurine uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human multicenter genetic study; cellular transport experiments; final issue year 2026, online 2025.
limitations
Investigational supplementation was proposed, not proven effective by this study.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Some disease variants had no measurable transport in the tested cells.
primary_references
Early-Onset Retinopathy in Patients With Variants in SLC6A6 Leading to Impaired Taurine Transport. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41343195/ · DOI 10.1001/jamaophthalmol.2025.4875
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 177–183
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human multicenter genetic study; cellular transport experiments; final issue year 2026, online 2025. · source_derived_draft · unverified_draft
## taurine-taut-new-variants Some disease variants had no measurable transport in the tested cells. SLC6A6 p.Thr249Ile and p.Ala294Thr missense variants showed complete loss of taurine transport in HEK293 cells and patient fibroblasts in the four-family study of seven affected individuals. Model: Human multicenter genetic study; cellular transport experiments; final issue year 2026, online 2025. Limitations: Investigational supplementation was proposed, not proven effective by this study. Evidence access: Primary abstract Early-Onset Retinopathy in Patients With Variants in SLC6A6 Leading to Impaired Taurine Transport. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41343195/ · DOI 10.1001/jamaophthalmol.2025.4875
Complete structured claim and evidence
Two weeks of low-protein or low-sulfur-amino-acid feeding lowered plasma taurine and increased renal taurine uptake while reducing fractional urinary excretion in the studied mouse strains.
Taurine → Renal taurine conservation in dietary-restricted mice source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
C3H/HeJ and C57BL/6J mice; in-vivo excretion and renal membrane transport.
limitations
Strain-specific responses; precursor restriction is not isolated taurine withdrawal.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The kidney conserved taurine when dietary supply of its precursors was restricted.
primary_references
Renal transport of taurine adapts to perturbed taurine homeostasis. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6952257/ · DOI 10.1073/pnas.79.6.2101
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 185–191
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C3H/HeJ and C57BL/6J mice; in-vivo excretion and renal membrane transport. · source_derived_draft · unverified_draft
## taurine-renal-mouse-conservation The kidney conserved taurine when dietary supply of its precursors was restricted. Two weeks of low-protein or low-sulfur-amino-acid feeding lowered plasma taurine and increased renal taurine uptake while reducing fractional urinary excretion in the studied mouse strains. Model: C3H/HeJ and C57BL/6J mice; in-vivo excretion and renal membrane transport. Limitations: Strain-specific responses; precursor restriction is not isolated taurine withdrawal. Evidence access: Primary abstract Renal transport of taurine adapts to perturbed taurine homeostasis. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6952257/ · DOI 10.1073/pnas.79.6.2101
Complete structured claim and evidence
A diet deficient in cysteine and methionine increased the Vmax of the rat high-affinity renal taurine uptake system without changing apparent Km.
Taurine → Renal taurine conservation in precursor-restricted rats source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat dietary adaptation and renal transport assays.
limitations
Adaptation over days does not establish equivalent regulation in all human disease states.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Conservation involved more transport capacity rather than greater binding affinity.
primary_references
Renal adaptation to alteration in dietary amino acid intake. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6881333/ · DOI 10.1152/ajprenal.1983.245.2.F159
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 193–199
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat dietary adaptation and renal transport assays. · source_derived_draft · unverified_draft
## taurine-renal-rat-capacity Conservation involved more transport capacity rather than greater binding affinity. A diet deficient in cysteine and methionine increased the Vmax of the rat high-affinity renal taurine uptake system without changing apparent Km. Model: Rat dietary adaptation and renal transport assays. Limitations: Adaptation over days does not establish equivalent regulation in all human disease states. Evidence access: Primary abstract Renal adaptation to alteration in dietary amino acid intake. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6881333/ · DOI 10.1152/ajprenal.1983.245.2.F159
Complete structured claim and evidence
Reconstituting the human MTO1-GTPBP3 complex with hypomodified mitochondrial tRNA, taurine and 5,10-methylene-THF produced the taurine-containing U34 modification.
Human mitochondrial tRNA modification protein / MTO1 → Mitochondrial tRNA 5-taurinomethyluridine / tau-m5U34 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, in-vitro reconstitution methods and results
experimental_model
Human enzyme-complex reconstitution and mass spectrometry.
limitations
The reaction mixture also contained GTP, ATP, FAD, NADH, NADPH and magnesium; their presence alone does not demonstrate each is individually limiting.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Two proteins join taurine and a folate-derived carbon unit onto mitochondrial tRNA.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 201–207
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme-complex reconstitution and mass spectrometry. · source_derived_draft · unverified_draft
## taurine-mto1-gtpbp3 Two proteins join taurine and a folate-derived carbon unit onto mitochondrial tRNA. Reconstituting the human MTO1-GTPBP3 complex with hypomodified mitochondrial tRNA, taurine and 5,10-methylene-THF produced the taurine-containing U34 modification. Model: Human enzyme-complex reconstitution and mass spectrometry. Limitations: The reaction mixture also contained GTP, ATP, FAD, NADH, NADPH and magnesium; their presence alone does not demonstrate each is individually limiting. Evidence access: Primary full text, in-vitro reconstitution methods and results Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Isotope tracing supported the beta-carbon of serine entering the methylene group of mitochondrial taurine-modified uridine through 5,10-methylene-THF.
5,10-Methylenetetrahydrofolate → Mitochondrial tRNA 5-taurinomethyluridine / tau-m5U34 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Figure 1 and metabolic-labeling experiments
experimental_model
Human HeLa metabolic labeling plus biochemical reconstitution.
limitations
A folate connection is not evidence for a benefit from folic acid supplementation in replete people.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Folate chemistry contributes part of the RNA mark; taurine supplies a different part.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 209–215
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human HeLa metabolic labeling plus biochemical reconstitution. · source_derived_draft · unverified_draft
## taurine-folate-carbon-donor Folate chemistry contributes part of the RNA mark; taurine supplies a different part. Isotope tracing supported the beta-carbon of serine entering the methylene group of mitochondrial taurine-modified uridine through 5,10-methylene-THF. Model: Human HeLa metabolic labeling plus biochemical reconstitution. Limitations: A folate connection is not evidence for a benefit from folic acid supplementation in replete people. Evidence access: Primary full text, Figure 1 and metabolic-labeling experiments Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Shmt2-mutant Chinese hamster ovary cells showed reduced mitochondrial tRNA taurine modification compared with wild type.
Chinese hamster mitochondrial serine hydroxymethyltransferase / Shmt2 → Mitochondrial tRNA 5-taurinomethyluridine / tau-m5U34 source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text, Figure 1F
experimental_model
CHO mutant-cell mass spectrometry.
limitations
This species-specific machinery defect is not a B6 or folate deprivation experiment.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
One-carbon supply can affect the same RNA mark even when the taurine molecule is present.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 217–223
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO mutant-cell mass spectrometry. · source_derived_draft · unverified_draft
## taurine-shmt2-mutation One-carbon supply can affect the same RNA mark even when the taurine molecule is present. Shmt2-mutant Chinese hamster ovary cells showed reduced mitochondrial tRNA taurine modification compared with wild type. Model: CHO mutant-cell mass spectrometry. Limitations: This species-specific machinery defect is not a B6 or folate deprivation experiment. Evidence access: Primary full text, Figure 1F Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Mitochondrial folate-transporter-mutant CHO cells showed reduced taurine modification of mitochondrial tRNA.
Chinese hamster mitochondrial folate transporter / Slc25a32 → Mitochondrial tRNA 5-taurinomethyluridine / tau-m5U34 source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary full text, Figure 1F
experimental_model
Chinese hamster ovary Mft mutant cells.
limitations
Compartment-specific transport failure is different from low total blood folate.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Getting folate into the mitochondrial compartment matters.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 225–231
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chinese hamster ovary Mft mutant cells. · source_derived_draft · unverified_draft
## taurine-folate-carrier-mutation Getting folate into the mitochondrial compartment matters. Mitochondrial folate-transporter-mutant CHO cells showed reduced taurine modification of mitochondrial tRNA. Model: Chinese hamster ovary Mft mutant cells. Limitations: Compartment-specific transport failure is different from low total blood folate. Evidence access: Primary full text, Figure 1F Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Taurine starvation reduced mitochondrial tRNA taurine modification in cultured cells, with corresponding dietary-depletion observations in cat liver and flatfish tissues.
Taurine → Mitochondrial tRNA 5-taurinomethyluridine / tau-m5U34 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Cultured-cell and dietary animal experiments.
limitations
Cats and flatfish differ from adult humans in endogenous taurine synthesis; no universal human plasma threshold was determined.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Insufficient taurine can leave fewer tRNAs carrying the normal mark.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 233–239
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cultured-cell and dietary animal experiments. · source_derived_draft · unverified_draft
## taurine-taurine-starvation-rna Insufficient taurine can leave fewer tRNAs carrying the normal mark. Taurine starvation reduced mitochondrial tRNA taurine modification in cultured cells, with corresponding dietary-depletion observations in cat liver and flatfish tissues. Model: Cultured-cell and dietary animal experiments. Limitations: Cats and flatfish differ from adult humans in endogenous taurine synthesis; no universal human plasma threshold was determined. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Taurine-depleted cultured cells accumulated mitochondrial tRNA cmnm5U, whose glycine-derived group replaces the taurine-derived group of tau-m5U.
Glycine → Mitochondrial tRNA 5-carboxymethylaminomethyluridine / cmnm5U34 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mass spectrometry of mitochondrial tRNAs from depleted cells.
limitations
Detection of an alternative mark does not establish complete functional rescue by glycine.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Low taurine changed the chemical identity of the RNA modification.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 241–247
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mass spectrometry of mitochondrial tRNAs from depleted cells. · source_derived_draft · unverified_draft
## taurine-glycine-substitution Low taurine changed the chemical identity of the RNA modification. Taurine-depleted cultured cells accumulated mitochondrial tRNA cmnm5U, whose glycine-derived group replaces the taurine-derived group of tau-m5U. Model: Mass spectrometry of mitochondrial tRNAs from depleted cells. Limitations: Detection of an alternative mark does not establish complete functional rescue by glycine. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Deleting GTPBP3 in human cells eliminated the normal taurine-containing wobble modification and reduced mitochondrial translation.
Human mitochondrial GTP-binding protein 3 / GTPBP3 → Mitochondrial translation in human GTPBP3-deficient cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human GTPBP3-knockout cultured cells.
limitations
Adding substrate cannot be assumed to substitute for an absent enzyme.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Removing the modifying machinery impaired mitochondrial protein production.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 249–255
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human GTPBP3-knockout cultured cells. · source_derived_draft · unverified_draft
## taurine-gtpbp3-translation Removing the modifying machinery impaired mitochondrial protein production. Deleting GTPBP3 in human cells eliminated the normal taurine-containing wobble modification and reduced mitochondrial translation. Model: Human GTPBP3-knockout cultured cells. Limitations: Adding substrate cannot be assumed to substitute for an absent enzyme. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
GTPBP3-knockout human cells exhibited impaired mitochondrial respiration alongside loss of taurine tRNA modification.
Human mitochondrial GTP-binding protein 3 / GTPBP3 → Mitochondrial respiration in human GTPBP3-deficient cells source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human cell knockout; respiratory measurements.
limitations
Same perturbation as the translation claim, not independent clinical evidence.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The RNA-processing defect reached the cell respiratory machinery.
primary_references
Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 257–263
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cell knockout; respiratory measurements. · source_derived_draft · unverified_draft
## taurine-gtpbp3-respiration The RNA-processing defect reached the cell respiratory machinery. GTPBP3-knockout human cells exhibited impaired mitochondrial respiration alongside loss of taurine tRNA modification. Model: Human cell knockout; respiratory measurements. Limitations: Same perturbation as the translation claim, not independent clinical evidence. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidence
Purified mature human GTPBP3 exhibited GTPase activity, and functional experiments linked that activity to tRNA modification.
Human mitochondrial GTP-binding protein 3 / GTPBP3 → Guanosine triphosphate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human enzyme kinetics and cellular/yeast functional studies.
limitations
Results depend on the mature protein construct; do not infer benefit from dietary nucleotide supplements.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The modifying complex includes a GTP-powered component.
primary_references
The human tRNA taurine modification enzyme GTPBP3 is an active GTPase linked to mitochondrial diseases. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33619562/ · DOI 10.1093/nar/gkab104
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 265–271
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme kinetics and cellular/yeast functional studies. · source_derived_draft · unverified_draft
## taurine-gtpbp3-gtpase The modifying complex includes a GTP-powered component. Purified mature human GTPBP3 exhibited GTPase activity, and functional experiments linked that activity to tRNA modification. Model: Human enzyme kinetics and cellular/yeast functional studies. Limitations: Results depend on the mature protein construct; do not infer benefit from dietary nucleotide supplements. Evidence access: Primary abstract The human tRNA taurine modification enzyme GTPBP3 is an active GTPase linked to mitochondrial diseases. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33619562/ · DOI 10.1093/nar/gkab104
Complete structured claim and evidence
Mto1-deficient experimental cells and mice showed defective mitochondrial translation with mistargeting and aggregation of nuclear-encoded mitochondrial proteins; chemical chaperones reduced cytotoxicity.
Mouse mitochondrial tRNA modification protein / Mto1 → Cytoplasmic proteostress following Mto1 loss in mouse models source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mto1 deficiency in experimental cells and mice.
limitations
The rescue used chemical chaperones, not proof that taurine treats absent Mto1.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Failure of mitochondrial translation can disturb protein handling beyond mitochondria.
primary_references
Defective Mitochondrial tRNA Taurine Modification Activates Global Proteostress and Leads to Mitochondrial Disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29320742/ · DOI 10.1016/j.celrep.2017.12.051
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 273–279
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mto1 deficiency in experimental cells and mice. · source_derived_draft · unverified_draft
## taurine-mto1-proteostress Failure of mitochondrial translation can disturb protein handling beyond mitochondria. Mto1-deficient experimental cells and mice showed defective mitochondrial translation with mistargeting and aggregation of nuclear-encoded mitochondrial proteins; chemical chaperones reduced cytotoxicity. Model: Mto1 deficiency in experimental cells and mice. Limitations: The rescue used chemical chaperones, not proof that taurine treats absent Mto1. Evidence access: Primary abstract Defective Mitochondrial tRNA Taurine Modification Activates Global Proteostress and Leads to Mitochondrial Disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29320742/ · DOI 10.1016/j.celrep.2017.12.051
Complete structured claim and evidence
Five patients in the ten-person MELAS trial showed a significant increase in leukocyte mitochondrial tRNA-Leu(UUR) taurine modification after high-dose taurine treatment.
Taurine → Mitochondrial tRNA 5-taurinomethyluridine / tau-m5U34 source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Open-label 52-week study; 9 or 12 g/day under clinical supervision.
limitations
Five molecular responders among ten patients; leukocyte measurements are not direct brain-tissue measurements.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A molecular response was measurable in a specific mitochondrial disease.
primary_references
Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 281–287
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Open-label 52-week study; 9 or 12 g/day under clinical supervision. · source_derived_draft · unverified_draft
## taurine-melas-rna-response A molecular response was measurable in a specific mitochondrial disease. Five patients in the ten-person MELAS trial showed a significant increase in leukocyte mitochondrial tRNA-Leu(UUR) taurine modification after high-dose taurine treatment. Model: Open-label 52-week study; 9 or 12 g/day under clinical supervision. Limitations: Five molecular responders among ten patients; leukocyte measurements are not direct brain-tissue measurements. Evidence access: Primary abstract Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
Complete structured claim and evidence
During the ten-patient 52-week open-label MELAS trial, six patients had no stroke-like episodes in the evaluation period and annual episode frequency fell from 2.22 to 0.72.
Taurine → Stroke-like episode frequency in the taurine MELAS trial source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Within-patient comparison without a placebo group.
limitations
The 60% response estimate had a wide 95% CI of 26.2–87.8%; no general anti-aging or energy inference.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The small disease-specific study reported fewer episodes during treatment.
primary_references
Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 289–295
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Within-patient comparison without a placebo group. · source_derived_draft · unverified_draft
## taurine-melas-episodes The small disease-specific study reported fewer episodes during treatment. During the ten-patient 52-week open-label MELAS trial, six patients had no stroke-like episodes in the evaluation period and annual episode frequency fell from 2.22 to 0.72. Model: Within-patient comparison without a placebo group. Limitations: The 60% response estimate had a wide 95% CI of 26.2–87.8%; no general anti-aging or energy inference. Evidence access: Primary abstract Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
Complete structured claim and evidence
Expression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate.
Human bile acid-CoA:amino acid N-acyltransferase / BAAT → Taurocholate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme.
limitations
Conjugated bile acid and free taurine are separate molecules.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Taurine becomes chemically attached to bile acids.
primary_references
Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 297–303
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme. · source_derived_draft · unverified_draft
## taurine-baat-taurine Taurine becomes chemically attached to bile acids. Expression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate. Model: Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme. Limitations: Conjugated bile acid and free taurine are separate molecules. Evidence access: Primary abstract Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Complete structured claim and evidence
The same expressed human BAAT also catalyzed glycine conjugation of cholic acid.
Human bile acid-CoA:amino acid N-acyltransferase / BAAT → Glycocholate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant human enzyme.
limitations
Shared enzyme use does not establish clinical competition or a need to balance glycine and taurine supplements.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Glycine and taurine converge on the same bile-conjugating enzyme.
primary_references
Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 305–311
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme. · source_derived_draft · unverified_draft
## taurine-baat-glycine Glycine and taurine converge on the same bile-conjugating enzyme. The same expressed human BAAT also catalyzed glycine conjugation of cholic acid. Model: Recombinant human enzyme. Limitations: Shared enzyme use does not establish clinical competition or a need to balance glycine and taurine supplements. Evidence access: Primary abstract Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Complete structured claim and evidence
Patients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients.
Human bile acid-CoA:amino acid N-acyltransferase / BAAT → Human hepatic bile acid amidation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Ten pediatric patients; bile chemistry and genetic investigation.
limitations
Not evidence that isolated dietary taurine shortage causes the same phenotype.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A broken conjugation enzyme affects both amino-acid routes.
primary_references
Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 313–319
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ten pediatric patients; bile chemistry and genetic investigation. · source_derived_draft · unverified_draft
## taurine-baat-loss A broken conjugation enzyme affects both amino-acid routes. Patients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients. Model: Ten pediatric patients; bile chemistry and genetic investigation. Limitations: Not evidence that isolated dietary taurine shortage causes the same phenotype. Evidence access: Primary abstract Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
Complete structured claim and evidence
The pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children.
Human hepatic bile acid amidation → Fat-soluble vitamin malabsorption in human bile acid amidation deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human genetic disease cohort and biochemical characterization.
limitations
The study tests conjugation failure, not taurine supplement efficacy or one universal vitamin deficit.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Failed bile chemistry can make fat-soluble nutrient absorption fail downstream.
primary_references
Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
trigger_kind
machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 321–327
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human genetic disease cohort and biochemical characterization. · source_derived_draft · unverified_draft
## taurine-bile-vitamin-absorption Failed bile chemistry can make fat-soluble nutrient absorption fail downstream. The pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children. Model: Human genetic disease cohort and biochemical characterization. Limitations: The study tests conjugation failure, not taurine supplement efficacy or one universal vitamin deficit. Evidence access: Primary abstract Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
Complete structured claim and evidence
Adding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion.
Taurocholate → Bilophila expansion in the milk-fat/taurocholate mouse experiments source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse dietary experiments with conjugate comparison.
limitations
The intervention was taurocholate, not free taurine alone; microbial community and host genotype matter.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Taurine-conjugated bile supplies sulfur that certain microbes can exploit.
primary_references
Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 329–335
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dietary experiments with conjugate comparison. · source_derived_draft · unverified_draft
## taurine-microbial-bilophila Taurine-conjugated bile supplies sulfur that certain microbes can exploit. Adding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion. Model: Mouse dietary experiments with conjugate comparison. Limitations: The intervention was taurocholate, not free taurine alone; microbial community and host genotype matter. Evidence access: Primary abstract Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Complete structured claim and evidence
Taurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility.
Taurocholate → Colitis in Il10-null mice in the taurocholate study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Il10-deficient and wild-type mouse comparisons.
limitations
Not a demonstration that taurine causes human inflammatory bowel disease.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A sulfur-using microbial route worsened inflammation in this susceptible model.
primary_references
Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 337–343
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Il10-deficient and wild-type mouse comparisons. · source_derived_draft · unverified_draft
## taurine-microbial-colitis A sulfur-using microbial route worsened inflammation in this susceptible model. Taurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility. Model: Il10-deficient and wild-type mouse comparisons. Limitations: Not a demonstration that taurine causes human inflammatory bowel disease. Evidence access: Primary abstract Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Complete structured claim and evidence
Supplying exogenous taurine enhanced microbiota-mediated resistance to subsequent enteric infection in mice.
Taurine → Taurine-associated microbial colonization resistance in mice source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse infection, microbiota and taurine intervention experiments.
limitations
This outcome differs from Il10-null colitis; neither result is a universal rule about intestinal taurine.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
In another setting, feeding microbes taurine improved pathogen resistance.
primary_references
Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 345–351
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse infection, microbiota and taurine intervention experiments. · source_derived_draft · unverified_draft
## taurine-microbial-protection In another setting, feeding microbes taurine improved pathogen resistance. Supplying exogenous taurine enhanced microbiota-mediated resistance to subsequent enteric infection in mice. Model: Mouse infection, microbiota and taurine intervention experiments. Limitations: This outcome differs from Il10-null colitis; neither result is a universal rule about intestinal taurine. Evidence access: Primary abstract Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Complete structured claim and evidence
Taurine-supported microbiota increased sulfide production, which inhibited respiration important for invasion by the tested enteric pathogens; sulfide sequestration promoted invasion.
Hydrogen sulfide / H2S → Respiration-dependent growth of tested enteric pathogens source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse colonization-resistance study with microbial and sulfide interventions.
limitations
Local microbial sulfide, circulating host sulfide and systemic sulfide toxicity are distinct exposures.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The microbial product blocked a pathway that pathogens needed.
primary_references
Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 353–359
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse colonization-resistance study with microbial and sulfide interventions. · source_derived_draft · unverified_draft
## taurine-microbial-sulfide The microbial product blocked a pathway that pathogens needed. Taurine-supported microbiota increased sulfide production, which inhibited respiration important for invasion by the tested enteric pathogens; sulfide sequestration promoted invasion. Model: Mouse colonization-resistance study with microbial and sulfide interventions. Limitations: Local microbial sulfide, circulating host sulfide and systemic sulfide toxicity are distinct exposures. Evidence access: Primary abstract Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Complete structured claim and evidence
Purified myeloperoxidase plus hydrogen peroxide, chloride and taurine generated taurine chloramine; removing chloride or peroxide, or inhibiting MPO, blocked generation.
Human myeloperoxidase / MPO → Taurine chloramine / TauCl source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Purified human MPO system and stimulated human neutrophils.
limitations
Taurine chloramine remains an oxidant; free taurine is not equivalent to every chloramine effect.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
An immune-cell oxidant reacts with taurine to make a different active molecule.
primary_references
Chlorination of taurine by human neutrophils. Evidence for hypochlorous acid generation. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6286728/ · DOI 10.1172/jci110652
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 361–367
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified human MPO system and stimulated human neutrophils. · source_derived_draft · unverified_draft
## taurine-mpo-chlorination An immune-cell oxidant reacts with taurine to make a different active molecule. Purified myeloperoxidase plus hydrogen peroxide, chloride and taurine generated taurine chloramine; removing chloride or peroxide, or inhibiting MPO, blocked generation. Model: Purified human MPO system and stimulated human neutrophils. Limitations: Taurine chloramine remains an oxidant; free taurine is not equivalent to every chloramine effect. Evidence access: Primary abstract Chlorination of taurine by human neutrophils. Evidence for hypochlorous acid generation. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6286728/ · DOI 10.1172/jci110652
Complete structured claim and evidence
Adding 0.5 mM taurine chloramine to activated RAW264.7 macrophages reduced measured nitrite output by 47%; cytosolic nitric-oxide-synthase activity was also inhibited by pretreatment.
Taurine chloramine / TauCl → Nitric oxide output from activated mouse RAW264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse RAW264.7 cells stimulated with interferon-gamma and LPS.
limitations
Millimolar derivative exposure does not establish the effect of oral taurine in humans.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The chlorinated derivative dampened one inflammatory output in cultured mouse cells.
primary_references
Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 369–375
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse RAW264.7 cells stimulated with interferon-gamma and LPS. · source_derived_draft · unverified_draft
## taurine-taucl-no The chlorinated derivative dampened one inflammatory output in cultured mouse cells. Adding 0.5 mM taurine chloramine to activated RAW264.7 macrophages reduced measured nitrite output by 47%; cytosolic nitric-oxide-synthase activity was also inhibited by pretreatment. Model: Mouse RAW264.7 cells stimulated with interferon-gamma and LPS. Limitations: Millimolar derivative exposure does not establish the effect of oral taurine in humans. Evidence access: Primary abstract Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Complete structured claim and evidence
Adding 0.5 mM taurine chloramine to activated RAW264.7 cells reduced TNF release by 43% in the reported assay.
Taurine chloramine / TauCl → TNF release from activated mouse RAW264.7 macrophages source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same mouse-cell experiment as the nitric-oxide result.
limitations
Two endpoints from one paper are not independent replications.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A second inflammatory signal also fell.
primary_references
Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 377–383
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same mouse-cell experiment as the nitric-oxide result. · source_derived_draft · unverified_draft
## taurine-taucl-tnf A second inflammatory signal also fell. Adding 0.5 mM taurine chloramine to activated RAW264.7 cells reduced TNF release by 43% in the reported assay. Model: Same mouse-cell experiment as the nitric-oxide result. Limitations: Two endpoints from one paper are not independent replications. Evidence access: Primary abstract Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Complete structured claim and evidence
Taurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study.
Taurine chloramine / TauCl → Mouse heme oxygenase 1 / Hmox1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Murine peritonitis, isolated macrophages and RAW264.7 cells.
limitations
This is a derivative and mouse immune-cell result, not evidence that taurine directly supplies or removes iron.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The derivative changed an enzyme involved in stress responses.
primary_references
Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 385–391
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Murine peritonitis, isolated macrophages and RAW264.7 cells. · source_derived_draft · unverified_draft
## taurine-taucl-ho1 The derivative changed an enzyme involved in stress responses. Taurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study. Model: Murine peritonitis, isolated macrophages and RAW264.7 cells. Limitations: This is a derivative and mouse immune-cell result, not evidence that taurine directly supplies or removes iron. Evidence access: Primary abstract Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Complete structured claim and evidence
HO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it.
Mouse heme oxygenase 1 / Hmox1 → Taurine-chloramine-induced mouse macrophage phagocytosis source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse macrophage pharmacological and genetic comparisons.
limitations
The mechanism concerns this phagocytosis assay, not all actions of taurine chloramine.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Removing HO-1 tested whether the observed effect needed that enzyme.
primary_references
Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 393–399
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage pharmacological and genetic comparisons. · source_derived_draft · unverified_draft
## taurine-ho1-required Removing HO-1 tested whether the observed effect needed that enzyme. HO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it. Model: Mouse macrophage pharmacological and genetic comparisons. Limitations: The mechanism concerns this phagocytosis assay, not all actions of taurine chloramine. Evidence access: Primary abstract Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Complete structured claim and evidence
RNAi knockdown of Lrrc8d strongly reduced swelling-evoked taurine release from primary rat astrocytes; Lrrc8a knockdown also suppressed release.
Rat LRRC8D / Lrrc8d → Rat astrocyte swelling-evoked taurine efflux source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary rat astrocytes; 30% hypoosmotic challenge and radiotracers.
limitations
RNAi reduction, not whole-animal gene deletion; this is efflux rather than SLC6A6 uptake.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Swollen brain-support cells release taurine through a channel with specific subunits.
primary_references
Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 401–407
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary rat astrocytes; 30% hypoosmotic challenge and radiotracers. · source_derived_draft · unverified_draft
## taurine-vrac-taurine Swollen brain-support cells release taurine through a channel with specific subunits. RNAi knockdown of Lrrc8d strongly reduced swelling-evoked taurine release from primary rat astrocytes; Lrrc8a knockdown also suppressed release. Model: Primary rat astrocytes; 30% hypoosmotic challenge and radiotracers. Limitations: RNAi reduction, not whole-animal gene deletion; this is efflux rather than SLC6A6 uptake. Evidence access: Primary abstract Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Complete structured claim and evidence
Lrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments.
Rat LRRC8D / Lrrc8d → Rat astrocyte swelling-evoked myo-inositol efflux source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary rat astrocytes and labeled myo-inositol.
limitations
Shared channel dependence does not prove competitive depletion or supplement synergy.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Taurine and inositol share part of the cell-volume release machinery.
primary_references
Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 409–415
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary rat astrocytes and labeled myo-inositol. · source_derived_draft · unverified_draft
## taurine-vrac-inositol Taurine and inositol share part of the cell-volume release machinery. Lrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments. Model: Primary rat astrocytes and labeled myo-inositol. Limitations: Shared channel dependence does not prove competitive depletion or supplement synergy. Evidence access: Primary abstract Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Complete structured claim and evidence
Applied taurine activated recombinant human alpha1 homomeric glycine receptors in oocytes and HEK293 cells; its potency and efficacy varied with the experimental receptor response.
Taurine → Human alpha1 homomeric glycine receptor source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human receptor expressed in Xenopus oocytes or human cells; electrophysiology.
limitations
Not a clinical sedative effect; chloride gradient and receptor composition shape cellular response.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Taurine can activate a receptor named for glycine.
primary_references
Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 417–423
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human receptor expressed in Xenopus oocytes or human cells; electrophysiology. · source_derived_draft · unverified_draft
## taurine-glycine-receptor-alpha1 Taurine can activate a receptor named for glycine. Applied taurine activated recombinant human alpha1 homomeric glycine receptors in oocytes and HEK293 cells; its potency and efficacy varied with the experimental receptor response. Model: Human receptor expressed in Xenopus oocytes or human cells; electrophysiology. Limitations: Not a clinical sedative effect; chloride gradient and receptor composition shape cellular response. Evidence access: Primary abstract Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Complete structured claim and evidence
Applied taurine also activated human alpha2 homomeric glycine receptors, with efficacy varying from weak to full agonism across tested conditions.
Taurine → Human alpha2 homomeric glycine receptor source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant human alpha2 receptor electrophysiology.
limitations
Avoid labeling taurine a universally weak or full agonist.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The receptor subtype and cell setting change the strength of taurine signaling.
primary_references
Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 425–431
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human alpha2 receptor electrophysiology. · source_derived_draft · unverified_draft
## taurine-glycine-receptor-alpha2 The receptor subtype and cell setting change the strength of taurine signaling. Applied taurine also activated human alpha2 homomeric glycine receptors, with efficacy varying from weak to full agonism across tested conditions. Model: Recombinant human alpha2 receptor electrophysiology. Limitations: Avoid labeling taurine a universally weak or full agonist. Evidence access: Primary abstract Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Complete structured claim and evidence
Taurine at 10–100 micromolar reduced excitability of mouse thalamocortical neurons and evoked tonic currents consistent with extrasynaptic alpha4beta2delta GABA-A receptors.
Taurine → Mouse extrasynaptic alpha4beta2delta GABA-A receptor source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse ventrobasal thalamic neurons and recombinant receptor comparisons.
limitations
Bath concentration is not an oral dose; this does not establish treatment of human anxiety or insomnia.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A low concentration changed neuronal firing in this mouse brain region.
primary_references
Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 433–439
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse ventrobasal thalamic neurons and recombinant receptor comparisons. · source_derived_draft · unverified_draft
## taurine-gabaa-tonic A low concentration changed neuronal firing in this mouse brain region. Taurine at 10–100 micromolar reduced excitability of mouse thalamocortical neurons and evoked tonic currents consistent with extrasynaptic alpha4beta2delta GABA-A receptors. Model: Mouse ventrobasal thalamic neurons and recombinant receptor comparisons. Limitations: Bath concentration is not an oral dose; this does not establish treatment of human anxiety or insomnia. Evidence access: Primary abstract Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Complete structured claim and evidence
Taurine-evoked currents were absent in relay neurons from GABA-A-receptor alpha4-subunit knockout mice.
Mouse extrasynaptic alpha4beta2delta GABA-A receptor → Mouse thalamic taurine-evoked tonic inhibition source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse alpha4-knockout thalamic neuron recordings.
limitations
Subunit dependence is local to this experimental response.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Removing a receptor subunit tested dependence of the current.
primary_references
Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 441–447
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse alpha4-knockout thalamic neuron recordings. · source_derived_draft · unverified_draft
## taurine-gabaa-knockout Removing a receptor subunit tested dependence of the current. Taurine-evoked currents were absent in relay neurons from GABA-A-receptor alpha4-subunit knockout mice. Model: Mouse alpha4-knockout thalamic neuron recordings. Limitations: Subunit dependence is local to this experimental response. Evidence access: Primary abstract Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Complete structured claim and evidence
Exposing skinned human type I and II muscle fibers to taurine for more than ten minutes increased the SR calcium accumulation rate; 10 and 20 mM produced similar rates, while 5 mM was slower.
Taurine → Human skeletal-muscle SR calcium accumulation rate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mechanically skinned human vastus lateralis fibers.
limitations
Intracellular bath exposure bypasses absorption and transport; it does not prove oral performance benefits.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Taurine affected how quickly muscle stored calcium.
primary_references
Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 449–455
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mechanically skinned human vastus lateralis fibers. · source_derived_draft · unverified_draft
## taurine-muscle-calcium-uptake Taurine affected how quickly muscle stored calcium. Exposing skinned human type I and II muscle fibers to taurine for more than ten minutes increased the SR calcium accumulation rate; 10 and 20 mM produced similar rates, while 5 mM was slower. Model: Mechanically skinned human vastus lateralis fibers. Limitations: Intracellular bath exposure bypasses absorption and transport; it does not prove oral performance benefits. Evidence access: Primary abstract Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Complete structured claim and evidence
Taurine slightly increased contractile calcium sensitivity in human type I fibers, but not type II fibers; maximum calcium-activated force was unchanged in both.
Taurine → Human muscle-fiber contractile calcium sensitivity source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same human skinned-fiber study.
limitations
Small preparation-specific effect; do not merge with rodent muscle or whole-person strength.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The contractile response differed between muscle fiber types.
primary_references
Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 457–463
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same human skinned-fiber study. · source_derived_draft · unverified_draft
## taurine-muscle-calcium-sensitivity The contractile response differed between muscle fiber types. Taurine slightly increased contractile calcium sensitivity in human type I fibers, but not type II fibers; maximum calcium-activated force was unchanged in both. Model: Same human skinned-fiber study. Limitations: Small preparation-specific effect; do not merge with rodent muscle or whole-person strength. Evidence access: Primary abstract Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Complete structured claim and evidence
At 20 mM, taurine had no detectable effect on the responsiveness of SR calcium-release channels in either human fiber type.
Taurine → Human skeletal-muscle SR calcium-release responsiveness source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human skinned type I and II muscle fibers.
limitations
The proposed action inside the SR lumen was a hypothesis, not a demonstrated binding target.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Faster calcium accumulation did not mean every calcium process increased.
primary_references
Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 465–471
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human skinned type I and II muscle fibers. · source_derived_draft · unverified_draft
## taurine-muscle-release-null Faster calcium accumulation did not mean every calcium process increased. At 20 mM, taurine had no detectable effect on the responsiveness of SR calcium-release channels in either human fiber type. Model: Human skinned type I and II muscle fibers. Limitations: The proposed action inside the SR lumen was a hypothesis, not a demonstrated binding target. Evidence access: Primary abstract Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Complete structured claim and evidence
In 120 adults with prehypertension randomized to 1.6 g/day taurine or placebo for 12 weeks, clinic systolic pressure fell by 7.2 versus 2.6 mmHg and ambulatory systolic pressure by 3.8 versus 0.3 mmHg.
Taurine → Blood pressure in the 120-participant taurine trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Randomized double-blind placebo-controlled human trial.
limitations
These are within-arm changes; the trial did not establish long-term cardiovascular-event reduction.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
One controlled trial found a modest blood-pressure reduction.
primary_references
Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 473–479
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Randomized double-blind placebo-controlled human trial. · source_derived_draft · unverified_draft
## taurine-bp-trial One controlled trial found a modest blood-pressure reduction. In 120 adults with prehypertension randomized to 1.6 g/day taurine or placebo for 12 weeks, clinic systolic pressure fell by 7.2 versus 2.6 mmHg and ambulatory systolic pressure by 3.8 versus 0.3 mmHg. Model: Randomized double-blind placebo-controlled human trial. Limitations: These are within-arm changes; the trial did not establish long-term cardiovascular-event reduction. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidence
The taurine arm in the same prehypertension trial improved both endothelium-dependent and endothelium-independent vasodilation.
Taurine → Vasodilation in the 120-participant taurine trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same 120-person randomized study.
limitations
Clinical and vascular endpoints from one trial are not independent trials.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Blood-vessel function changed along with blood pressure.
primary_references
Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 481–487
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same 120-person randomized study. · source_derived_draft · unverified_draft
## taurine-vascular-dilation Blood-vessel function changed along with blood pressure. The taurine arm in the same prehypertension trial improved both endothelium-dependent and endothelium-independent vasodilation. Model: Same 120-person randomized study. Limitations: Clinical and vascular endpoints from one trial are not independent trials. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidence
Taurine supplementation increased measured plasma hydrogen sulfide in the blood-pressure trial; changes in pressure were negatively correlated with H2S and taurine concentrations.
Taurine → Plasma hydrogen sulfide in the taurine blood-pressure trial source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human randomized trial with biomarker correlations.
limitations
Correlation within the trial does not prove H2S mediated the clinical blood-pressure effect.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The study linked the response to a sulfur signaling molecule.
primary_references
Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human randomized trial with biomarker correlations. · source_derived_draft · unverified_draft
## taurine-human-h2s The study linked the response to a sulfur signaling molecule. Taurine supplementation increased measured plasma hydrogen sulfide in the blood-pressure trial; changes in pressure were negatively correlated with H2S and taurine concentrations. Model: Human randomized trial with biomarker correlations. Limitations: Correlation within the trial does not prove H2S mediated the clinical blood-pressure effect. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidence
Taurine treatment reduced agonist-induced vascular reactivity through inhibition of TRPC3-mediated calcium influx in human mesenteric artery experiments.
Taurine → TRPC3-mediated calcium influx in human mesenteric arteries source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human artery preparations in the translational blood-pressure study.
limitations
Do not infer that oral taurine directly binds TRPC3; the signaling pathway and clinical mediation are distinct.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The mechanistic experiments implicated a calcium entry channel.
primary_references
Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 497–503
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human artery preparations in the translational blood-pressure study. · source_derived_draft · unverified_draft
## taurine-human-trpc3 The mechanistic experiments implicated a calcium entry channel. Taurine treatment reduced agonist-induced vascular reactivity through inhibition of TRPC3-mediated calcium influx in human mesenteric artery experiments. Model: Human artery preparations in the translational blood-pressure study. Limitations: Do not infer that oral taurine directly binds TRPC3; the signaling pathway and clinical mediation are distinct. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidence
The same study reported reduced TRPC3-mediated calcium influx and vascular reactivity in mouse mesenteric artery experiments after taurine treatment.
Taurine → TRPC3-mediated calcium influx in mouse mesenteric arteries source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse vascular experiments paired with the human study.
limitations
Mouse and human preparations are linked evidence, not identical biological records.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The vascular mechanism was also examined in mouse arteries.
primary_references
Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 505–511
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse vascular experiments paired with the human study. · source_derived_draft · unverified_draft
## taurine-mouse-trpc3 The vascular mechanism was also examined in mouse arteries. The same study reported reduced TRPC3-mediated calcium influx and vascular reactivity in mouse mesenteric artery experiments after taurine treatment. Model: Mouse vascular experiments paired with the human study. Limitations: Mouse and human preparations are linked evidence, not identical biological records. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidence
Deleting Cdo1 in mouse mesenchymal/osteolineage cells reduced support for leukemia growth and prolonged survival in the transplanted leukemia model.
Mouse cysteine dioxygenase / Cdo1 → Myeloid leukemia growth in the taurine niche experiments source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Figure 2 and niche experiments
experimental_model
Conditional mouse Cdo1 deletion, coculture and leukemia transplantation.
limitations
An established leukemia model does not measure cancer incidence in healthy supplement users.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The tumor-supporting tissue supplied taurine to leukemia cells.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 513–519
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse Cdo1 deletion, coculture and leukemia transplantation. · source_derived_draft · unverified_draft
## taurine-niche-mouse-cdo1 The tumor-supporting tissue supplied taurine to leukemia cells. Deleting Cdo1 in mouse mesenchymal/osteolineage cells reduced support for leukemia growth and prolonged survival in the transplanted leukemia model. Model: Conditional mouse Cdo1 deletion, coculture and leukemia transplantation. Limitations: An established leukemia model does not measure cancer incidence in healthy supplement users. Evidence access: Primary full text, Figure 2 and niche experiments Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
Inhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients.
Human cysteine dioxygenase / CDO1 → Patient-derived human AML cell growth in taurine experiments source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Figure 2h–i
experimental_model
Matched human stromal/AML cocultures.
limitations
Ex-vivo dependency does not establish an effective or safe clinical inhibitor.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Patient-derived support cells also provided a growth-supporting pathway.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 521–527
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Matched human stromal/AML cocultures. · source_derived_draft · unverified_draft
## taurine-niche-human-cdo1 Patient-derived support cells also provided a growth-supporting pathway. Inhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients. Model: Matched human stromal/AML cocultures. Limitations: Ex-vivo dependency does not establish an effective or safe clinical inhibitor. Evidence access: Primary full text, Figure 2h–i Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
Genetic loss of Slc6a6 impaired progression in mouse myeloid leukemia models.
Mouse taurine transporter / Slc6a6 → Myeloid leukemia growth in the taurine niche experiments source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse loss-of-function and in-vivo leukemia experiments.
limitations
This does not negate taurine requirements of normal retina and heart.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Leukemia cells needed taurine uptake in these models.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 529–535
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse loss-of-function and in-vivo leukemia experiments. · source_derived_draft · unverified_draft
## taurine-leukemia-taut-loss Leukemia cells needed taurine uptake in these models. Genetic loss of Slc6a6 impaired progression in mouse myeloid leukemia models. Model: Mouse loss-of-function and in-vivo leukemia experiments. Limitations: This does not negate taurine requirements of normal retina and heart. Evidence access: Primary abstract Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
Slc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments.
Mouse taurine transporter / Slc6a6 → mTOR signaling and glycolysis in mouse taurine-dependent leukemia cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Figure 5
experimental_model
Mouse leukemia multiomics, signaling and metabolic experiments.
limitations
This pathway is not established as a universal response to taurine in healthy human cells.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Transport was connected to growth signaling and fuel use.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 537–543
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia multiomics, signaling and metabolic experiments. · source_derived_draft · unverified_draft
## taurine-leukemia-mtor Transport was connected to growth signaling and fuel use. Slc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments. Model: Mouse leukemia multiomics, signaling and metabolic experiments. Limitations: This pathway is not established as a universal response to taurine in healthy human cells. Evidence access: Primary full text, Figure 5 Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
Expression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells.
Mouse Ras-related GTP-binding protein A / Rraga → mTOR signaling and glycolysis in mouse taurine-dependent leukemia cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Figure 5p–s and associated results
experimental_model
Mouse leukemia expression-rescue experiments.
limitations
Rescue does not identify taurine as a direct physical ligand of RAGA.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A downstream rescue tested the signaling chain.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 545–551
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia expression-rescue experiments. · source_derived_draft · unverified_draft
## taurine-leukemia-rag-rescue A downstream rescue tested the signaling chain. Expression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells. Model: Mouse leukemia expression-rescue experiments. Limitations: Rescue does not identify taurine as a direct physical ligand of RAGA. Evidence access: Primary full text, Figure 5p–s and associated results Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
Exogenous taurine increased leukemia-cell colony formation and accelerated disease progression in the tested immunocompetent mouse leukemia model.
Taurine → Myeloid leukemia growth in the taurine niche experiments source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Extended Data Figure 5o–r and results
experimental_model
Mouse leukemia supplementation experiments, with separate patient-derived cell colony assays.
limitations
Not a human trial or proof that taurine initiates leukemia in healthy people.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Additional taurine worsened an existing malignancy in this experimental setting.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 553–559
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia supplementation experiments, with separate patient-derived cell colony assays. · source_derived_draft · unverified_draft
## taurine-leukemia-supplement Additional taurine worsened an existing malignancy in this experimental setting. Exogenous taurine increased leukemia-cell colony formation and accelerated disease progression in the tested immunocompetent mouse leukemia model. Model: Mouse leukemia supplementation experiments, with separate patient-derived cell colony assays. Limitations: Not a human trial or proof that taurine initiates leukemia in healthy people. Evidence access: Primary full text, Extended Data Figure 5o–r and results Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
TAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments.
Human taurine transporter / SLC6A6 → Patient-derived human AML cell growth in taurine experiments source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Ex-vivo human AML; venetoclax-resistance expression analyses.
limitations
Measured experimental combination effect, not a proven clinical interaction between taurine supplements and venetoclax.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Blocking nutrient uptake affected response to an anticancer drug in patient-derived cells.
primary_references
Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 561–567
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ex-vivo human AML; venetoclax-resistance expression analyses. · source_derived_draft · unverified_draft
## taurine-leukemia-venetoclax Blocking nutrient uptake affected response to an anticancer drug in patient-derived cells. TAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments. Model: Ex-vivo human AML; venetoclax-resistance expression analyses. Limitations: Measured experimental combination effect, not a proven clinical interaction between taurine supplements and venetoclax. Evidence access: Primary abstract Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidence
The 2023 study reported lower circulating taurine with age in its human samples, alongside corresponding age comparisons in mice and monkeys.
Taurine → Human circulating taurine across age source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human age-group observations; separate animal datasets.
limitations
Association alone does not establish deficiency as a cause or specify a universal threshold.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The original aging paper reported a fall in blood taurine.
primary_references
Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
trigger_kind
biomarker_context Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 569–575
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human age-group observations; separate animal datasets. · source_derived_draft · unverified_draft
## taurine-aging-decline The original aging paper reported a fall in blood taurine. The 2023 study reported lower circulating taurine with age in its human samples, alongside corresponding age comparisons in mice and monkeys. Model: Human age-group observations; separate animal datasets. Limitations: Association alone does not establish deficiency as a cause or specify a universal threshold. Evidence access: Primary abstract Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidence
The 2025 study found circulating taurine increased or remained unchanged with age in three geographically distinct human cohorts, with longitudinal and cross-sectional analyses and supporting nonhuman datasets.
Taurine → Human circulating taurine across age source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human cohorts plus nonhuman primates and mice; repeated and cross-sectional measurements.
limitations
A biomarker challenge does not by itself refute every animal supplementation outcome.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Later data did not reproduce a consistent age-related decline.
primary_references
Is taurine an aging biomarker? · 2025 · https://pubmed.ncbi.nlm.nih.gov/40472098/ · DOI 10.1126/science.adl2116
trigger_kind
biomarker_context Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 577–583
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cohorts plus nonhuman primates and mice; repeated and cross-sectional measurements. · source_derived_draft · unverified_draft
## taurine-aging-not-universal Later data did not reproduce a consistent age-related decline. The 2025 study found circulating taurine increased or remained unchanged with age in three geographically distinct human cohorts, with longitudinal and cross-sectional analyses and supporting nonhuman datasets. Model: Human cohorts plus nonhuman primates and mice; repeated and cross-sectional measurements. Limitations: A biomarker challenge does not by itself refute every animal supplementation outcome. Evidence access: Primary abstract Is taurine an aging biomarker? · 2025 · https://pubmed.ncbi.nlm.nih.gov/40472098/ · DOI 10.1126/science.adl2116
Complete structured claim and evidence
In 137 physically active and inactive men aged 20–93, circulating taurine was not associated with age, muscle mass, strength, physical performance or mitochondrial function.
Taurine → Taurine associations with physical and mitochondrial function in 137 men source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Human observational study of men spanning adult ages.
limitations
No randomized taurine intervention; findings do not establish equivalence in women or every tissue.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
Another human dataset did not support blood taurine as a simple aging signal.
primary_references
Experimental Evidence Against Taurine Deficiency as a Driver of Aging in Humans. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41061678/ · DOI 10.1111/acel.70191
trigger_kind
biomarker_context Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 585–591
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human observational study of men spanning adult ages. · source_derived_draft · unverified_draft
## taurine-aging-men-null Another human dataset did not support blood taurine as a simple aging signal. In 137 physically active and inactive men aged 20–93, circulating taurine was not associated with age, muscle mass, strength, physical performance or mitochondrial function. Model: Human observational study of men spanning adult ages. Limitations: No randomized taurine intervention; findings do not establish equivalence in women or every tissue. Evidence access: Primary abstract Experimental Evidence Against Taurine Deficiency as a Driver of Aging in Humans. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41061678/ · DOI 10.1111/acel.70191
Complete structured claim and evidence
Starting 1000 mg/kg/day taurine at 14 months increased median lifespan by approximately 10–12% in the reported male and female mouse cohorts.
Taurine → Mouse lifespan in the 2023 taurine supplementation study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, lifespan results and Figure 1
experimental_model
C57BL/6J mice treated daily until death; same chow in both arms.
limitations
High animal exposure is not a human dose or proof of human lifespan extension.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The mouse intervention reported longer survival.
primary_references
Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 593–599
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C57BL/6J mice treated daily until death; same chow in both arms. · source_derived_draft · unverified_draft
## taurine-aging-mouse-lifespan The mouse intervention reported longer survival. Starting 1000 mg/kg/day taurine at 14 months increased median lifespan by approximately 10–12% in the reported male and female mouse cohorts. Model: C57BL/6J mice treated daily until death; same chow in both arms. Limitations: High animal exposure is not a human dose or proof of human lifespan extension. Evidence access: Primary full text, lifespan results and Figure 1 Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidence
Taurine supplementation extended C. elegans lifespan across the reported worm experiments, with dose-dependent effects.
Taurine → C. elegans lifespan in the 2023 taurine study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text, Figure 1 and supplementary-cohort description
experimental_model
C. elegans intervention cohorts in the 2023 study.
limitations
Organism-specific exposure and metabolism; not an additional human trial.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
A separate organism also showed a survival response.
primary_references
Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 601–607
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C. elegans intervention cohorts in the 2023 study. · source_derived_draft · unverified_draft
## taurine-aging-worm-lifespan A separate organism also showed a survival response. Taurine supplementation extended C. elegans lifespan across the reported worm experiments, with dose-dependent effects. Model: C. elegans intervention cohorts in the 2023 study. Limitations: Organism-specific exposure and metabolism; not an additional human trial. Evidence access: Primary full text, Figure 1 and supplementary-cohort description Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidence
Taurine treatment improved several measured health-related outcomes in monkeys in the 2023 study.
Taurine → Measured health outcomes in taurine-treated monkeys source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Nonhuman-primate supplementation arm.
limitations
The study did not establish longer primate or human lifespan; health measures should not be relabeled survival.
nutrient_topic
Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
plain_language
The primate arm measured health outcomes rather than lifespan extension.
primary_references
Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 609–615
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Nonhuman-primate supplementation arm. · source_derived_draft · unverified_draft
## taurine-aging-monkey-health The primate arm measured health outcomes rather than lifespan extension. Taurine treatment improved several measured health-related outcomes in monkeys in the 2023 study. Model: Nonhuman-primate supplementation arm. Limitations: The study did not establish longer primate or human lifespan; health measures should not be relabeled survival. Evidence access: Primary abstract Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidence
Human CDO1 oxidizes cysteine to cysteine sulfinic acid using molecular oxygen and a non-heme iron center.
Human cysteine dioxygenase / CDO1 → L-Cysteine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/molybdenum-research/17135237.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ccd6f2de98887d17d935999238a88d8901fe8a66bb9b48c9cbd5d179bf180d6", "start_char": 0, "end_char": 1343, "text_sha256": "3ccd6f2de98887d17d935999238a88d8901fe8a66bb9b48c9cbd5d179bf180d6"}
experimental_model
Purified human CDO1 crystallography, substrate binding, metal analysis and mutants
exposure
L-cysteine oxidation with molecular oxygen
limitations
The overall reaction and iron requirement are recorded; disputed detailed structural intermediates are not assigned as settled.
nutrient_topic
Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
organism
Homo sapiens
plain_language
Iron-dependent CDO1 starts an upstream sulfur-breakdown route.
primary_references
[mo-p17135237] An insight into the mechanism of human cysteine dioxygenase. Key roles of the thioether-bonded tyrosine-cysteine cofactor. (2007). https://pubmed.ncbi.nlm.nih.gov/17135237/ DOI: 10.1074/jbc.m609337200
tissue_or_cell_type
Recombinant human cysteine dioxygenase
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 677–688
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human CDO1 crystallography, substrate binding, metal analysis and mutants · source_derived_draft · unverified_draft
### mo-cdo-csa Human CDO1 oxidizes cysteine to cysteine sulfinic acid using molecular oxygen and a non-heme iron center. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron-dependent CDO1 starts an upstream sulfur-breakdown route. organism: Homo sapiens tissue_or_cell_type: Recombinant human cysteine dioxygenase experimental_model: Purified human CDO1 crystallography, substrate binding, metal analysis and mutants limitations: The overall reaction and iron requirement are recorded; disputed detailed structural intermediates are not assigned as settled. exposure: L-cysteine oxidation with molecular oxygen evidence_span: {"source_cache": "artifacts/molybdenum-research/17135237.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ccd6f2de98887d17d935999238a88d8901fe8a66bb9b48c9cbd5d179bf180d6", "start_char": 0, "end_char": 1343, "text_sha256": "3ccd6f2de98887d17d935999238a88d8901fe8a66bb9b48c9cbd5d179bf180d6"} [mo-p17135237] An insight into the mechanism of human cysteine dioxygenase. Key roles of the thioether-bonded tyrosine-cysteine cofactor. (2007). https://pubmed.ncbi.nlm.nih.gov/17135237/ DOI: 10.1074/jbc.m609337200
Complete structured claim and evidence
Ten weeks of beta-alanine supplementation did not change muscle taurine in this study.
Beta-alanine → Human skeletal-muscle taurine content source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human muscle-biopsy study.
limitations
Does not exclude effects under other exposures or in other species.
nutrient_topic
Carnosine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnosine / beta-alanyl-L-histidine
plain_language
A proposed precursor interaction did not cause measurable depletion here.
primary_references
Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. · 2007 · https://pubmed.ncbi.nlm.nih.gov/16868650/ · DOI 10.1007/s00726-006-0364-4
Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19) · lines 220–226
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human muscle-biopsy study. · source_derived_draft · unverified_draft
## carnosine-taurine-negative A proposed precursor interaction did not cause measurable depletion here. Ten weeks of beta-alanine supplementation did not change muscle taurine in this study. Model: Human muscle-biopsy study. Limitations: Does not exclude effects under other exposures or in other species. Evidence access: Primary abstract Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. · 2007 · https://pubmed.ncbi.nlm.nih.gov/16868650/ · DOI 10.1007/s00726-006-0364-4
Complete structured claim and evidence
Taurine flux depended on LRRC8 proteins in the tested cells.
LRRC8 heteromeric volume-regulated anion channel / VRAC → Cellular taurine efflux source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chloride-research/24790029.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9fc0ba50276b74ac5cd7aa29c4c8af4917132a43259b45363b5c16a19b775334", "start_char": 0, "end_char": 896, "text_sha256": "9fc0ba50276b74ac5cd7aa29c4c8af4917132a43259b45363b5c16a19b775334"}
experimental_model
Genome-wide screen, gene disruption and rescue
exposure
LRRC8 knockout and isoform coexpression
limitations
Channel composition and cellular volume response; no dietary intervention.
nutrient_topic
Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
organism
Human cell lines
plain_language
The channel system also connects chloride handling to movement of an organic osmolyte.
primary_references
[chloride-p24790029] Identification of LRRC8 heteromers as an essential component of the volume-regulated anion channel VRAC. (2014). https://pubmed.ncbi.nlm.nih.gov/24790029/ DOI: 10.1126/science.1252826
tissue_or_cell_type
Plasma membrane
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 497–508
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genome-wide screen, gene disruption and rescue · source_derived_draft · unverified_draft
### chloride-vrac-taurine Taurine flux depended on LRRC8 proteins in the tested cells. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The channel system also connects chloride handling to movement of an organic osmolyte. organism: Human cell lines tissue_or_cell_type: Plasma membrane experimental_model: Genome-wide screen, gene disruption and rescue limitations: Channel composition and cellular volume response; no dietary intervention. exposure: LRRC8 knockout and isoform coexpression evidence_span: {"source_cache": "artifacts/chloride-research/24790029.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9fc0ba50276b74ac5cd7aa29c4c8af4917132a43259b45363b5c16a19b775334", "start_char": 0, "end_char": 896, "text_sha256": "9fc0ba50276b74ac5cd7aa29c4c8af4917132a43259b45363b5c16a19b775334"} [chloride-p24790029] Identification of LRRC8 heteromers as an essential component of the volume-regulated anion channel VRAC. (2014). https://pubmed.ncbi.nlm.nih.gov/24790029/ DOI: 10.1126/science.1252826
Complete structured claim and evidence
Taurine pretreatment prevented the reported guanidinoacetate-related inhibition of complex II, complex II–III and sodium/potassium ATPase activity.
Taurine → Rat striatal respiratory complex II activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"}
experimental_model
Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment
exposure
Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment
limitations
Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined.
nutrient_topic
Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
organism
Young rats and rat striatal preparations
plain_language
Taurine protected selected enzyme measurements in this rat experiment.
primary_references
[creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005
tissue_or_cell_type
Striatum
trigger_kind
machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 776–787
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment · source_derived_draft · unverified_draft
### creatine-taurine-gaa-enzyme Taurine pretreatment prevented the reported guanidinoacetate-related inhibition of complex II, complex II–III and sodium/potassium ATPase activity. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Taurine protected selected enzyme measurements in this rat experiment. organism: Young rats and rat striatal preparations tissue_or_cell_type: Striatum experimental_model: Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment limitations: Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined. exposure: Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment evidence_span: {"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"} [creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005
Complete structured claim and evidence
PLP-dependent human CBS condenses serine with homocysteine to produce cystathionine.
Human cystathionine beta-synthase / CBS → Cystathionine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Methionine-derived sulfur enters cysteine synthesis.
experimental_model
Recombinant truncated human CBS crystallography
limitations
Enzyme chemistry alone does not predict whole-body homocysteine during mild deficiency.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
This B6-dependent step channels homocysteine into transsulfuration.
primary_references
[b6-cbs-2001] Structure of human cystathionine beta-synthase: a unique pyridoxal 5'-phosphate-dependent heme protein. (2001). https://pmc.ncbi.nlm.nih.gov/articles/PMC149156/ DOI: 10.1093/emboj/20.15.3910
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 517–527
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant truncated human CBS crystallography · source_derived_draft · unverified_draft
### b6-met-cbs-condensation PLP-dependent human CBS condenses serine with homocysteine to produce cystathionine. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This B6-dependent step channels homocysteine into transsulfuration. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant truncated human CBS crystallography limitations: Enzyme chemistry alone does not predict whole-body homocysteine during mild deficiency. cross_nutrient: Methionine-derived sulfur enters cysteine synthesis. [b6-cbs-2001] Structure of human cystathionine beta-synthase: a unique pyridoxal 5'-phosphate-dependent heme protein. (2001). https://pmc.ncbi.nlm.nih.gov/articles/PMC149156/ DOI: 10.1093/emboj/20.15.3910
Complete structured claim and evidence
Human CTH cleaves cystathionine to cysteine, 2-oxobutanoate and ammonia in a PLP-dependent reaction.
Human cystathionine gamma-lyase / CTH → Cystathionine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B6-dependent sulfur transfer supplies cysteine; glutathione synthesis requires additional enzymes.
experimental_model
Purified human CTH apo/holo crystal structures and assays
limitations
Purified-enzyme evidence does not define dietary requirements or cellular PLP thresholds.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
This step releases cysteine for downstream metabolism.
primary_references
[b6-cth-structure-2009] Structural Basis for the Inhibition Mechanism of Human Cystathionine gamma-Lyase, an Enzyme Responsible for the Production of H2S (2009). https://doi.org/10.1074/jbc.M805459200 DOI: 10.1074/jbc.M805459200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 554–564
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human CTH apo/holo crystal structures and assays · source_derived_draft · unverified_draft
### b6-met-cth-cleavage Human CTH cleaves cystathionine to cysteine, 2-oxobutanoate and ammonia in a PLP-dependent reaction. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This step releases cysteine for downstream metabolism. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified human CTH apo/holo crystal structures and assays limitations: Purified-enzyme evidence does not define dietary requirements or cellular PLP thresholds. cross_nutrient: B6-dependent sulfur transfer supplies cysteine; glutathione synthesis requires additional enzymes. [b6-cth-structure-2009] Structural Basis for the Inhibition Mechanism of Human Cystathionine gamma-Lyase, an Enzyme Responsible for the Production of H2S (2009). https://doi.org/10.1074/jbc.M805459200 DOI: 10.1074/jbc.M805459200
Complete structured claim and evidence
Human SHMT2 uses PLP to couple serine-to-glycine conversion with transfer of a one-carbon unit to tetrahydrofolate.
SHMT2 → 5,10-Methylenetetrahydrofolate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
PLP (B6) and THF (folate) cooperate in one reaction.
experimental_model
Purified human SHMT1 and SHMT2; structures and solution oligomerization
limitations
Reaction is reversible; assembly assays do not establish flux in every cell.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
The enzyme connects B6-dependent amino-acid chemistry to folate chemistry.
primary_references
[b6-shmt-2015] How pyridoxal 5'-phosphate differentially regulates human cytosolic and mitochondrial serine hydroxymethyltransferase oligomeric state (2015). https://febs.onlinelibrary.wiley.com/doi/10.1111/febs.13211 DOI: 10.1111/febs.13211
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 614–624
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human SHMT1 and SHMT2; structures and solution oligomerization · source_derived_draft · unverified_draft
### b6-met-shmt2-onecarbon Human SHMT2 uses PLP to couple serine-to-glycine conversion with transfer of a one-carbon unit to tetrahydrofolate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme connects B6-dependent amino-acid chemistry to folate chemistry. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified human SHMT1 and SHMT2; structures and solution oligomerization limitations: Reaction is reversible; assembly assays do not establish flux in every cell. cross_nutrient: PLP (B6) and THF (folate) cooperate in one reaction. [b6-shmt-2015] How pyridoxal 5'-phosphate differentially regulates human cytosolic and mitochondrial serine hydroxymethyltransferase oligomeric state (2015). https://febs.onlinelibrary.wiley.com/doi/10.1111/febs.13211 DOI: 10.1111/febs.13211
Complete structured claim and evidence
The human PNPO structure localized tightly bound FMN at the conserved catalytic site of the homodimer.
Flavin mononucleotide → Pyridoxine 5-prime-phosphate oxidase / PNPO source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B2-FMN is a cofactor for B6 activation.
evidence_location
Results: kinetic properties; Table 1; FMN-binding structure
experimental_model
Recombinant human PNPO expressed in E. coli; crystallography and purified-enzyme kinetics at 37 C.
exposure
Purified-enzyme assay
limitations
Biochemical evidence does not establish a dietary threshold or supplementation benefit.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Homo sapiens
plain_language
PNPO uses the FMN form of vitamin B2.
primary_references
[musayev2003] Structure and properties of recombinant human pyridoxine 5'-phosphate oxidase. (2003). https://pubmed.ncbi.nlm.nih.gov/12824491/ DOI: 10.1110/ps.0356203
tissue_or_cell_type
Purified recombinant enzyme; no intact tissue
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1136–1148
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PNPO expressed in E. coli; crystallography and purified-enzyme kinetics at 37 C. · source_derived_draft · unverified_draft
### b2-pnpo-fmn-binding The human PNPO structure localized tightly bound FMN at the conserved catalytic site of the homodimer. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: PNPO uses the FMN form of vitamin B2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant enzyme; no intact tissue experimental_model: Recombinant human PNPO expressed in E. coli; crystallography and purified-enzyme kinetics at 37 C. limitations: Biochemical evidence does not establish a dietary threshold or supplementation benefit. exposure: Purified-enzyme assay cross_nutrient: B2-FMN is a cofactor for B6 activation. evidence_location: Results: kinetic properties; Table 1; FMN-binding structure [musayev2003] Structure and properties of recombinant human pyridoxine 5'-phosphate oxidase. (2003). https://pubmed.ncbi.nlm.nih.gov/12824491/ DOI: 10.1110/ps.0356203
Complete structured claim and evidence
Purified human PNPO converted PNP to PLP with a turnover number of 0.19 per second at 37 C.
Pyridoxine 5-prime-phosphate oxidase / PNPO → Pyridoxine 5-prime-phosphate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B2-dependent oxidation activates one B6 precursor.
evidence_location
Results: kinetic properties; Table 1; FMN-binding structure
experimental_model
Recombinant human PNPO expressed in E. coli; crystallography and purified-enzyme kinetics at 37 C.
exposure
Purified-enzyme assay
limitations
Biochemical evidence does not establish a dietary threshold or supplementation benefit.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Homo sapiens
plain_language
PNPO changes phosphorylated pyridoxine into active B6.
primary_references
[musayev2003] Structure and properties of recombinant human pyridoxine 5'-phosphate oxidase. (2003). https://pubmed.ncbi.nlm.nih.gov/12824491/ DOI: 10.1110/ps.0356203
tissue_or_cell_type
Purified recombinant enzyme; no intact tissue
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1150–1162
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PNPO expressed in E. coli; crystallography and purified-enzyme kinetics at 37 C. · source_derived_draft · unverified_draft
### b2-pnpo-pnp-oxidation Purified human PNPO converted PNP to PLP with a turnover number of 0.19 per second at 37 C. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: PNPO changes phosphorylated pyridoxine into active B6. organism: Homo sapiens tissue_or_cell_type: Purified recombinant enzyme; no intact tissue experimental_model: Recombinant human PNPO expressed in E. coli; crystallography and purified-enzyme kinetics at 37 C. limitations: Biochemical evidence does not establish a dietary threshold or supplementation benefit. exposure: Purified-enzyme assay cross_nutrient: B2-dependent oxidation activates one B6 precursor. evidence_location: Results: kinetic properties; Table 1; FMN-binding structure [musayev2003] Structure and properties of recombinant human pyridoxine 5'-phosphate oxidase. (2003). https://pubmed.ncbi.nlm.nih.gov/12824491/ DOI: 10.1110/ps.0356203
Complete structured claim and evidence
Human PDXK assays directly measured ATP-dependent conversion of pyridoxal to PLP, a reaction distinct from PNPO oxidation.
Pyridoxal kinase / PDXK → Pyridoxal source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Separates the B6 phosphorylation step from the B2-dependent oxidation step.
evidence_location
Abstract
experimental_model
Recombinant human PDXK expressed in E. coli; PL-to-PLP kinetics and unliganded/MgATP-bound structures.
exposure
Purified-enzyme assay
limitations
This biochemical route does not establish that dietary pyridoxal bypasses all consequences of PNPO disease.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Homo sapiens
plain_language
Not every route to active B6 passes through PNPO.
primary_references
[safo2007] Crystal Structure of human pyridoxal kinase: structural basis of M(+) and M(2+) activation. (2007). https://pubmed.ncbi.nlm.nih.gov/17766369/ DOI: 10.1110/ps.073022107
tissue_or_cell_type
Purified recombinant enzyme; no intact tissue
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1192–1204
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PDXK expressed in E. coli; PL-to-PLP kinetics and unliganded/MgATP-bound structures. · source_derived_draft · unverified_draft
### b2-pdxk-pyridoxal-route Human PDXK assays directly measured ATP-dependent conversion of pyridoxal to PLP, a reaction distinct from PNPO oxidation. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Not every route to active B6 passes through PNPO. organism: Homo sapiens tissue_or_cell_type: Purified recombinant enzyme; no intact tissue experimental_model: Recombinant human PDXK expressed in E. coli; PL-to-PLP kinetics and unliganded/MgATP-bound structures. limitations: This biochemical route does not establish that dietary pyridoxal bypasses all consequences of PNPO disease. exposure: Purified-enzyme assay cross_nutrient: Separates the B6 phosphorylation step from the B2-dependent oxidation step. evidence_location: Abstract [safo2007] Crystal Structure of human pyridoxal kinase: structural basis of M(+) and M(2+) activation. (2007). https://pubmed.ncbi.nlm.nih.gov/17766369/ DOI: 10.1110/ps.073022107
Complete structured claim and evidence
After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma.
Pantethine → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Pharmacokinetic/metabolic study in four children with nephropathic cystinosis
exposure
Historical oral D-pantethine exposures 70–1000 mg/kg/day.
limitations
Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine.
primary_references
[b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
tissue_or_cell_type
Plasma after oral D-pantethine
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1467–1479
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacokinetic/metabolic study in four children with nephropathic cystinosis · source_derived_draft · unverified_draft
### b5-clin-pantethine-human-products After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine. organism: Homo sapiens tissue_or_cell_type: Plasma after oral D-pantethine experimental_model: Pharmacokinetic/metabolic study in four children with nephropathic cystinosis limitations: Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform. exposure: Historical oral D-pantethine exposures 70–1000 mg/kg/day. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
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.

Transport failure can deplete tissues despite extracellular supply

Condition: machinery_impairment · Biallelic SLC6A6 variants with variable residual transport.

Normal role: SLC6A6 concentrates taurine inside cells.

Recorded consequence: Markedly reduced uptake and tissue taurine accompany retinal disease; some variants also have cardiac disease.

Scope: Rare families, cell studies and a two-sibling treatment follow-up.

An oxidation defect changes the hypotaurine/taurine pattern

Condition: machinery_impairment · Fmo1 gene deletion.

Normal role: FMO1 converts hypotaurine to taurine.

Recorded consequence: Urinary hypotaurine accumulates while taurine decreases.

Scope: Mouse knockout and metabolomics.

Taurine shortage changes mitochondrial tRNA chemistry

Condition: nutrient_deficiency · Taurine-starved cells or animal diets.

Normal role: Taurine supplies the amino-sulfonate portion of tau-m5U.

Recorded consequence: Normal modification decreases and a glycine-containing alternative appears in depleted cells.

Scope: Cell experiments, cat liver and flatfish tissue.

Available taurine cannot replace a broken RNA-modification system

Condition: machinery_impairment · GTPBP3 or Mto1 loss, or hamster one-carbon/folate-transporter mutations.

Normal role: MTO1/GTPBP3 use taurine and folate-derived carbon for tRNA modification.

Recorded consequence: Modification, translation and respiration decline; Mto1 deficiency can cause broader proteostress.

Scope: Human cultured cells, hamster mutant cells and mouse models; species recorded separately.

Mutant mitochondrial tRNA is a distinct clinical context

Condition: machinery_impairment · Pathogenic mitochondrial tRNA variants associated with MELAS.

Normal role: Modified mitochondrial tRNA supports decoding.

Recorded consequence: The small open-label taurine study observed modification increases in five patients and fewer clinical episodes overall.

Scope: Ten patients, 52 weeks of supervised treatment.

Bile-conjugation failure can impair other nutrient absorption

Condition: machinery_impairment · Inherited bile acid amidation defects.

Normal role: BAAT attaches glycine or taurine to bile acids.

Recorded consequence: Conjugates are absent and fat-soluble vitamin deficiency can occur downstream.

Scope: Ten pediatric patients.

Low precursor supply triggers renal conservation

Condition: nutrient_deficiency · Low-protein/sulfur-amino-acid diets or cysteine/methionine restriction.

Normal role: Renal transport adjusts taurine retention.

Recorded consequence: Lower urinary loss and greater uptake capacity conserve taurine.

Scope: Separate mouse-strain and rat feeding studies.

Blood taurine is not a universal aging-deficiency threshold

Condition: biomarker_context · Interpretation of a lower or higher concentration across age.

Normal role: Circulating taurine is one measured compartment.

Recorded consequence: Published cohorts disagree on age trajectories; a tissue-deficiency diagnosis cannot follow from a universal decline assumption.

Scope: 2023 and 2025 human observational datasets.

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.

Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19)AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19)AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead 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.

Does circulating taurine consistently decline with age?The 2023 paper reported age-related decline and proposed taurine deficiency as an aging driver; independent 2025 human cohort analyses found stable or increased levels, and another male cohort found no age association. These oppose a universal circulating-taurine decline, rather than correcting a draft label.Read the recorded disagreement

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.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Taurine

The mechanisms

Purified human CSAD decarboxylated L-cysteine sulfinic acid to hypotaurine in PLP-containing enzyme assays.

The purified human CSAD characterized in this study was a PLP-dependent enzyme, linking its decarboxylation chemistry to the active cofactor form of vitamin B6.

Human CSAD also catalyzed L-cysteic-acid decarboxylation to taurine in vitro.

Recombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay.

RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine.

Recombinant human FMO1 catalyzed oxygenation of hypotaurine to taurine in vitro.

Human FMO1 converted hypotaurine to taurine with either NADPH or NADH as the reducing cofactor in the reported assays.

Fmo1-null mice accumulated urinary hypotaurine and had less urinary taurine than wild-type mice.

Liver-specific Cdo1 deletion increased extrahepatic CDO abundance and hypotaurine; mice maintained taurine, glutathione and sulfate despite a taurine-free diet.

Human TauT structures and uptake assays characterized sodium- and chloride-dependent taurine transport and substrate recognition.

Replacing sodium strongly reduced taurine uptake in reconstituted human placental membranes; uptake kinetics supported two sodium ions per taurine.

Taurine uptake by reconstituted human placental membranes required chloride; chloride kinetics supported one chloride per taurine.

Human TauT structures captured beta-alanine and taurine as separately bound substrate analogues at the transporter binding site.

The human TauT study captured guanidinoacetate-bound transporter structures as part of its substrate-recognition analysis.

The homozygous SLC6A6 p.Ala78Glu variant was associated with approximately 95% lower taurine uptake in patient peripheral blood mononuclear cells despite membrane localization of the variant protein.

The two brothers carrying homozygous SLC6A6 p.Ala78Glu had panretinal degeneration and markedly reduced taurine in plasma, muscle and brain.

In two siblings with SLC6A6 p.Gly399Val and about 15% residual transport, supervised taurine treatment at 100 mg/kg/day normalized blood taurine and corrected cardiomyopathy after 24 months.

In the younger, six-year-old sibling in the p.Gly399Val family, taurine treatment was associated with arrested retinal degeneration and clinically improved vision over follow-up.

SLC6A6 p.Thr249Ile and p.Ala294Thr missense variants showed complete loss of taurine transport in HEK293 cells and patient fibroblasts in the four-family study of seven affected individuals.

Two weeks of low-protein or low-sulfur-amino-acid feeding lowered plasma taurine and increased renal taurine uptake while reducing fractional urinary excretion in the studied mouse strains.

A diet deficient in cysteine and methionine increased the Vmax of the rat high-affinity renal taurine uptake system without changing apparent Km.

Reconstituting the human MTO1-GTPBP3 complex with hypomodified mitochondrial tRNA, taurine and 5,10-methylene-THF produced the taurine-containing U34 modification.

Isotope tracing supported the beta-carbon of serine entering the methylene group of mitochondrial taurine-modified uridine through 5,10-methylene-THF.

Shmt2-mutant Chinese hamster ovary cells showed reduced mitochondrial tRNA taurine modification compared with wild type.

Mitochondrial folate-transporter-mutant CHO cells showed reduced taurine modification of mitochondrial tRNA.

Taurine starvation reduced mitochondrial tRNA taurine modification in cultured cells, with corresponding dietary-depletion observations in cat liver and flatfish tissues.

Taurine-depleted cultured cells accumulated mitochondrial tRNA cmnm5U, whose glycine-derived group replaces the taurine-derived group of tau-m5U.

Deleting GTPBP3 in human cells eliminated the normal taurine-containing wobble modification and reduced mitochondrial translation.

GTPBP3-knockout human cells exhibited impaired mitochondrial respiration alongside loss of taurine tRNA modification.

Purified mature human GTPBP3 exhibited GTPase activity, and functional experiments linked that activity to tRNA modification.

Mto1-deficient experimental cells and mice showed defective mitochondrial translation with mistargeting and aggregation of nuclear-encoded mitochondrial proteins; chemical chaperones reduced cytotoxicity.

Five patients in the ten-person MELAS trial showed a significant increase in leukocyte mitochondrial tRNA-Leu(UUR) taurine modification after high-dose taurine treatment.

During the ten-patient 52-week open-label MELAS trial, six patients had no stroke-like episodes in the evaluation period and annual episode frequency fell from 2.22 to 0.72.

Expression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate.

The same expressed human BAAT also catalyzed glycine conjugation of cholic acid.

Patients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients.

The pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children.

Adding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion.

Taurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility.

Supplying exogenous taurine enhanced microbiota-mediated resistance to subsequent enteric infection in mice.

Taurine-supported microbiota increased sulfide production, which inhibited respiration important for invasion by the tested enteric pathogens; sulfide sequestration promoted invasion.

Purified myeloperoxidase plus hydrogen peroxide, chloride and taurine generated taurine chloramine; removing chloride or peroxide, or inhibiting MPO, blocked generation.

Adding 0.5 mM taurine chloramine to activated RAW264.7 macrophages reduced measured nitrite output by 47%; cytosolic nitric-oxide-synthase activity was also inhibited by pretreatment.

Adding 0.5 mM taurine chloramine to activated RAW264.7 cells reduced TNF release by 43% in the reported assay.

Taurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study.

HO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it.

RNAi knockdown of Lrrc8d strongly reduced swelling-evoked taurine release from primary rat astrocytes; Lrrc8a knockdown also suppressed release.

Lrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments.

Applied taurine activated recombinant human alpha1 homomeric glycine receptors in oocytes and HEK293 cells; its potency and efficacy varied with the experimental receptor response.

Applied taurine also activated human alpha2 homomeric glycine receptors, with efficacy varying from weak to full agonism across tested conditions.

Taurine at 10–100 micromolar reduced excitability of mouse thalamocortical neurons and evoked tonic currents consistent with extrasynaptic alpha4beta2delta GABA-A receptors.

Taurine-evoked currents were absent in relay neurons from GABA-A-receptor alpha4-subunit knockout mice.

Exposing skinned human type I and II muscle fibers to taurine for more than ten minutes increased the SR calcium accumulation rate; 10 and 20 mM produced similar rates, while 5 mM was slower.

Taurine slightly increased contractile calcium sensitivity in human type I fibers, but not type II fibers; maximum calcium-activated force was unchanged in both.

At 20 mM, taurine had no detectable effect on the responsiveness of SR calcium-release channels in either human fiber type.

In 120 adults with prehypertension randomized to 1.6 g/day taurine or placebo for 12 weeks, clinic systolic pressure fell by 7.2 versus 2.6 mmHg and ambulatory systolic pressure by 3.8 versus 0.3 mmHg.

The taurine arm in the same prehypertension trial improved both endothelium-dependent and endothelium-independent vasodilation.

Taurine supplementation increased measured plasma hydrogen sulfide in the blood-pressure trial; changes in pressure were negatively correlated with H2S and taurine concentrations.

Taurine treatment reduced agonist-induced vascular reactivity through inhibition of TRPC3-mediated calcium influx in human mesenteric artery experiments.

The same study reported reduced TRPC3-mediated calcium influx and vascular reactivity in mouse mesenteric artery experiments after taurine treatment.

Deleting Cdo1 in mouse mesenchymal/osteolineage cells reduced support for leukemia growth and prolonged survival in the transplanted leukemia model.

Inhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients.

Genetic loss of Slc6a6 impaired progression in mouse myeloid leukemia models.

Slc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments.

Expression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells.

Exogenous taurine increased leukemia-cell colony formation and accelerated disease progression in the tested immunocompetent mouse leukemia model.

TAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments.

The 2023 study reported lower circulating taurine with age in its human samples, alongside corresponding age comparisons in mice and monkeys.

The 2025 study found circulating taurine increased or remained unchanged with age in three geographically distinct human cohorts, with longitudinal and cross-sectional analyses and supporting nonhuman datasets.

In 137 physically active and inactive men aged 20–93, circulating taurine was not associated with age, muscle mass, strength, physical performance or mitochondrial function.

Starting 1000 mg/kg/day taurine at 14 months increased median lifespan by approximately 10–12% in the reported male and female mouse cohorts.

Taurine supplementation extended C. elegans lifespan across the reported worm experiments, with dose-dependent effects.

Taurine treatment improved several measured health-related outcomes in monkeys in the 2023 study.

Human CDO1 oxidizes cysteine to cysteine sulfinic acid using molecular oxygen and a non-heme iron center.

Ten weeks of beta-alanine supplementation did not change muscle taurine in this study.

Taurine flux depended on LRRC8 proteins in the tested cells.

Taurine pretreatment prevented the reported guanidinoacetate-related inhibition of complex II, complex II–III and sodium/potassium ATPase activity.

PLP-dependent human CBS condenses serine with homocysteine to produce cystathionine.