Hydrogen sulfide / H2S

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

evidence_access

Primary abstract

experimental_model

Dietary/add-back mouse experiments reported in the primary study.

limitations

Donor identity and exposure matter; this is not a human H2S or methionine treatment recommendation.

nutrient_topic

L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine

plain_language

Restoring sulfur support changed the net tumor response.

primary_references

Methionine restriction-induced sulfur deficiency impairs antitumour immunity partially through gut microbiota. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37537369/ · DOI 10.1038/s42255-023-00854-3

L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 476–482

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Dietary/add-back mouse experiments reported in the primary study. · source_derived_draft · unverified_draft

## methionine-sulfur-rescue Restoring sulfur support changed the net tumor response. Supplementation with an H2S donor, a precursor or methionine restored antitumor immune responses in the tested restriction setting. Model: Dietary/add-back mouse experiments reported in the primary study. Limitations: Donor identity and exposure matter; this is not a human H2S or methionine treatment recommendation. Evidence access: Primary abstract Methionine restriction-induced sulfur deficiency impairs antitumour immunity partially through gut microbiota. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37537369/ · DOI 10.1038/s42255-023-00854-3

evidence_access

Primary abstract

experimental_model

In vitro five-step bacterial enzyme system.

limitations

Environmental gene distribution does not quantify human intestinal flux.

nutrient_topic

Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine

plain_language

The sulfur and carbon skeleton enter separate products.

primary_references

In Vitro Reconstitution of a Five-Step Pathway for Bacterial Ergothioneine Catabolism. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33544568/ · DOI 10.1021/acschembio.0c00968

Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 272–278

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · In vitro five-step bacterial enzyme system. · source_derived_draft · unverified_draft

## ergothioneine-catabolic-products The sulfur and carbon skeleton enter separate products. The reconstituted bacterial pathway converted ergothioneine into glutamate, trimethylamine, hydrogen sulfide, carbon dioxide and ammonia. Model: In vitro five-step bacterial enzyme system. Limitations: Environmental gene distribution does not quantify human intestinal flux. Evidence access: Primary abstract In Vitro Reconstitution of a Five-Step Pathway for Bacterial Ergothioneine Catabolism. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33544568/ · DOI 10.1021/acschembio.0c00968

evidence_access

Publisher abstract/introduction plus the authors' article and supplementary legends reproduced in an indexed document. This is source-derived extraction, not raw-data verification. Main-text OCR corrupts some micro-unit symbols; ambiguous doses and binding constants are deliberately not transcribed.

experimental_condition

substrate-omission baseline controls present · L-Ergothioneine Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_condition

substrate-omission baseline controls omitted · 3-Mercaptopyruvate Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "ergothioneine with 3-mercaptopyruvate omitted", "comparator": "substrate-omission baseline controls", "endpoint": "detectable H2S signal", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "ergothioneine", "state": "present"}, {"entity_slug": "3-mercaptopyruvate", "state": "omitted"}]} Explicit extracted experimental comparison; source-derived draft.

experimental_model

Recombinant MPST and isolated mitochondria; substrate-omission controls.

interpretation_status

Source-derived research curation; not independent raw-data verification.

limitations

This control is not evidence of a human 3-mercaptopyruvate deficiency threshold or a universal inability to release sulfur in other systems.

nutrient_topic

Ergothioneine mitochondrial supplement; shared molecular requirements are not demonstrated dietary interactions. · L-Ergothioneine

plain_language

Ergothioneine alone did not replace the substrate.

primary_references

Sprenger et al. Ergothioneine controls mitochondrial function and exercise performance via direct activation of MPST. DOI 10.1016/j.cmet.2025.01.024; PMID 39965563; https://pubmed.ncbi.nlm.nih.gov/39965563/

source_locator

Figures S3K-S3L; Results

Ergothioneine: mitochondrial transport, MPST and sulfur-handling dependencies (2026-10-02) · lines 65–65

Original AI-assisted curation of five primary studies with publication identifiers, experimental locators and access limitations. Additive chapter supplement, not publisher full text. · supports · Recombinant MPST and isolated mitochondria; substrate-omission controls. · source_derived_draft · unverified_draft

Without 3-mercaptopyruvate, ergothioneine produced no detected H2S in the MPST and isolated-mitochondria assays.

assay_pH

11

evidence_access

Publisher abstract/introduction plus the authors' article and supplementary legends reproduced in an indexed document. This is source-derived extraction, not raw-data verification. Main-text OCR corrupts some micro-unit symbols; ambiguous doses and binding constants are deliberately not transcribed.

experimental_condition

substrate conditions without ergothioneine added · L-Ergothioneine Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_condition

substrate conditions without ergothioneine present · 3-Mercaptopyruvate Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "ergothioneine plus 3-mercaptopyruvate", "comparator": "substrate conditions without ergothioneine", "endpoint": "AzMC H2S-associated signal", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "ergothioneine", "state": "added"}, {"entity_slug": "3-mercaptopyruvate", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.

experimental_model

Purified human MPST activity assay using AzMC; reported buffer pH 11.

interpretation_status

Source-derived research curation; not independent raw-data verification.

limitations

The alkaline biochemical assay does not establish the same flux at physiological pH. Product signal is not proof of a structurally identified ergothioneine persulfide.

nutrient_topic

Ergothioneine mitochondrial supplement; shared molecular requirements are not demonstrated dietary interactions. · L-Ergothioneine

plain_language

Enzyme activation still needs its sulfur substrate.

primary_references

Sprenger et al. Ergothioneine controls mitochondrial function and exercise performance via direct activation of MPST. DOI 10.1016/j.cmet.2025.01.024; PMID 39965563; https://pubmed.ncbi.nlm.nih.gov/39965563/

source_locator

Figure 3G; Figure S3K; STAR Methods, Recombinant MPST activity

Ergothioneine: mitochondrial transport, MPST and sulfur-handling dependencies (2026-10-02) · lines 57–57

Original AI-assisted curation of five primary studies with publication identifiers, experimental locators and access limitations. Additive chapter supplement, not publisher full text. · supports · Purified human MPST activity assay using AzMC; reported buffer pH 11. · source_derived_draft · unverified_draft

Ergothioneine plus 3-mercaptopyruvate supported H2S release by recombinant human MPST.

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays

exposure

Cysteine-sulfinate and H2S pathway experiments

limitations

Cell-specific contributions; a higher concentration is not a direct measurement of pathway flux.

nutrient_topic

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

organism

Homo sapiens

plain_language

The sulfur disturbance extends beyond sulfite, but its precise route remains unresolved.

primary_references

[mo-p33271457] The role of glutamate oxaloacetate transaminases in sulfite biosynthesis and H₂S metabolism. (2021). https://pubmed.ncbi.nlm.nih.gov/33271457/ DOI: 10.1016/j.redox.2020.101800

tissue_or_cell_type

HEK293T cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 703–714

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays · source_derived_draft · unverified_draft

### mo-suox-h2s SUOX deficiency was accompanied by increased H2S steady-state levels without upregulation of the known H2S-producing pathways. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sulfur disturbance extends beyond sulfite, but its precise route remains unresolved. organism: Homo sapiens tissue_or_cell_type: HEK293T cells experimental_model: CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays limitations: Cell-specific contributions; a higher concentration is not a direct measurement of pathway flux. exposure: Cysteine-sulfinate and H2S pathway experiments evidence_span: {"source_cache": "artifacts/molybdenum-research/33271457.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617", "start_char": 0, "end_char": 1479, "text_sha256": "619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617"} [mo-p33271457] The role of glutamate oxaloacetate transaminases in sulfite biosynthesis and H₂S metabolism. (2021). https://pubmed.ncbi.nlm.nih.gov/33271457/ DOI: 10.1016/j.redox.2020.101800

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

Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 489–495

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

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

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

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

evidence_span

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experimental_model

Patient fibroblasts, biosynthesis inhibition and mouse genetics

exposure

Genetic or pharmacological CoQ depletion and in-vitro repletion

limitations

Tissue-specific disease models; mouse residual percentages are not diagnostic human thresholds.

nutrient_topic

Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system

organism

Human fibroblasts/HeLa cells and Pdss2 mutant mice

plain_language

CoQ connects energy metabolism to sulfur disposal.

primary_references

[coq10-p27856618] Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/27856618/ DOI: 10.15252/emmm.201606356

tissue_or_cell_type

Sulfide oxidation and tissue CoQ

Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 528–539

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient fibroblasts, biosynthesis inhibition and mouse genetics · source_derived_draft · unverified_draft

### coq10-sqor-electron-acceptor CoQ serves as electron acceptor for SQOR at the start of mitochondrial sulfide oxidation. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CoQ connects energy metabolism to sulfur disposal. organism: Human fibroblasts/HeLa cells and Pdss2 mutant mice tissue_or_cell_type: Sulfide oxidation and tissue CoQ experimental_model: Patient fibroblasts, biosynthesis inhibition and mouse genetics limitations: Tissue-specific disease models; mouse residual percentages are not diagnostic human thresholds. exposure: Genetic or pharmacological CoQ depletion and in-vitro repletion evidence_span: {"source_cache": "artifacts/coq10-research/27856618.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485", "start_char": 0, "end_char": 1261, "text_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485"} [coq10-p27856618] Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/27856618/ DOI: 10.15252/emmm.201606356

evidence_access

Primary abstract

experimental_model

Immunocompetent male/female mouse tumor models with microbiome and sulfur interventions.

limitations

Microbial sulfur production is not identical to host CBS/CTH flux.

nutrient_topic

L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine

plain_language

Dietary sulfur supply also changes support coming from gut microbes.

primary_references

Methionine restriction-induced sulfur deficiency impairs antitumour immunity partially through gut microbiota. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37537369/ · DOI 10.1038/s42255-023-00854-3

L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 460–466

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Immunocompetent male/female mouse tumor models with microbiome and sulfur interventions. · source_derived_draft · unverified_draft

## methionine-restriction-microbial-sulfur Dietary sulfur supply also changes support coming from gut microbes. Methionine restriction reduced microbial hydrogen-sulfide production and impaired immune-cell survival/activation in the study models. Model: Immunocompetent male/female mouse tumor models with microbiome and sulfur interventions. Limitations: Microbial sulfur production is not identical to host CBS/CTH flux. Evidence access: Primary abstract Methionine restriction-induced sulfur deficiency impairs antitumour immunity partially through gut microbiota. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37537369/ · DOI 10.1038/s42255-023-00854-3

evidence_access

Primary indexed abstract and figure descriptions.

experimental_model

Purified human sulfide:quinone oxidoreductase; transient kinetics and flavin spectroscopy.

interpretation_status

Source-derived research curation; not independent raw-data verification.

limitations

Enzyme-bound FAD is not extracellular FMN. This study did not test dietary B2 deficiency or combined B2 and ergothioneine treatment.

nutrient_topic

Ergothioneine mitochondrial supplement; shared molecular requirements are not demonstrated dietary interactions. · L-Ergothioneine

plain_language

Sulfur disposal has a flavin-dependent electron relay.

primary_references

Mishanina et al. Transient Kinetic Analysis of Hydrogen Sulfide Oxidation Catalyzed by Human Sulfide Quinone Oxidoreductase. DOI 10.1074/jbc.M115.682369; PMID 26318450; https://pubmed.ncbi.nlm.nih.gov/26318450/

source_locator

Abstract and Figure 1

Ergothioneine: mitochondrial transport, MPST and sulfur-handling dependencies (2026-10-02) · lines 129–129

Original AI-assisted curation of five primary studies with publication identifiers, experimental locators and access limitations. Additive chapter supplement, not publisher full text. · supports · Purified human sulfide:quinone oxidoreductase; transient kinetics and flavin spectroscopy. · source_derived_draft · unverified_draft

Bound FAD cycles between reduction by sulfide and oxidation by ubiquinone during human SQOR catalysis.

evidence_access

Primary indexed abstract. Physiological acceptor assignment is a kinetic interpretation, not a direct measurement of flux in a patient.

experimental_model

Purified human SQOR in nanodiscs; steady-state and rapid-kinetic assays.

interpretation_status

Source-derived research curation; not independent raw-data verification.

limitations

Predominant acceptor is a kinetic interpretation; alternative acceptors can work in other assay conditions. Ergothioneine and nutrient depletion were not tested.

nutrient_topic

Ergothioneine mitochondrial supplement; shared molecular requirements are not demonstrated dietary interactions. · L-Ergothioneine

plain_language

Glutathione also participates in disposal of sulfide-derived sulfur.

primary_references

Landry et al. H2S oxidation by nanodisc-embedded human sulfide quinone oxidoreductase. DOI 10.1074/jbc.M117.788547; PMID 28512131; https://pubmed.ncbi.nlm.nih.gov/28512131/

source_locator

Abstract

Ergothioneine: mitochondrial transport, MPST and sulfur-handling dependencies (2026-10-02) · lines 137–137

Original AI-assisted curation of five primary studies with publication identifiers, experimental locators and access limitations. Additive chapter supplement, not publisher full text. · supports · Purified human SQOR in nanodiscs; steady-state and rapid-kinetic assays. · source_derived_draft · unverified_draft

Nanodisc-embedded human SQOR transferred sulfane sulfur to glutathione; kinetics supported GSH as the predominant physiological acceptor.

evidence_access

Primary abstract

experimental_model

Mouse-centered brown-adipocyte and in vivo experimental program.

limitations

Abstract does not fully resolve each chemical intermediate; do not equate free H2S, CysSSH and protein-bound persulfides.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Sulfur chemistry fed back to the transcription machinery.

primary_references

Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 396–402

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-centered brown-adipocyte and in vivo experimental program. · source_derived_draft · unverified_draft

## l-cysteine-cars2-ebf2-persulfidation Sulfur chemistry fed back to the transcription machinery. Cars2-derived cysteine persulfide/H2S signaling promoted EBF2 persulfidation and interaction with PPARgamma or BRG1, supporting thermogenic gene recruitment. Model: Mouse-centered brown-adipocyte and in vivo experimental program. Limitations: Abstract does not fully resolve each chemical intermediate; do not equate free H2S, CysSSH and protein-bound persulfides. Evidence access: Primary abstract Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690

evidence_access

Primary abstract

experimental_model

Mouse high-fat-diet and brown-adipocyte experiments.

limitations

Abstract-only intervention details; no human dose, route equivalence or cysteine-plus-B6 synergy is established.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

A B6-derived coenzyme and a sulfur donor were separately tested inputs to this pathway.

primary_references

Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 412–418

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse high-fat-diet and brown-adipocyte experiments. · source_derived_draft · unverified_draft

## l-cysteine-cars2-plp-intervention A B6-derived coenzyme and a sulfur donor were separately tested inputs to this pathway. PLP treatment or an H2S donor improved brown-adipocyte function and reduced obesity progression in the reported high-fat-fed mouse experiments. Model: Mouse high-fat-diet and brown-adipocyte experiments. Limitations: Abstract-only intervention details; no human dose, route equivalence or cysteine-plus-B6 synergy is established. Evidence access: Primary abstract Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690

evidence_access

Primary abstract

experimental_model

Human and yeast CBS kinetics, with human enzyme kept as this record’s subject.

limitations

Relative pathway dominance in a tissue cannot be read directly from purified-enzyme substrate tests.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

An enzyme that helps synthesize cysteine can also use it in sulfur-gas production.

primary_references

Relative contributions of cystathionine beta-synthase and gamma-cystathionase to H2S biogenesis via alternative trans-sulfuration reactions. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19531479/ · DOI 10.1074/jbc.M109.010868

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 284–290

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human and yeast CBS kinetics, with human enzyme kept as this record’s subject. · source_derived_draft · unverified_draft

## l-cysteine-cbs-h2s-branch An enzyme that helps synthesize cysteine can also use it in sulfur-gas production. Purified human CBS favored H2S production through replacement of cysteine by homocysteine over the tested alternative cysteine reactions. Model: Human and yeast CBS kinetics, with human enzyme kept as this record’s subject. Limitations: Relative pathway dominance in a tissue cannot be read directly from purified-enzyme substrate tests. Evidence access: Primary abstract Relative contributions of cystathionine beta-synthase and gamma-cystathionase to H2S biogenesis via alternative trans-sulfuration reactions. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19531479/ · DOI 10.1074/jbc.M109.010868

evidence_access

Primary abstract and primary figure descriptions

experimental_model

Purified human MPST kinetics; concentrations and acceptors varied.

limitations

Some small-thiol assays used millimolar concentrations; these are not demonstrated effects of oral cysteine or lipoic acid.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Sharing a sulfur-transfer route does not make these acceptors equally effective inside cells.

primary_references

Structure and kinetic analysis of H2S production by human mercaptopyruvate sulfurtransferase. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23698001/ · DOI 10.1074/jbc.M113.466177

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 460–466

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human MPST kinetics; concentrations and acceptors varied. · source_derived_draft · unverified_draft

## l-cysteine-mpst-acceptor-choice Sharing a sulfur-transfer route does not make these acceptors equally effective inside cells. Human MPST supported H2S production with thioredoxin and several low-molecular-weight acceptors, including cysteine, glutathione and dihydrolipoic acid. Model: Purified human MPST kinetics; concentrations and acceptors varied. Limitations: Some small-thiol assays used millimolar concentrations; these are not demonstrated effects of oral cysteine or lipoic acid. Evidence access: Primary abstract and primary figure descriptions Structure and kinetic analysis of H2S production by human mercaptopyruvate sulfurtransferase. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23698001/ · DOI 10.1074/jbc.M113.466177

evidence_access

Primary abstract

experimental_model

Simulation based on purified CBS/CSE kinetics with assumed equimolar enzyme concentrations.

limitations

A modeled 25–70% contribution is not a directly measured universal human tissue fraction.

nutrient_topic

L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine

plain_language

Methylation-cycle chemistry can influence a sulfur-signaling branch.

primary_references

Relative contributions of cystathionine beta-synthase and gamma-cystathionase to H2S biogenesis via alternative trans-sulfuration reactions. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19531479/ · DOI 10.1074/jbc.M109.010868

L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 292–298

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Simulation based on purified CBS/CSE kinetics with assumed equimolar enzyme concentrations. · source_derived_draft · unverified_draft

## l-cysteine-sam-sulfur-partition Methylation-cycle chemistry can influence a sulfur-signaling branch. Kinetic simulations predicted that SAM-dependent activation changes the relative CBS contribution to H2S generation at specified substrate concentrations. Model: Simulation based on purified CBS/CSE kinetics with assumed equimolar enzyme concentrations. Limitations: A modeled 25–70% contribution is not a directly measured universal human tissue fraction. Evidence access: Primary abstract Relative contributions of cystathionine beta-synthase and gamma-cystathionase to H2S biogenesis via alternative trans-sulfuration reactions. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19531479/ · DOI 10.1074/jbc.M109.010868

acting_entity

s-allylcysteine

dose

Not specified in accessed abstract

duration

Not specified in accessed abstract

evidence_access

Primary abstract

experimental_comparison

Purified SAC and black garlic extract tested separately

experimental_model

Bovine aortic endothelial BAE-1 cells

interpretation_status

Source-derived research curation; not independent primary verification

limitations

Bovine cells; does not identify direct chemical release versus enzyme-dependent production.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Bos taurus

plain_language

Sulfur signaling was measured in another experimental system.

primary_references

[37062967] Improving endothelial health with food-derived H2S donors: an in vitro study with S-allyl cysteine and with a black-garlic extract enriched in sulfur-containing compounds. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37062967/ · DOI 10.1039/d3fo00412k

route

Cell culture

tissue_or_cell_type

Bovine aortic endothelial BAE-1 cells

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 266–273

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Bovine aortic endothelial BAE-1 cells · source_derived_draft · unverified_draft

## s-allylcysteine-bovine-h2s Sulfur signaling was measured in another experimental system. Purified SAC increased the H2S release readout in bovine aortic endothelial cells. Model: Bovine aortic endothelial BAE-1 cells Limitations: Bovine cells; does not identify direct chemical release versus enzyme-dependent production. Evidence access: Primary abstract [37062967] Improving endothelial health with food-derived H2S donors: an in vitro study with S-allyl cysteine and with a black-garlic extract enriched in sulfur-containing compounds. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37062967/ · DOI 10.1039/d3fo00412k Structured context: {"organism": "Bos taurus", "tissue_or_cell_type": "Bovine aortic endothelial BAE-1 cells", "dose": "Not specified in accessed abstract", "duration": "Not specified in accessed abstract", "route": "Cell culture", "experimental_comparison": "Purified SAC and black garlic extract tested separately", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}

acting_entity

s-allylcysteine

dose

SAC 50 mg/kg/day; PAG 10 mg/kg/day

duration

Seven-day pretreatment; assessed 48 hours after infarction

evidence_access

Primary abstract

experimental_comparison

Saline, SAC, SAC plus PAG, and PAG-alone groups

experimental_model

Acute myocardial infarction; left ventricular and plasma measurements

interpretation_status

Source-derived research curation; not independent primary verification

limitations

CSE is CTH; not proof that SAC is directly cleaved to H2S or that enzyme activity increases in people.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Rattus norvegicus

plain_language

A sulfur-producing enzyme changed activity.

primary_references

[17766469] S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17766469/ · DOI 10.1152/ajpheart.00853.2007

route

Administration route not specified in accessed abstract

tissue_or_cell_type

Acute myocardial infarction; left ventricular and plasma measurements

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 239–246

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Acute myocardial infarction; left ventricular and plasma measurements · source_derived_draft · unverified_draft

## s-allylcysteine-cth-activity A sulfur-producing enzyme changed activity. SAC pretreatment increased left ventricular CSE activity in infarcted rats from 1.23 to 2.75 micromol/g protein/hour. Model: Acute myocardial infarction; left ventricular and plasma measurements Limitations: CSE is CTH; not proof that SAC is directly cleaved to H2S or that enzyme activity increases in people. Evidence access: Primary abstract [17766469] S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17766469/ · DOI 10.1152/ajpheart.00853.2007 Structured context: {"organism": "Rattus norvegicus", "tissue_or_cell_type": "Acute myocardial infarction; left ventricular and plasma measurements", "dose": "SAC 50 mg/kg/day; PAG 10 mg/kg/day", "duration": "Seven-day pretreatment; assessed 48 hours after infarction", "route": "Administration route not specified in accessed abstract", "experimental_comparison": "Saline, SAC, SAC plus PAG, and PAG-alone groups", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}

acting_entity

s-allylcysteine

dose

SAC 50 mg/kg/day; PAG 10 mg/kg/day

duration

Seven-day pretreatment; assessed 48 hours after infarction

evidence_access

Primary abstract

experimental_comparison

Saline, SAC, SAC plus PAG, and PAG-alone groups

experimental_model

Acute myocardial infarction; left ventricular and plasma measurements

interpretation_status

Source-derived research curation; not independent primary verification

limitations

Historical sulfide assay result; exact chemical species and analytical selectivity require full-text assessment.

nutrient_topic

S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC

organism

Rattus norvegicus

plain_language

The sulfur signal had its own measured endpoint.

primary_references

[17766469] S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17766469/ · DOI 10.1152/ajpheart.00853.2007

route

Administration route not specified in accessed abstract

tissue_or_cell_type

Acute myocardial infarction; left ventricular and plasma measurements

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 248–255

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Acute myocardial infarction; left ventricular and plasma measurements · source_derived_draft · unverified_draft

## s-allylcysteine-rat-h2s The sulfur signal had its own measured endpoint. SAC-treated infarcted rats had higher measured plasma H2S than controls and SAC-plus-PAG rats. Model: Acute myocardial infarction; left ventricular and plasma measurements Limitations: Historical sulfide assay result; exact chemical species and analytical selectivity require full-text assessment. Evidence access: Primary abstract [17766469] S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17766469/ · DOI 10.1152/ajpheart.00853.2007 Structured context: {"organism": "Rattus norvegicus", "tissue_or_cell_type": "Acute myocardial infarction; left ventricular and plasma measurements", "dose": "SAC 50 mg/kg/day; PAG 10 mg/kg/day", "duration": "Seven-day pretreatment; assessed 48 hours after infarction", "route": "Administration route not specified in accessed abstract", "experimental_comparison": "Saline, SAC, SAC plus PAG, and PAG-alone groups", "acting_entity": "s-allylcysteine", "interpretation_status": "Source-derived research curation; not independent primary verification"}