GSSG

cross_nutrient

B2-FAD supports GSH recycling; selenium-dependent GPX use of GSH is a separate reaction.

evidence_location

Results: NADPH binding; Fig 1 consensus cycle; GSH/GSSG complexes

experimental_model

Purified human glutathione reductase crystals with natural substrates, 0.95-1.1-A resolution, chemically reduced controls.

exposure

Purified-enzyme assay

limitations

GSR is not glutathione peroxidase; this record does not show that B2 improves selenium repletion.

nutrient_topic

Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)

organism

Homo sapiens

plain_language

This enzyme recycles glutathione after oxidation.

primary_references

[berkholz2008] Catalytic cycle of human glutathione reductase near 1 A resolution. (2008). https://pubmed.ncbi.nlm.nih.gov/18638483/ DOI: 10.1016/j.jmb.2008.06.083

tissue_or_cell_type

Purified human GSR

Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1332–1344

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human glutathione reductase crystals with natural substrates, 0.95-1.1-A resolution, chemically reduced controls. · source_derived_draft · unverified_draft

### b2-gsr-gssg-to-gsh GSR reduces one glutathione-disulfide molecule to two reduced glutathione molecules using the NADPH/FAD catalytic relay. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This enzyme recycles glutathione after oxidation. organism: Homo sapiens tissue_or_cell_type: Purified human GSR experimental_model: Purified human glutathione reductase crystals with natural substrates, 0.95-1.1-A resolution, chemically reduced controls. limitations: GSR is not glutathione peroxidase; this record does not show that B2 improves selenium repletion. exposure: Purified-enzyme assay cross_nutrient: B2-FAD supports GSH recycling; selenium-dependent GPX use of GSH is a separate reaction. evidence_location: Results: NADPH binding; Fig 1 consensus cycle; GSH/GSSG complexes [berkholz2008] Catalytic cycle of human glutathione reductase near 1 A resolution. (2008). https://pubmed.ncbi.nlm.nih.gov/18638483/ DOI: 10.1016/j.jmb.2008.06.083

evidence_span

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experimental_model

Purified mammalian enzymes and expression comparison

exposure

CHAC1/CHAC2 substrate and kinetics comparison

limitations

Human kinetics and yeast structure are distinct; this does not establish a universal turnover rate in vivo.

nutrient_topic

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

organism

Human and mouse enzymes; yeast structural homolog

plain_language

Substrate identity matters even within one degradation family.

primary_references

[glutathione-p27913623] ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione. (2017). https://pubmed.ncbi.nlm.nih.gov/27913623/ DOI: 10.1074/jbc.m116.727479

tissue_or_cell_type

Cytosolic glutathione turnover

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 619–630

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified mammalian enzymes and expression comparison · source_derived_draft · unverified_draft

### glutathione-chac1-gssg-null CHAC1 likewise lacked activity against GSSG in this comparison. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Substrate identity matters even within one degradation family. organism: Human and mouse enzymes; yeast structural homolog tissue_or_cell_type: Cytosolic glutathione turnover experimental_model: Purified mammalian enzymes and expression comparison limitations: Human kinetics and yeast structure are distinct; this does not establish a universal turnover rate in vivo. exposure: CHAC1/CHAC2 substrate and kinetics comparison evidence_span: {"source_cache": "artifacts/glutathione-research/27913623.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694", "start_char": 0, "end_char": 1617, "text_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694"} [glutathione-p27913623] ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione. (2017). https://pubmed.ncbi.nlm.nih.gov/27913623/ DOI: 10.1074/jbc.m116.727479

evidence_span

{"source_cache": "artifacts/glutathione-research/27913623.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694", "start_char": 0, "end_char": 1617, "text_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694"}

experimental_model

Purified mammalian enzymes and expression comparison

exposure

CHAC1/CHAC2 substrate and kinetics comparison

limitations

Human kinetics and yeast structure are distinct; this does not establish a universal turnover rate in vivo.

nutrient_topic

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

organism

Human and mouse enzymes; yeast structural homolog

plain_language

Reduced and oxidized glutathione were not interchangeable substrates.

primary_references

[glutathione-p27913623] ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione. (2017). https://pubmed.ncbi.nlm.nih.gov/27913623/ DOI: 10.1074/jbc.m116.727479

tissue_or_cell_type

Cytosolic glutathione turnover

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 606–617

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified mammalian enzymes and expression comparison · source_derived_draft · unverified_draft

### glutathione-chac2-gssg-null CHAC2 showed no activity against oxidized glutathione in the substrate comparison. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced and oxidized glutathione were not interchangeable substrates. organism: Human and mouse enzymes; yeast structural homolog tissue_or_cell_type: Cytosolic glutathione turnover experimental_model: Purified mammalian enzymes and expression comparison limitations: Human kinetics and yeast structure are distinct; this does not establish a universal turnover rate in vivo. exposure: CHAC1/CHAC2 substrate and kinetics comparison evidence_span: {"source_cache": "artifacts/glutathione-research/27913623.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694", "start_char": 0, "end_char": 1617, "text_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694"} [glutathione-p27913623] ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione. (2017). https://pubmed.ncbi.nlm.nih.gov/27913623/ DOI: 10.1074/jbc.m116.727479

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/molybdenum-research/25777939.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1768480178724867d4c7a98f723cfd1a0010f7973eae4a4baea3d1261a06fdd2", "start_char": 0, "end_char": 2017, "text_sha256": "1768480178724867d4c7a98f723cfd1a0010f7973eae4a4baea3d1261a06fdd2"}

experimental_model

Sulfite/thiosulfate incubation of rat cortical slices and cell-free GSSG

exposure

One- versus three-hour incubations; 10 micromolar sulfite redox observations

limitations

Concentration, duration and preparation matter; GPx activity is not evidence of selenium depletion.

nutrient_topic

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

organism

Rattus norvegicus; cell-free comparison

plain_language

A chemical increase in measured GSH outside cells is different from restoring a living antioxidant system.

primary_references

[mo-p25777939] In vitro evidence that sulfite impairs glutamatergic neurotransmission and inhibits glutathione metabolism-related enzymes in rat cerebral cortex. (2015). https://pubmed.ncbi.nlm.nih.gov/25777939/ DOI: 10.1016/j.ijdevneu.2015.03.005

tissue_or_cell_type

Cerebral cortex

trigger_kind

machinery_impairment Imported condition classification; unverified.

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1431–1442

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sulfite/thiosulfate incubation of rat cortical slices and cell-free GSSG · source_derived_draft · unverified_draft

### mo-sulfite-gssg-chemical At 500 micromolar, sulfite increased measured GSH in a cell-free GSSG solution, consistent with disulfide-bond chemistry. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chemical increase in measured GSH outside cells is different from restoring a living antioxidant system. organism: Rattus norvegicus; cell-free comparison tissue_or_cell_type: Cerebral cortex experimental_model: Sulfite/thiosulfate incubation of rat cortical slices and cell-free GSSG limitations: Concentration, duration and preparation matter; GPx activity is not evidence of selenium depletion. exposure: One- versus three-hour incubations; 10 micromolar sulfite redox observations evidence_span: {"source_cache": "artifacts/molybdenum-research/25777939.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1768480178724867d4c7a98f723cfd1a0010f7973eae4a4baea3d1261a06fdd2", "start_char": 0, "end_char": 2017, "text_sha256": "1768480178724867d4c7a98f723cfd1a0010f7973eae4a4baea3d1261a06fdd2"} [mo-p25777939] In vitro evidence that sulfite impairs glutamatergic neurotransmission and inhibits glutathione metabolism-related enzymes in rat cerebral cortex. (2015). https://pubmed.ncbi.nlm.nih.gov/25777939/ DOI: 10.1016/j.ijdevneu.2015.03.005

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/biotin-research/34818536.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "48bcb3951c9b630862fdda839e0a54b80abe9e2cf2e79d0bfb7547e2af317523", "start_char": 35800, "end_char": 36138, "text_sha256": "b1dd7e5022ba64d19114d853d2f75c43e061cdca76e1938e95c19379e96c3933"}

experimental_model

Primary human-islet tracer metabolomics and PC knockdown under inflammatory/nitrosative stress

exposure

Glucose tracer, PC knockdown and nitric-oxide donor exposure

limitations

Genetic perturbation of PC in isolated islets is not dietary biotin depletion or evidence that biotin supplements raise glutathione in replete people.

nutrient_topic

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

organism

Homo sapiens

plain_language

PC connects carbon metabolism to the cell’s ability to maintain glutathione.

primary_references

[b7-p34818536] Glucose metabolism and pyruvate carboxylase enhance glutathione synthesis and restrict oxidative stress in pancreatic islets. (2021). https://pubmed.ncbi.nlm.nih.gov/34818536/ DOI: 10.1016/j.celrep.2021.110037

tissue_or_cell_type

Primary human pancreatic islets

trigger_kind

machinery_impairment Imported condition classification; unverified.

Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 871–882

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human-islet tracer metabolomics and PC knockdown under inflammatory/nitrosative stress · source_derived_draft · unverified_draft

### b7-pc-islet-gsh Genetic depletion of PC in human islets reduced glutathione and the GSH/GSSG ratio under nitrosative stress. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: PC connects carbon metabolism to the cell’s ability to maintain glutathione. organism: Homo sapiens tissue_or_cell_type: Primary human pancreatic islets experimental_model: Primary human-islet tracer metabolomics and PC knockdown under inflammatory/nitrosative stress limitations: Genetic perturbation of PC in isolated islets is not dietary biotin depletion or evidence that biotin supplements raise glutathione in replete people. exposure: Glucose tracer, PC knockdown and nitric-oxide donor exposure evidence_span: {"source_cache": "artifacts/biotin-research/34818536.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "48bcb3951c9b630862fdda839e0a54b80abe9e2cf2e79d0bfb7547e2af317523", "start_char": 35800, "end_char": 36138, "text_sha256": "b1dd7e5022ba64d19114d853d2f75c43e061cdca76e1938e95c19379e96c3933"} [b7-p34818536] Glucose metabolism and pyruvate carboxylase enhance glutathione synthesis and restrict oxidative stress in pancreatic islets. (2021). https://pubmed.ncbi.nlm.nih.gov/34818536/ DOI: 10.1016/j.celrep.2021.110037

evidence_access

Primary abstract

experimental_model

Human NSCLC cell study.

limitations

A ratio alone does not establish which synthesis, oxidation, conjugation or export flux caused the change.

nutrient_topic

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

plain_language

The redox balance shifted alongside toxicity.

primary_references

Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 132–138

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cell study. · source_derived_draft · unverified_draft

## cucurbitacin-b-redox-ratio The redox balance shifted alongside toxicity. Cucurbitacin B exposure lowered the GSH/GSSG ratio in the human NSCLC experiments. Model: Human NSCLC cell study. Limitations: A ratio alone does not establish which synthesis, oxidation, conjugation or export flux caused the change. Evidence access: Primary abstract Cucurbitacin B potently suppresses non-small-cell lung cancer growth: identification of intracellular thiols as critical targets. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23340170/ · DOI 10.1016/j.canlet.2013.01.008

evidence_access

Primary abstract

experimental_model

Cultured human endothelial cells.

limitations

GSR expression does not establish increased flux or correction of riboflavin deficiency.

nutrient_topic

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

plain_language

This connects the response to glutathione recycling.

primary_references

Uptake and protective effects of ergothioneine in human endothelial cells. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25022513/ · DOI 10.1124/jpet.114.214049

Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 296–302

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

## ergothioneine-endothelial-gsr This connects the response to glutathione recycling. Ergothioneine increased glutathione reductase expression in human brain microvascular endothelial cells. Model: Cultured human endothelial cells. Limitations: GSR expression does not establish increased flux or correction of riboflavin deficiency. Evidence access: Primary abstract Uptake and protective effects of ergothioneine in human endothelial cells. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25022513/ · DOI 10.1124/jpet.114.214049

dose

Sulfanilic acid 1 micromolar-1 mM; mitochondrial depolarization reported at 1 mM

duration

Acute calcium time course; other assay intervals not specified in abstract

evidence_access

Primary PubMed abstract; unrecovered method details explicitly retained.

evidence_scope

literature_reviewed; source-specific experimental curation

experimental_model

Rat pancreatic AR42J cell line

limitations

The metabolite was administered directly. No measured oral tartrazine-to-pancreas exposure or pancreatitis outcome is established. Oxidant production was reported to be calcium-independent.

nutrient_topic

Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine

organism

Rat pancreatic AR42J cell line

plain_language

Sulfanilic acid lowered the GSH/GSSG ratio in AR42J cells.

primary_references

Sulfanilic acid increases intracellular free-calcium concentration, induces reactive oxygen species production and impairs trypsin secretion in pancreatic AR42J cells. (2018). https://pubmed.ncbi.nlm.nih.gov/29986830/ DOI: 10.1016/j.fct.2018.07.001

route

In vitro metabolite exposure

tissue

Calcium, redox, mitochondrial and secretory assays

Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 160–169

Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Rat pancreatic AR42J cell line · source_derived_draft · unverified_draft

## tartrazine-metabolite-gsh Sulfanilic acid lowered the GSH/GSSG ratio in AR42J cells. Model/species: Rat pancreatic AR42J cell line Tissue: Calcium, redox, mitochondrial and secretory assays Exposure: Sulfanilic acid 1 micromolar-1 mM; mitochondrial depolarization reported at 1 mM Route: In vitro metabolite exposure Duration: Acute calcium time course; other assay intervals not specified in abstract Limits: The metabolite was administered directly. No measured oral tartrazine-to-pancreas exposure or pancreatitis outcome is established. Oxidant production was reported to be calcium-independent. Primary reference: Sulfanilic acid increases intracellular free-calcium concentration, induces reactive oxygen species production and impairs trypsin secretion in pancreatic AR42J cells. (2018). https://pubmed.ncbi.nlm.nih.gov/29986830/ DOI: 10.1016/j.fct.2018.07.001 Access: Primary PubMed abstract; unrecovered method details explicitly retained.

evidence_span

{"source_cache": "artifacts/theanine-research/34922485.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282", "start_char": 0, "end_char": 1703, "text_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282"}

experimental_model

Chemotherapy-associated intestinal injury experiment

exposure

Cystine plus theanine during 5-fluorouracil exposure

limitations

Combination product, not isolated theanine. Preservation of antitumor activity in the tested model does not establish compatibility with every human chemotherapy regimen.

nutrient_topic

L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine

organism

Mice

plain_language

This result belongs to the tested two-ingredient mixture and its chemotherapy context.

primary_references

[theanine-p34922485] Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model. (2021). https://pubmed.ncbi.nlm.nih.gov/34922485/ DOI: 10.1186/s12885-021-09057-z

tissue_or_cell_type

Intestinal redox balance and crypt injury

L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 783–794

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemotherapy-associated intestinal injury experiment · source_derived_draft · unverified_draft

### theanine-ct-diarrhea The cystine-theanine mixture reduced diarrhea in the mouse chemotherapy model. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This result belongs to the tested two-ingredient mixture and its chemotherapy context. organism: Mice tissue_or_cell_type: Intestinal redox balance and crypt injury experimental_model: Chemotherapy-associated intestinal injury experiment limitations: Combination product, not isolated theanine. Preservation of antitumor activity in the tested model does not establish compatibility with every human chemotherapy regimen. exposure: Cystine plus theanine during 5-fluorouracil exposure evidence_span: {"source_cache": "artifacts/theanine-research/34922485.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282", "start_char": 0, "end_char": 1703, "text_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282"} [theanine-p34922485] Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model. (2021). https://pubmed.ncbi.nlm.nih.gov/34922485/ DOI: 10.1186/s12885-021-09057-z

evidence_span

{"source_cache": "artifacts/theanine-research/34922485.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282", "start_char": 0, "end_char": 1703, "text_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282"}

experimental_model

Chemotherapy-associated intestinal injury experiment

exposure

Cystine plus theanine during 5-fluorouracil exposure

limitations

Combination product, not isolated theanine. Preservation of antitumor activity in the tested model does not establish compatibility with every human chemotherapy regimen.

nutrient_topic

L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine

organism

Mice

plain_language

This result belongs to the tested two-ingredient mixture and its chemotherapy context.

primary_references

[theanine-p34922485] Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model. (2021). https://pubmed.ncbi.nlm.nih.gov/34922485/ DOI: 10.1186/s12885-021-09057-z

tissue_or_cell_type

Intestinal redox balance and crypt injury

L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 757–768

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemotherapy-associated intestinal injury experiment · source_derived_draft · unverified_draft

### theanine-ct-redox The cystine-theanine mixture restored the intestinal GSH/GSSG ratio during 5-fluorouracil exposure. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This result belongs to the tested two-ingredient mixture and its chemotherapy context. organism: Mice tissue_or_cell_type: Intestinal redox balance and crypt injury experimental_model: Chemotherapy-associated intestinal injury experiment limitations: Combination product, not isolated theanine. Preservation of antitumor activity in the tested model does not establish compatibility with every human chemotherapy regimen. exposure: Cystine plus theanine during 5-fluorouracil exposure evidence_span: {"source_cache": "artifacts/theanine-research/34922485.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282", "start_char": 0, "end_char": 1703, "text_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282"} [theanine-p34922485] Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model. (2021). https://pubmed.ncbi.nlm.nih.gov/34922485/ DOI: 10.1186/s12885-021-09057-z

evidence_span

{"source_cache": "artifacts/theanine-research/34922485.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282", "start_char": 0, "end_char": 1703, "text_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282"}

experimental_model

Chemotherapy-associated intestinal injury experiment

exposure

Cystine plus theanine during 5-fluorouracil exposure

limitations

Combination product, not isolated theanine. Preservation of antitumor activity in the tested model does not establish compatibility with every human chemotherapy regimen.

nutrient_topic

L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine

organism

Mice

plain_language

This result belongs to the tested two-ingredient mixture and its chemotherapy context.

primary_references

[theanine-p34922485] Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model. (2021). https://pubmed.ncbi.nlm.nih.gov/34922485/ DOI: 10.1186/s12885-021-09057-z

tissue_or_cell_type

Intestinal redox balance and crypt injury

L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 770–781

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemotherapy-associated intestinal injury experiment · source_derived_draft · unverified_draft

### theanine-ct-ros The cystine-theanine mixture reduced reactive oxygen species in intestinal crypts. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This result belongs to the tested two-ingredient mixture and its chemotherapy context. organism: Mice tissue_or_cell_type: Intestinal redox balance and crypt injury experimental_model: Chemotherapy-associated intestinal injury experiment limitations: Combination product, not isolated theanine. Preservation of antitumor activity in the tested model does not establish compatibility with every human chemotherapy regimen. exposure: Cystine plus theanine during 5-fluorouracil exposure evidence_span: {"source_cache": "artifacts/theanine-research/34922485.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282", "start_char": 0, "end_char": 1703, "text_sha256": "5828410d2c083fec47a3c7e1907b801a2dc616dbbb7e5ed36e59d503bceeb282"} [theanine-p34922485] Oral administration of cystine and theanine attenuates 5-fluorouracil-induced intestinal mucositis and diarrhea by suppressing both glutathione level decrease and ROS production in the small intestine of mucositis mouse model. (2021). https://pubmed.ncbi.nlm.nih.gov/34922485/ DOI: 10.1186/s12885-021-09057-z

evidence_span

{"source_cache": "artifacts/glutathione-research/9642155.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "701b6cbdc44486c0b9423d7c30f52b282f1407958c7dde45d4aa1d3751718a72", "start_char": 0, "end_char": 1538, "text_sha256": "701b6cbdc44486c0b9423d7c30f52b282f1407958c7dde45d4aa1d3751718a72"}

experimental_model

Purified GAPDH oxidation and radiolabeled disulfide assays

exposure

Hydrogen peroxide versus GSSG and glutaredoxin

limitations

This particular assay separates oxidation from glutathionylation; it does not establish one universal effect for all modified proteins.

nutrient_topic

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

organism

Human GAPDH; human or bacterial glutaredoxin

plain_language

Reaction conditions can change the direction of a redox enzyme’s effect.

primary_references

[glutathione-p9642155] Studies on the mechanism of oxidative modification of human glyceraldehyde-3-phosphate dehydrogenase by glutathione: catalysis by glutaredoxin. (1998). https://pubmed.ncbi.nlm.nih.gov/9642155/ DOI: 10.1006/bbrc.1998.8695

tissue_or_cell_type

Cell-free enzyme system

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 866–877

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified GAPDH oxidation and radiolabeled disulfide assays · source_derived_draft · unverified_draft

### glutathione-glrx-gapdh-tagging Recombinant human glutaredoxin enhanced GAPDH S-glutathionylation under the tested GSSG conditions. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reaction conditions can change the direction of a redox enzyme’s effect. organism: Human GAPDH; human or bacterial glutaredoxin tissue_or_cell_type: Cell-free enzyme system experimental_model: Purified GAPDH oxidation and radiolabeled disulfide assays limitations: This particular assay separates oxidation from glutathionylation; it does not establish one universal effect for all modified proteins. exposure: Hydrogen peroxide versus GSSG and glutaredoxin evidence_span: {"source_cache": "artifacts/glutathione-research/9642155.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "701b6cbdc44486c0b9423d7c30f52b282f1407958c7dde45d4aa1d3751718a72", "start_char": 0, "end_char": 1538, "text_sha256": "701b6cbdc44486c0b9423d7c30f52b282f1407958c7dde45d4aa1d3751718a72"} [glutathione-p9642155] Studies on the mechanism of oxidative modification of human glyceraldehyde-3-phosphate dehydrogenase by glutathione: catalysis by glutaredoxin. (1998). https://pubmed.ncbi.nlm.nih.gov/9642155/ DOI: 10.1006/bbrc.1998.8695

evidence_span

{"source_cache": "artifacts/glutathione-research/8670053.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3", "start_char": 0, "end_char": 1433, "text_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3"}

experimental_model

Membrane-vesicle transport assays

exposure

ATP-dependent GSSG uptake into vesicles

limitations

Vesicle uptake reflects cellular export; the GSH null result applies specifically to the tested 100 micromolar condition.

nutrient_topic

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

organism

Human HL60 and HeLa systems

plain_language

Oxidized glutathione can be exported instead of recycled locally.

primary_references

[glutathione-p8670053] ATP-dependent glutathione disulphide transport mediated by the MRP gene-encoded conjugate export pump. (1996). https://pubmed.ncbi.nlm.nih.gov/8670053/ DOI: 10.1042/bj3140433

tissue_or_cell_type

MRP-overexpressing membranes

Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 723–734

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Membrane-vesicle transport assays · source_derived_draft · unverified_draft

### glutathione-mrp-gssg MRP1 mediated ATP-dependent GSSG transport; the HeLa-vesicle Km was 93 ± 26 micromolar. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized glutathione can be exported instead of recycled locally. organism: Human HL60 and HeLa systems tissue_or_cell_type: MRP-overexpressing membranes experimental_model: Membrane-vesicle transport assays limitations: Vesicle uptake reflects cellular export; the GSH null result applies specifically to the tested 100 micromolar condition. exposure: ATP-dependent GSSG uptake into vesicles evidence_span: {"source_cache": "artifacts/glutathione-research/8670053.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3", "start_char": 0, "end_char": 1433, "text_sha256": "9178e466ea8bd18f0957cc65594934ec1681ad7483e6ac64d79c4b8d8ca2afc3"} [glutathione-p8670053] ATP-dependent glutathione disulphide transport mediated by the MRP gene-encoded conjugate export pump. (1996). https://pubmed.ncbi.nlm.nih.gov/8670053/ DOI: 10.1042/bj3140433

experimental_model

Animal selenium status and erythrocyte glutathione-peroxidase biochemistry.

limitations

This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit.

organism

Rat

Selenium: literature corrections and mechanism additions · lines 954–963

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Animal selenium status and erythrocyte glutathione-peroxidase biochemistry. · secondary_verified · secondary_verified

## gpx1-peroxide-reduction GPX1 uses glutathione to remove hydrogen peroxide. Classical GPX1 couples hydrogen-peroxide reduction to oxidation of reduced glutathione; water and glutathione disulfide are products. Experimental model: Animal selenium status and erythrocyte glutathione-peroxidase biochemistry. Organism: Rat Limitations: This experiment-specific relationship does not establish a human dietary-deficiency threshold or supplementation benefit. Primary reference: [Selenium: biochemical role as a component of glutathione peroxidase](https://pubmed.ncbi.nlm.nih.gov/4686466/)

cell_type

MCF-7 transfectants

experimental_model

GPX2 cDNA expression and enzyme assays

limitations

Expression model; not an intestinal clinical outcome.

organism

human

Selenium: literature corrections and mechanism additions · lines 642–652

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · GPX2 cDNA expression and enzyme assays · secondary_verified · secondary_verified

## gpx2-reduces-peroxide GPX2 can remove peroxide using glutathione. Expressed human GPX2 exhibited glutathione-dependent hydrogen-peroxide reduction. Organism: human Cell type: MCF-7 transfectants Experimental model: GPX2 cDNA expression and enzyme assays Limitations: Expression model; not an intestinal clinical outcome. Primary reference: [Expression, characterization, and tissue distribution of a new cellular selenium-dependent glutathione peroxidase, GSHPx-GI](https://pubmed.ncbi.nlm.nih.gov/8428933/)

cell_type

plasma

experimental_model

Purified enzyme kinetics

limitations

Assay glutathione availability does not define every physiological electron donor.

organism

human

Selenium: literature corrections and mechanism additions · lines 678–688

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Purified enzyme kinetics · secondary_verified · secondary_verified

## gpx3-reduces-extracellular-peroxide GPX3 can remove peroxide outside cells. Purified human plasma glutathione peroxidase reduced hydrogen peroxide using glutathione. Organism: human Cell type: plasma Experimental model: Purified enzyme kinetics Limitations: Assay glutathione availability does not define every physiological electron donor. Primary reference: [Characterization of the major hydroperoxide-reducing activity of human plasma. Purification and properties of a selenium-dependent glutathione peroxidase.](https://www.sciencedirect.com/science/article/pii/S0021925818453926)