NO

evidence_span

{"source_cache": "artifacts/hbot-research/10749833.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687", "start_char": 0, "end_char": 1283, "text_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687"}

experimental_model

Regional cerebral blood flow and electroencephalography in anaesthetised rats

exposure

Oxygen at 1, 3, 4 and 5 ATA with L-NAME, L-arginine, nitric oxide donors or MK-801

limitations

A time-course study at toxic pressures. It shows the nitric oxide effect reverses with exposure time, which a single time point would miss.

nutrient_topic

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

organism

Rat

plain_language

Early on there is too little of this molecule, later too much.

primary_references

[hbot-p10749833] Nitric oxide and cerebral blood flow responses to hyperbaric oxygen. (2000). https://pubmed.ncbi.nlm.nih.gov/10749833/ DOI: 10.1152/jappl.2000.88.4.1381

tissue_or_cell_type

Brain

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 205–216

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow and electroencephalography in anaesthetised rats · source_derived_draft · unverified_draft

### hbot-no-production-rises-late A relative lack of nitric oxide activity contributed to the early decrease in blood flow, but as exposure was prolonged nitric oxide production increased and augmented blood flow in anticipation of neuronal excitation. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Early on there is too little of this molecule, later too much. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow and electroencephalography in anaesthetised rats limitations: A time-course study at toxic pressures. It shows the nitric oxide effect reverses with exposure time, which a single time point would miss. exposure: Oxygen at 1, 3, 4 and 5 ATA with L-NAME, L-arginine, nitric oxide donors or MK-801 evidence_span: {"source_cache": "artifacts/hbot-research/10749833.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687", "start_char": 0, "end_char": 1283, "text_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687"} [hbot-p10749833] Nitric oxide and cerebral blood flow responses to hyperbaric oxygen. (2000). https://pubmed.ncbi.nlm.nih.gov/10749833/ DOI: 10.1152/jappl.2000.88.4.1381

evidence_span

{"source_cache": "artifacts/citrulline-research/31514202.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d", "start_char": 0, "end_char": 991, "text_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d"}

experimental_model

Cryo-EM structures in multiple functional states

exposure

NO-bound and other functional enzyme states

limitations

Structural signal transduction, not a clinical citrulline efficacy experiment.

nutrient_topic

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

organism

Human soluble guanylate cyclase alpha1-beta1

plain_language

NO is a signal received by another enzyme, rather than the final vascular response.

primary_references

[citrulline-p31514202] Structural insights into the mechanism of human soluble guanylate cyclase. (2019). https://pubmed.ncbi.nlm.nih.gov/31514202/ DOI: 10.1038/s41586-019-1584-6

tissue_or_cell_type

NO sensor, transducer and catalytic modules

Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 684–695

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM structures in multiple functional states · source_derived_draft · unverified_draft

### citrulline-no-sgc NO binding to the beta1 H-NOX region drove structural changes that increased human soluble guanylate cyclase activity. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: NO is a signal received by another enzyme, rather than the final vascular response. organism: Human soluble guanylate cyclase alpha1-beta1 tissue_or_cell_type: NO sensor, transducer and catalytic modules experimental_model: Cryo-EM structures in multiple functional states limitations: Structural signal transduction, not a clinical citrulline efficacy experiment. exposure: NO-bound and other functional enzyme states evidence_span: {"source_cache": "artifacts/citrulline-research/31514202.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d", "start_char": 0, "end_char": 991, "text_sha256": "e3001c79d449d8a5545278fdaa6dd7a2dd9e1a67b6e4553d78bbc5848a35362d"} [citrulline-p31514202] Structural insights into the mechanism of human soluble guanylate cyclase. (2019). https://pubmed.ncbi.nlm.nih.gov/31514202/ DOI: 10.1038/s41586-019-1584-6

evidence_span

{"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"}

experimental_model

Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays

exposure

Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase

limitations

Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step.

nutrient_topic

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

organism

Rat

plain_language

Superoxide destroys the molecule that keeps vessels relaxed, and removing superoxide removes the effect.

primary_references

[hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313

tissue_or_cell_type

Brain

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 166–177

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays · source_derived_draft · unverified_draft

### hbot-no-inactivation Brain nitric oxide metabolite levels fell by 31% and correlated with the fall in blood flow, while estimated hydroxyl radical production rose by 56%, and the blood-flow decrease was completely abolished by intravascular superoxide dismutase. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Superoxide destroys the molecule that keeps vessels relaxed, and removing superoxide removes the effect. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays limitations: Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step. exposure: Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase evidence_span: {"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"} [hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313

evidence_span

{"source_cache": "artifacts/citrulline-research/1378832.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "265be186f6d8172b272e7b1e75b4fbae12a6df78c7396cad499bce2b195b1206", "start_char": 0, "end_char": 1652, "text_sha256": "265be186f6d8172b272e7b1e75b4fbae12a6df78c7396cad499bce2b195b1206"}

experimental_model

Functional expression and reporter-cell coculture

exposure

NOS3 transfection and calcium ionophore A23187

limitations

Heterologous expression; reporter activation supports bioactive NO production, not a clinical calcium supplementation effect.

nutrient_topic

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

organism

Human NOS3 expressed in NIH3T3 cells; rat reporter fibroblasts

plain_language

Arginine feeds an enzyme that makes the signal NO while also producing citrulline.

primary_references

[citrulline-p1378832] Cloning and expression of a cDNA encoding human endothelium-derived relaxing factor/nitric oxide synthase. (1992). https://pubmed.ncbi.nlm.nih.gov/1378832/ DOI: 10.1016/s0021-9258(18)42066-2

tissue_or_cell_type

Arginine conversion and NO-dependent reporter guanylate cyclase activity

Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 463–474

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Functional expression and reporter-cell coculture · source_derived_draft · unverified_draft

### citrulline-nos-no Cells expressing human endothelial NOS produced bioactive NO that increased guanylate cyclase activity in cocultured reporter cells. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Arginine feeds an enzyme that makes the signal NO while also producing citrulline. organism: Human NOS3 expressed in NIH3T3 cells; rat reporter fibroblasts tissue_or_cell_type: Arginine conversion and NO-dependent reporter guanylate cyclase activity experimental_model: Functional expression and reporter-cell coculture limitations: Heterologous expression; reporter activation supports bioactive NO production, not a clinical calcium supplementation effect. exposure: NOS3 transfection and calcium ionophore A23187 evidence_span: {"source_cache": "artifacts/citrulline-research/1378832.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "265be186f6d8172b272e7b1e75b4fbae12a6df78c7396cad499bce2b195b1206", "start_char": 0, "end_char": 1652, "text_sha256": "265be186f6d8172b272e7b1e75b4fbae12a6df78c7396cad499bce2b195b1206"} [citrulline-p1378832] Cloning and expression of a cDNA encoding human endothelium-derived relaxing factor/nitric oxide synthase. (1992). https://pubmed.ncbi.nlm.nih.gov/1378832/ DOI: 10.1016/s0021-9258(18)42066-2

evidence_span

{"source_cache": "artifacts/dihydrocapsaicin-research/36007275.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b", "start_char": 0, "end_char": 1605, "text_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b"}

experimental_model

Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays

exposure

Dihydrocapsaicin from below 50 up to 500 micromolar, against capsaicin and vitamin C

limitations

The only head-to-head cytotoxicity comparison in this collection. Concentrations of 100 micromolar and above are far higher than any plasma level reported here.

nutrient_topic

Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin

organism

Human

plain_language

It raises the signal that relaxes blood vessels, and mops up free radicals in a test tube.

primary_references

[dhc-p36007275] Beneficial effects of capsaicin and dihydrocapsaicin on endothelial inflammation, nitric oxide production and antioxidant activity. (2022). https://pubmed.ncbi.nlm.nih.gov/36007275/ DOI: 10.1016/j.biopha.2022.113521

tissue_or_cell_type

Vascular endothelium

Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 686–697

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays · source_derived_draft · unverified_draft

### dhc-nitric-oxide-and-radicals Nitric oxide production was significantly induced by dihydrocapsaicin and by capsaicin compared with vehicle control, and similar to capsaicin and vitamin C, dihydrocapsaicin scavenged DPPH free radicals in vitro. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: It raises the signal that relaxes blood vessels, and mops up free radicals in a test tube. organism: Human tissue_or_cell_type: Vascular endothelium experimental_model: Primary human endothelial cells stimulated with tumour necrosis factor alpha, with viability, adhesion and radical scavenging assays limitations: The only head-to-head cytotoxicity comparison in this collection. Concentrations of 100 micromolar and above are far higher than any plasma level reported here. exposure: Dihydrocapsaicin from below 50 up to 500 micromolar, against capsaicin and vitamin C evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/36007275.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b", "start_char": 0, "end_char": 1605, "text_sha256": "b04a74a345c83df1454aa34ad591c7cefd04325de39cde8d5118bbea005aba3b"} [dhc-p36007275] Beneficial effects of capsaicin and dihydrocapsaicin on endothelial inflammation, nitric oxide production and antioxidant activity. (2022). https://pubmed.ncbi.nlm.nih.gov/36007275/ DOI: 10.1016/j.biopha.2022.113521

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

Not proof of lowered human blood pressure or independence from arginine and NOS cofactors.

nutrient_topic

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

organism

Bos taurus

plain_language

The downstream gas signal was measured separately.

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 284–291

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-no The downstream gas signal was measured separately. SAC increased the NO-release readout in BAE-1 cells. Model: Bovine aortic endothelial BAE-1 cells Limitations: Not proof of lowered human blood pressure or independence from arginine and NOS cofactors. 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"}

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"}

experimental_model

Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression

exposure

Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5

limitations

Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established.

nutrient_topic

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

organism

Homo sapiens proteins and HEK cells

plain_language

The molybdenum-binding cysteine is critical for this reaction.

primary_references

[mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

tissue_or_cell_type

Purified redox system and human cell model

trigger_kind

machinery_impairment Imported condition classification; unverified.

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1067–1078

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression · source_derived_draft · unverified_draft

### mo-marc-c273a The C273A mARC1 variant abolished nitrite-dependent NO formation. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The molybdenum-binding cysteine is critical for this reaction. organism: Homo sapiens proteins and HEK cells tissue_or_cell_type: Purified redox system and human cell model experimental_model: Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression limitations: Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established. exposure: Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5 evidence_span: {"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"} [mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"}

experimental_model

Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression

exposure

Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5

limitations

Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established.

nutrient_topic

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

organism

Homo sapiens proteins and HEK cells

plain_language

A chemically similar metal could not replace molybdenum in this reaction.

primary_references

[mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

tissue_or_cell_type

Purified redox system and human cell model

trigger_kind

machinery_impairment Imported condition classification; unverified.

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1080–1091

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression · source_derived_draft · unverified_draft

### mo-marc-tungsten Replacing molybdenum with tungsten during recombinant mARC1 production abolished NO formation. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chemically similar metal could not replace molybdenum in this reaction. organism: Homo sapiens proteins and HEK cells tissue_or_cell_type: Purified redox system and human cell model experimental_model: Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression limitations: Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established. exposure: Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5 evidence_span: {"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"} [mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

evidence_span

{"source_cache": "artifacts/molybdenum-research/41337830.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4cac9c7485dc06caae98c3fd1d54e64b47290a13869b96bfbee654dafdc2b20c", "start_char": 0, "end_char": 826, "text_sha256": "4cac9c7485dc06caae98c3fd1d54e64b47290a13869b96bfbee654dafdc2b20c"}

experimental_model

Electrochemically driven human SUOX nitrite-reductase assays

exposure

Benzyl-viologen mediator; pH-dependent assays

limitations

Artificial electron mediator and millimolar substrate affinity; physiological NO flux is not established.

nutrient_topic

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

organism

Homo sapiens protein

plain_language

The laboratory reaction does not require every component used in the normal cellular pathway.

primary_references

[mo-p41337830] An electrochemical perspective on human sulfite oxidase as a potential nitrite reductase. (2026). https://pubmed.ncbi.nlm.nih.gov/41337830/ DOI: 10.1016/j.jinorgbio.2025.113159

tissue_or_cell_type

Purified enzyme on electrochemical system

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1106–1117

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrochemically driven human SUOX nitrite-reductase assays · source_derived_draft · unverified_draft

### mo-suox-nitrite-electrochemical Electrochemical human SUOX nitrite reduction had a reported Km of 3.5 mM at pH 7; a heme-free variant behaved similarly in that system. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The laboratory reaction does not require every component used in the normal cellular pathway. organism: Homo sapiens protein tissue_or_cell_type: Purified enzyme on electrochemical system experimental_model: Electrochemically driven human SUOX nitrite-reductase assays limitations: Artificial electron mediator and millimolar substrate affinity; physiological NO flux is not established. exposure: Benzyl-viologen mediator; pH-dependent assays evidence_span: {"source_cache": "artifacts/molybdenum-research/41337830.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4cac9c7485dc06caae98c3fd1d54e64b47290a13869b96bfbee654dafdc2b20c", "start_char": 0, "end_char": 826, "text_sha256": "4cac9c7485dc06caae98c3fd1d54e64b47290a13869b96bfbee654dafdc2b20c"} [mo-p41337830] An electrochemical perspective on human sulfite oxidase as a potential nitrite reductase. (2026). https://pubmed.ncbi.nlm.nih.gov/41337830/ DOI: 10.1016/j.jinorgbio.2025.113159

evidence_span

{"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"}

experimental_model

LPS-stimulated macrophage experiments

exposure

Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract

limitations

These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent.

nutrient_topic

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

organism

Mouse RAW264 macrophages

plain_language

Output from the stimulated pathway decreased.

primary_references

[nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973

tissue_or_cell_type

Inflammatory mediator secretion and signaling

Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 237–248

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-stimulated macrophage experiments · source_derived_draft · unverified_draft

### nasunin-no-output Nasunin reduced LPS-induced nitric-oxide production. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Output from the stimulated pathway decreased. organism: Mouse RAW264 macrophages tissue_or_cell_type: Inflammatory mediator secretion and signaling experimental_model: LPS-stimulated macrophage experiments limitations: These measurements do not prove direct binding to Akt, p38, NF-kappa-B or NOS2; reduced NOS2 expression is not direct enzyme inhibition. Response is LPS/cell-context dependent. exposure: Dose-dependent nasunin treatment; exact dose/time not reported in indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/28812425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf", "start_char": 0, "end_char": 1094, "text_sha256": "7a697b4eb979f1e6349bc79f4d2ed0d3994de51dfed777a71fb04740819eeabf"} [nasunin-p28812425] Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways. (2017). https://pubmed.ncbi.nlm.nih.gov/28812425/ DOI: 10.1080/09168451.2017.1362973

evidence_access

Primary abstract

experimental_model

Rat cerebellar NOS preparation; separated partial reactions.

limitations

Purified preparation; residual enzyme reductant supported a limited first reaction without added NADPH. This does not imply physiological NOS is NADPH independent.

nutrient_topic

L-Arginine collection; tissue, species, dose and formulation distinctions retained. · L-Arginine

plain_language

The next reaction produces the signal and recycles the carbon skeleton.

primary_references

Characteristics of the nitric oxide synthase-catalyzed conversion of arginine to N-hydroxyarginine, the first oxygenation step in the enzymic synthesis of nitric oxide. · 1995 · https://pubmed.ncbi.nlm.nih.gov/7530247/ · DOI 10.1074/jbc.270.4.1721

L-Arginine: transport, metabolic branches, nutrient interactions, availability and discovery questions (2026-09-18) · lines 78–84

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat cerebellar NOS preparation; separated partial reactions. · source_derived_draft · unverified_draft

## arg-nos-second The next reaction produces the signal and recycles the carbon skeleton. The second oxygenation yielded NO and citrulline and required added NADPH and calcium/calmodulin. Model: Rat cerebellar NOS preparation; separated partial reactions. Limitations: Purified preparation; residual enzyme reductant supported a limited first reaction without added NADPH. This does not imply physiological NOS is NADPH independent. Evidence access: Primary abstract Characteristics of the nitric oxide synthase-catalyzed conversion of arginine to N-hydroxyarginine, the first oxygenation step in the enzymic synthesis of nitric oxide. · 1995 · https://pubmed.ncbi.nlm.nih.gov/7530247/ · DOI 10.1074/jbc.270.4.1721

cell_type

plasma and platelets

experimental_model

Gpx3 knockout

limitations

Individual oxidant intermediates were not fully isolated.

organism

mouse

Selenium: literature corrections and mechanism additions · lines 714–724

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx3 knockout · secondary_verified · secondary_verified

## gpx3-supports-no-platelet-restraint GPX3 may help preserve nitric oxide's platelet-inhibitory signal. Redox and platelet measurements support GPX3 preservation of NO-mediated platelet restraint. Organism: mouse Cell type: plasma and platelets Experimental model: Gpx3 knockout Limitations: Individual oxidant intermediates were not fully isolated. Primary reference: [Glutathione Peroxidase-3 Deficiency Promotes Platelet-dependent Thrombosis in vivo](https://pmc.ncbi.nlm.nih.gov/articles/PMC3107543/)

evidence_access

Primary abstract

experimental_model

Rodent osteoblast-like cell cultures; 2.5–100 micromolar vanadate.

limitations

Mixed cell models are named explicitly; NO is a proposed mediator, not proven sole cause of growth effects.

nutrient_topic

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

plain_language

A growth-related exposure can engage nitrosative signaling at higher concentrations.

primary_references

Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10988345/ · DOI 10.1016/s0014-2999(00)00356-3

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 326–332

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rodent osteoblast-like cell cultures; 2.5–100 micromolar vanadate. · source_derived_draft · unverified_draft

## vanadium-bone-no A growth-related exposure can engage nitrosative signaling at higher concentrations. Vanadate increased NO release above 50 micromolar in the tested rat UMR106 and mouse MC3T3-E1 osteoblast-like cultures, with a biphasic concentration response. Model: Rodent osteoblast-like cell cultures; 2.5–100 micromolar vanadate. Limitations: Mixed cell models are named explicitly; NO is a proposed mediator, not proven sole cause of growth effects. Evidence access: Primary abstract Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10988345/ · DOI 10.1016/s0014-2999(00)00356-3

evidence_access

Primary abstract

experimental_model

Rat UMR106 and mouse MC3T3-E1 culture program.

limitations

Mimicry is not equivalent to selective blockade and rescue of the proposed vanadate mechanism.

nutrient_topic

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

plain_language

A donor experiment supports a possible downstream mediator.

primary_references

Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10988345/ · DOI 10.1016/s0014-2999(00)00356-3

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 334–340

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat UMR106 and mouse MC3T3-E1 culture program. · source_derived_draft · unverified_draft

## vanadium-bone-no-donor A donor experiment supports a possible downstream mediator. The NO donor sodium nitroprusside reduced growth and alkaline-phosphatase activity, mimicking part of the vanadate phenotype. Model: Rat UMR106 and mouse MC3T3-E1 culture program. Limitations: Mimicry is not equivalent to selective blockade and rescue of the proposed vanadate mechanism. Evidence access: Primary abstract Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10988345/ · DOI 10.1016/s0014-2999(00)00356-3

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_location

Results: NOS Induction; Figure 3

evidence_span

enhanced endothelial NOS immunoreactivity

experimental_model

Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry.

exposure

Dietary thiamine removal plus daily pyrithiamine in mice or rats

limitations

Immunostaining is not a direct nitric oxide flux measurement and does not establish a protective or damaging net effect.

nutrient_topic

Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)

organism

Mus musculus

plain_language

The blood-vessel lining increased its endothelial nitric oxide synthase signal.

primary_references

[calingasan-1998-bbb-iron-nos] Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC1852979/ DOI: 10.1016/S0002-9440(10)65602-7

tissue_or_cell_type

Thalamic microvessel walls

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1197–1209

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry. · source_derived_draft · unverified_draft

### thiamine-def-mouse-endothelial-nos3 Thalamic microvessel endothelial NOS immunoreactivity increased after ten days of the mouse depletion protocol. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood-vessel lining increased its endothelial nitric oxide synthase signal. organism: Mus musculus tissue_or_cell_type: Thalamic microvessel walls experimental_model: Adult male C57BL/6 mice and Fischer 344 Brown Norway F1 rats; thiamine-deficient diet plus pyrithiamine 0.5 mg/kg/day intraperitoneally; staged brain histochemistry. limitations: Immunostaining is not a direct nitric oxide flux measurement and does not establish a protective or damaging net effect. evidence_location: Results: NOS Induction; Figure 3 evidence_span: enhanced endothelial NOS immunoreactivity exposure: Dietary thiamine removal plus daily pyrithiamine in mice or rats [calingasan-1998-bbb-iron-nos] Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC1852979/ DOI: 10.1016/S0002-9440(10)65602-7

evidence_span

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experimental_model

Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor

exposure

2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days

limitations

Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here.

nutrient_topic

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

organism

Rat

plain_language

Within a day the growth signals rise; within a week there are new vessels and repaired muscle.

primary_references

[hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

tissue_or_cell_type

Skeletal muscle

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 686–697

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor · source_derived_draft · unverified_draft

### hbot-no-vegf-bfgf Treatment significantly increased nitrate, VEGF and basic fibroblast growth factor levels and stabilised HIF-1alpha within one day, promoting blood vessel formation at 3 to 7 days and muscle healing at 5 to 7 days after contusion. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Within a day the growth signals rise; within a week there are new vessels and repaired muscle. organism: Rat tissue_or_cell_type: Skeletal muscle experimental_model: Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor limitations: Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here. exposure: 2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days evidence_span: {"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"} [hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Human volunteers, mice, and endothelial nitric oxide synthase knockout mice

exposure

2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments

limitations

The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel.

nutrient_topic

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

organism

Human and mouse

plain_language

Remove the enzyme that makes nitric oxide and the cells stay in the marrow.

primary_references

[hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

tissue_or_cell_type

Bone marrow and peripheral blood

trigger_kind

machinery_impairment Imported condition classification; unverified.

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 569–580

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteers, mice, and endothelial nitric oxide synthase knockout mice · source_derived_draft · unverified_draft

### hbot-nos3-required Stem cell mobilisation did not occur in knockout mice lacking genes for endothelial nitric oxide synthase, and pretreatment of wild-type mice with a nitric oxide synthase inhibitor prevented the elevation in stem cell factor and circulating stem cells. Condition category: machinery_impairment nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Remove the enzyme that makes nitric oxide and the cells stay in the marrow. organism: Human and mouse tissue_or_cell_type: Bone marrow and peripheral blood experimental_model: Human volunteers, mice, and endothelial nitric oxide synthase knockout mice limitations: The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel. exposure: 2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments evidence_span: {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"} [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays

exposure

Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase

limitations

Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step.

nutrient_topic

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

organism

Rat

plain_language

Giving the enzyme that clears superoxide kept the vessels open.

primary_references

[hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313

tissue_or_cell_type

Brain

trigger_kind

machinery_impairment Imported condition classification; unverified.

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 179–190

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays · source_derived_draft · unverified_draft

### hbot-sod-rescue Administration of superoxide dismutase into the circulation before exposure completely abolished the decrease in regional cerebral blood flow at 5 ATA. Condition category: machinery_impairment nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Giving the enzyme that clears superoxide kept the vessels open. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays limitations: Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step. exposure: Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase evidence_span: {"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"} [hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Rat mucosal pharmacology.

limitations

Supports pathway ordering; not direct proof of each cell source or a human MSG–arginine interaction.

nutrient_topic

Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate

plain_language

Nitric oxide and serotonin signaling interact upstream of the nerve response.

primary_references

Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005

trigger_kind

machinery_impairment Imported condition classification; unverified.

Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 170–176

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat mucosal pharmacology. · source_derived_draft · unverified_draft

## monosodium-glutamate-nos-gate Nitric oxide and serotonin signaling interact upstream of the nerve response. NOS inhibition blocked glutamate-evoked vagal firing; an NO donor mimicked firing and its response was blocked by 5-HT3 antagonism. Model: Rat mucosal pharmacology. Limitations: Supports pathway ordering; not direct proof of each cell source or a human MSG–arginine interaction. Evidence access: Primary abstract Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005

evidence_access

Primary abstract

experimental_model

Mouse plasma applied to human endothelial culture.

limitations

Cross-species ex vivo experiment, not human oral fisetin exposure.

nutrient_topic

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

plain_language

A plasma-transfer experiment tested effects on recipient cells.

primary_references

Senolytic Treatment With Fisetin Reverses Age-Related Endothelial Dysfunction Partially Mediated by SASP Factor CXCL12. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42021544/ · DOI 10.1111/acel.70500

Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 264–270

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse plasma applied to human endothelial culture. · source_derived_draft · unverified_draft

## fisetin-cross-species-plasma A plasma-transfer experiment tested effects on recipient cells. Old-mouse plasma reduced NO-related bioactivity and increased mitochondrial oxidative stress in cultured human aortic endothelial cells; fisetin treatment of donor mice attenuated these effects. Model: Mouse plasma applied to human endothelial culture. Limitations: Cross-species ex vivo experiment, not human oral fisetin exposure. Evidence access: Primary abstract Senolytic Treatment With Fisetin Reverses Age-Related Endothelial Dysfunction Partially Mediated by SASP Factor CXCL12. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42021544/ · DOI 10.1111/acel.70500

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Patient vascular testing, hypomorphic mice and molecular experiments

exposure

ASL loss; extracellular arginine; nitrite or NO donor interventions

limitations

Rare genetic deficiency; molecular scaffolding is distinct from supplying enough circulating arginine.

nutrient_topic

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

organism

Human ASL deficiency and Asl-deficient mice, model specified

plain_language

Providing arginine did not bypass every function of ASL.

primary_references

[citrulline-p22081021] Requirement of argininosuccinate lyase for systemic nitric oxide production. (2011). https://pubmed.ncbi.nlm.nih.gov/22081021/ DOI: 10.1038/nm.2544

tissue_or_cell_type

Arginine synthesis, NOS-associated protein complex and vasculature

trigger_kind

machinery_impairment Imported condition classification; unverified.

Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 632–643

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient vascular testing, hypomorphic mice and molecular experiments · source_derived_draft · unverified_draft

### citrulline-asl-external-arginine ASL loss impaired use of extracellular arginine for NO production as well as reducing endogenous arginine synthesis. Condition category: machinery_impairment nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing arginine did not bypass every function of ASL. organism: Human ASL deficiency and Asl-deficient mice, model specified tissue_or_cell_type: Arginine synthesis, NOS-associated protein complex and vasculature experimental_model: Patient vascular testing, hypomorphic mice and molecular experiments limitations: Rare genetic deficiency; molecular scaffolding is distinct from supplying enough circulating arginine. exposure: ASL loss; extracellular arginine; nitrite or NO donor interventions evidence_span: {"source_cache": "artifacts/citrulline-research/22081021.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b", "start_char": 0, "end_char": 1137, "text_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b"} [citrulline-p22081021] Requirement of argininosuccinate lyase for systemic nitric oxide production. (2011). https://pubmed.ncbi.nlm.nih.gov/22081021/ DOI: 10.1038/nm.2544

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/citrulline-research/22081021.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b", "start_char": 0, "end_char": 1137, "text_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b"}

experimental_model

Patient vascular testing, hypomorphic mice and molecular experiments

exposure

ASL loss; extracellular arginine; nitrite or NO donor interventions

limitations

Rare genetic deficiency; molecular scaffolding is distinct from supplying enough circulating arginine.

nutrient_topic

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

organism

Human ASL deficiency and Asl-deficient mice, model specified

plain_language

An intact downstream enzyme matters to the NO pathway.

primary_references

[citrulline-p22081021] Requirement of argininosuccinate lyase for systemic nitric oxide production. (2011). https://pubmed.ncbi.nlm.nih.gov/22081021/ DOI: 10.1038/nm.2544

tissue_or_cell_type

Arginine synthesis, NOS-associated protein complex and vasculature

trigger_kind

machinery_impairment Imported condition classification; unverified.

Citrulline: arginine recycling, nitrogen disposal 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 · Patient vascular testing, hypomorphic mice and molecular experiments · source_derived_draft · unverified_draft

### citrulline-asl-no-low ASL deficiency reduced nitric-oxide synthesis in the studied humans and mice. Condition category: machinery_impairment nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: An intact downstream enzyme matters to the NO pathway. organism: Human ASL deficiency and Asl-deficient mice, model specified tissue_or_cell_type: Arginine synthesis, NOS-associated protein complex and vasculature experimental_model: Patient vascular testing, hypomorphic mice and molecular experiments limitations: Rare genetic deficiency; molecular scaffolding is distinct from supplying enough circulating arginine. exposure: ASL loss; extracellular arginine; nitrite or NO donor interventions evidence_span: {"source_cache": "artifacts/citrulline-research/22081021.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b", "start_char": 0, "end_char": 1137, "text_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b"} [citrulline-p22081021] Requirement of argininosuccinate lyase for systemic nitric oxide production. (2011). https://pubmed.ncbi.nlm.nih.gov/22081021/ DOI: 10.1038/nm.2544

evidence_span

{"source_cache": "artifacts/citrulline-research/22081021.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b", "start_char": 0, "end_char": 1137, "text_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b"}

experimental_model

Patient vascular testing, hypomorphic mice and molecular experiments

exposure

ASL loss; extracellular arginine; nitrite or NO donor interventions

limitations

Rare genetic deficiency; molecular scaffolding is distinct from supplying enough circulating arginine.

nutrient_topic

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

organism

Human ASL deficiency and Asl-deficient mice, model specified

plain_language

This enzyme helps organize the machinery as well as catalyze a reaction.

primary_references

[citrulline-p22081021] Requirement of argininosuccinate lyase for systemic nitric oxide production. (2011). https://pubmed.ncbi.nlm.nih.gov/22081021/ DOI: 10.1038/nm.2544

tissue_or_cell_type

Arginine synthesis, NOS-associated protein complex and vasculature

Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 645–656

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient vascular testing, hypomorphic mice and molecular experiments · source_derived_draft · unverified_draft

### citrulline-asl-scaffold Mechanistic experiments identified a structural ASL role in assembly of a multiprotein complex required for NO production. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: This enzyme helps organize the machinery as well as catalyze a reaction. organism: Human ASL deficiency and Asl-deficient mice, model specified tissue_or_cell_type: Arginine synthesis, NOS-associated protein complex and vasculature experimental_model: Patient vascular testing, hypomorphic mice and molecular experiments limitations: Rare genetic deficiency; molecular scaffolding is distinct from supplying enough circulating arginine. exposure: ASL loss; extracellular arginine; nitrite or NO donor interventions evidence_span: {"source_cache": "artifacts/citrulline-research/22081021.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b", "start_char": 0, "end_char": 1137, "text_sha256": "2f9f02564dadd246299fe5eded3ddb08e3c68f08d27cae8b16f2506fe9eaf68b"} [citrulline-p22081021] Requirement of argininosuccinate lyase for systemic nitric oxide production. (2011). https://pubmed.ncbi.nlm.nih.gov/22081021/ DOI: 10.1038/nm.2544

acting_entity

optimized-aged-black-garlic-2023

dose

Optimized aged black garlic extract providing 0.25 mg SAC/day

duration

Twelve weeks

evidence_access

Primary abstract

experimental_comparison

Randomized triple-blind placebo-controlled extract trial

experimental_model

Grade I hypertensive participants receiving antihypertensive treatment

interpretation_status

Source-derived research curation; not independent primary verification

limitations

SAC-standardized extract, not purified SAC. Background antihypertensives continued; reported blood NO is a study assay endpoint.

nutrient_topic

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

organism

Homo sapiens

plain_language

Human formulation evidence is available, with ingredient attribution unresolved.

primary_references

[37686723] Antihypertensive Effects of an Optimized Aged Garlic Extract in Subjects with Grade I Hypertension and Antihypertensive Drug Therapy: A Randomized, Triple-Blind Controlled Trial. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37686723/ · DOI 10.3390/nu15173691

route

Oral

tissue_or_cell_type

Grade I hypertensive participants receiving antihypertensive treatment

S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 437–444

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Grade I hypertensive participants receiving antihypertensive treatment · source_derived_draft · unverified_draft

## s-allylcysteine-extract-no Human formulation evidence is available, with ingredient attribution unresolved. The randomized extract trial reported increased blood NO readout after 12 weeks. Model: Grade I hypertensive participants receiving antihypertensive treatment Limitations: SAC-standardized extract, not purified SAC. Background antihypertensives continued; reported blood NO is a study assay endpoint. Evidence access: Primary abstract [37686723] Antihypertensive Effects of an Optimized Aged Garlic Extract in Subjects with Grade I Hypertension and Antihypertensive Drug Therapy: A Randomized, Triple-Blind Controlled Trial. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37686723/ · DOI 10.3390/nu15173691 Structured context: {"organism": "Homo sapiens", "tissue_or_cell_type": "Grade I hypertensive participants receiving antihypertensive treatment", "dose": "Optimized aged black garlic extract providing 0.25 mg SAC/day", "duration": "Twelve weeks", "route": "Oral", "experimental_comparison": "Randomized triple-blind placebo-controlled extract trial", "acting_entity": "optimized-aged-black-garlic-2023", "interpretation_status": "Source-derived research curation; not independent primary verification"}

evidence_span

{"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"}

experimental_model

Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression

exposure

Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5

limitations

Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established.

nutrient_topic

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

organism

Homo sapiens proteins and HEK cells

plain_language

Acidity changed the reaction rate in this assay.

primary_references

[mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

tissue_or_cell_type

Purified redox system and human cell model

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1054–1065

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression · source_derived_draft · unverified_draft

### mo-marc-ph Lowering assay pH from 7.5 to 6.5 increased the reported mARC NO-formation rate by nearly threefold. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acidity changed the reaction rate in this assay. organism: Homo sapiens proteins and HEK cells tissue_or_cell_type: Purified redox system and human cell model experimental_model: Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression limitations: Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established. exposure: Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5 evidence_span: {"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"} [mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

evidence_span

{"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"}

experimental_model

Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression

exposure

Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5

limitations

Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established.

nutrient_topic

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

organism

Homo sapiens proteins and HEK cells

plain_language

mARC1 can also make NO from nitrite under suitable conditions.

primary_references

[mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

tissue_or_cell_type

Purified redox system and human cell model

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1028–1039

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression · source_derived_draft · unverified_draft

### mo-marc1-nitrite Reduced human mARC1 generated nitric oxide from nitrite in the reconstituted electron-transfer chain. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: mARC1 can also make NO from nitrite under suitable conditions. organism: Homo sapiens proteins and HEK cells tissue_or_cell_type: Purified redox system and human cell model experimental_model: Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression limitations: Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established. exposure: Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5 evidence_span: {"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"} [mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

evidence_span

{"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"}

experimental_model

Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression

exposure

Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5

limitations

Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established.

nutrient_topic

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

organism

Homo sapiens proteins and HEK cells

plain_language

mARC2 shares this conditional NO-forming capability.

primary_references

[mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

tissue_or_cell_type

Purified redox system and human cell model

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1041–1052

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression · source_derived_draft · unverified_draft

### mo-marc2-nitrite Reduced human mARC2 also catalyzed nitrite-to-NO conversion. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: mARC2 shares this conditional NO-forming capability. organism: Homo sapiens proteins and HEK cells tissue_or_cell_type: Purified redox system and human cell model experimental_model: Recombinant human mARC1/mARC2, active-site mutation, tungsten replacement and HEK expression limitations: Shows nitrite-reducing capacity; its share of NO production in normal people and response to mineral intake are not established. exposure: Reduced enzyme, nitrite, NADH/CYB5/CYB5R; pH 7.5 versus 6.5 evidence_span: {"source_cache": "artifacts/molybdenum-research/24500710.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b", "start_char": 0, "end_char": 1585, "text_sha256": "e4c2ab41c945d420266290d0241752039d7de2cb6223f9c64c7d0525c5688d9b"} [mo-p24500710] Nitrite reductase and nitric-oxide synthase activity of the mitochondrial molybdopterin enzymes mARC1 and mARC2. (2014). https://pubmed.ncbi.nlm.nih.gov/24500710/ DOI: 10.1074/jbc.m114.555177

evidence_span

{"source_cache": "artifacts/molybdenum-research/31167903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9fb7f72eba7a1a254ae8e20991ee5d9ecbffc01de2a1dfc5879cf34bdbf98b45", "start_char": 0, "end_char": 962, "text_sha256": "9fb7f72eba7a1a254ae8e20991ee5d9ecbffc01de2a1dfc5879cf34bdbf98b45"}

experimental_model

Human SUOX kinetics, spectroscopy and electron-transfer variants

exposure

Nitrite with sulfite and cytochrome c

limitations

Biochemical capacity; contribution to human physiology requires separate evidence.

nutrient_topic

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

organism

Homo sapiens protein

plain_language

SUOX can perform additional redox chemistry under the tested conditions.

primary_references

[mo-p31167903] Mechanism of nitrite-dependent NO synthesis by human sulfite oxidase. (2019). https://pubmed.ncbi.nlm.nih.gov/31167903/ DOI: 10.1042/bcj20190143

tissue_or_cell_type

Purified human sulfite oxidase

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1093–1104

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SUOX kinetics, spectroscopy and electron-transfer variants · source_derived_draft · unverified_draft

### mo-suox-nitrite Human SUOX reduced nitrite to NO at the molybdenum center, with steady-state turnover supported in a sulfite/cytochrome-c system. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: SUOX can perform additional redox chemistry under the tested conditions. organism: Homo sapiens protein tissue_or_cell_type: Purified human sulfite oxidase experimental_model: Human SUOX kinetics, spectroscopy and electron-transfer variants limitations: Biochemical capacity; contribution to human physiology requires separate evidence. exposure: Nitrite with sulfite and cytochrome c evidence_span: {"source_cache": "artifacts/molybdenum-research/31167903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9fb7f72eba7a1a254ae8e20991ee5d9ecbffc01de2a1dfc5879cf34bdbf98b45", "start_char": 0, "end_char": 962, "text_sha256": "9fb7f72eba7a1a254ae8e20991ee5d9ecbffc01de2a1dfc5879cf34bdbf98b45"} [mo-p31167903] Mechanism of nitrite-dependent NO synthesis by human sulfite oxidase. (2019). https://pubmed.ncbi.nlm.nih.gov/31167903/ DOI: 10.1042/bcj20190143

evidence_span

{"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"}

experimental_model

Recombinant human XDH variants with urate, superoxide and NO assays

exposure

Xanthine, oxygen and inorganic nitrite assays

limitations

The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response.

nutrient_topic

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

organism

Homo sapiens protein

plain_language

One variant raised several outputs at once.

primary_references

[mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864

tissue_or_cell_type

Purified human enzyme

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 807–818

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human XDH variants with urate, superoxide and NO assays · source_derived_draft · unverified_draft

### mo-xor-h1221r His1221Arg increased urate, superoxide and NO formation relative to wild type in xanthine-supplied assays. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: One variant raised several outputs at once. organism: Homo sapiens protein tissue_or_cell_type: Purified human enzyme experimental_model: Recombinant human XDH variants with urate, superoxide and NO assays limitations: The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response. exposure: Xanthine, oxygen and inorganic nitrite assays evidence_span: {"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"} [mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864

evidence_span

{"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"}

experimental_model

Recombinant human XDH variants with urate, superoxide and NO assays

exposure

Xanthine, oxygen and inorganic nitrite assays

limitations

The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response.

nutrient_topic

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

organism

Homo sapiens protein

plain_language

Another variant changed the balance of products differently.

primary_references

[mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864

tissue_or_cell_type

Purified human enzyme

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 820–831

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human XDH variants with urate, superoxide and NO assays · source_derived_draft · unverified_draft

### mo-xor-i703v Ile703Val increased urate and NO formation without increasing superoxide formation in the reported comparison. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another variant changed the balance of products differently. organism: Homo sapiens protein tissue_or_cell_type: Purified human enzyme experimental_model: Recombinant human XDH variants with urate, superoxide and NO assays limitations: The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response. exposure: Xanthine, oxygen and inorganic nitrite assays evidence_span: {"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"} [mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864

evidence_span

{"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"}

experimental_model

Recombinant human XDH variants with urate, superoxide and NO assays

exposure

Xanthine, oxygen and inorganic nitrite assays

limitations

The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response.

nutrient_topic

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

organism

Homo sapiens protein

plain_language

Changing the available electron acceptor changed the products.

primary_references

[mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864

tissue_or_cell_type

Purified human enzyme

Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 794–805

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human XDH variants with urate, superoxide and NO assays · source_derived_draft · unverified_draft

### mo-xor-nitrite Human XOR reduced nitrite to NO under the tested reducing conditions, and nitrite decreased XOR-driven superoxide production. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the available electron acceptor changed the products. organism: Homo sapiens protein tissue_or_cell_type: Purified human enzyme experimental_model: Recombinant human XDH variants with urate, superoxide and NO assays limitations: The 2023 Fig. 6E corrigendum corrects a displayed panel; authors state data and conclusions are unchanged. Enzyme activity is not a clinical benefit or dietary response. exposure: Xanthine, oxygen and inorganic nitrite assays evidence_span: {"source_cache": "artifacts/molybdenum-research/37713777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9", "start_char": 0, "end_char": 1655, "text_sha256": "30e93ea24784120403bef1dfe72cf46411f1af88946b9cc1cba3d4c45a367bf9"} [mo-p37713777] Natural mutations of human XDH promote the nitrite (NO2-)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health? (2023). https://pubmed.ncbi.nlm.nih.gov/37713777/ DOI: 10.1016/j.redox.2023.102864

evidence_access

Primary abstract

experimental_model

Acute labeled-nitrite human study.

limitations

Does not quantify interactions with prescription nitrates or prove long-term harm.

nutrient_topic

CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family

plain_language

Making more nitrated lipid coincided with less of another NO response.

primary_references

Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016

Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 334–340

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Acute labeled-nitrite human study. · source_derived_draft · unverified_draft

## cla-no-diversion Making more nitrated lipid coincided with less of another NO response. CLA coadministration reduced labeled NO–deoxyhemoglobin formation and attenuated nitrite-associated vasodilation and platelet inhibition. Model: Acute labeled-nitrite human study. Limitations: Does not quantify interactions with prescription nitrates or prove long-term harm. Evidence access: Primary abstract Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016