Component

Nitrite / NO2(-)

Nitrite / NO2(-). Species, exposure and limitations are retained in each linked claim.

14 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Reduced human mARC1 generated nitric oxide from nitrite in the reconstituted electron-transfer chain.

    Experimental context and source evidence
    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
    Complete structured claim and evidence
  2. Reduced human mARC2 also catalyzed nitrite-to-NO conversion.

    Experimental context and source evidence
    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
    Complete structured claim and evidence
  3. Human SUOX reduced nitrite to NO at the molybdenum center, with steady-state turnover supported in a sulfite/cytochrome-c system.

    Human sulfite oxidase / SUOX → Nitrite / NO2(-) source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence
  4. Human XOR reduced nitrite to NO under the tested reducing conditions, and nitrite decreased XOR-driven superoxide production.

    Human xanthine oxidoreductase / XDH → Nitrite / NO2(-) source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Plasma NOx remained elevated for 8 h after beetroot juice and 5 h after whole beetroot despite undetectable plasma betanin.

    Experimental context and source evidence
    dose
    250 mL beetroot juice or 300 g whole beetroot versus placebo
    duration
    Baseline and 1, 2, 3, 5 and 8 h
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Ten healthy men in a randomized crossover study
    limitations
    An undetectable parent compound is not proof of zero absorption. Food matrix, degradation and analytical methods differ from the cactus pear study. NOx is not itself a measurement of a betanin mechanism. Mixed-food nitrate-related observation; not a claim that betalains generate NO or mediate nitrate-associated performance effects.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Ten healthy men in a randomized crossover study
    plain_language
    Plasma NOx remained elevated for 8 h after beetroot juice and 5 h after whole beetroot despite undetectable plasma betanin.
    primary_references
    The plasma bioavailability of nitrate and betanin from Beta vulgaris rubra in humans. (2017). https://pubmed.ncbi.nlm.nih.gov/26873098/ DOI: 10.1007/s00394-016-1173-5
    route
    Oral food/drink
    tissue
    Venous plasma

    Betalains: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 537–545

    Original AI-assisted curation of twelve primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Ten healthy men in a randomized crossover study · source_derived_draft · unverified_draft

    ## betalains-beetroot-nox-separate Plasma NOx remained elevated for 8 h after beetroot juice and 5 h after whole beetroot despite undetectable plasma betanin. Model/species: Ten healthy men in a randomized crossover study Tissue: Venous plasma Exposure: 250 mL beetroot juice or 300 g whole beetroot versus placebo Route: Oral food/drink Duration: Baseline and 1, 2, 3, 5 and 8 h Limits: An undetectable parent compound is not proof of zero absorption. Food matrix, degradation and analytical methods differ from the cactus pear study. NOx is not itself a measurement of a betanin mechanism. Mixed-food nitrate-related observation; not a claim that betalains generate NO or mediate nitrate-associated performance effects. Primary reference: The plasma bioavailability of nitrate and betanin from Beta vulgaris rubra in humans. (2017). https://pubmed.ncbi.nlm.nih.gov/26873098/ DOI: 10.1007/s00394-016-1173-5
    Complete structured claim and evidence
  2. Betanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL.

    Betanin → Lipid peroxidation source_derived_draftungraded
    Experimental context and source evidence
    dose
    Experimental betanin addition; concentration not specified in accessed abstract
    duration
    Oxidation time courses; duration not specified in accessed abstract
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Isolated human LDL and MPO/nitrite biochemical system
    limitations
    Oxidation products were not chemically identified; clinical LDL lowering was not tested.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Isolated human LDL and MPO/nitrite biochemical system
    plain_language
    Betanin reduced lipid hydroperoxide formation during MPO/nitrite-mediated oxidation of human LDL.
    primary_references
    Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
    route
    In vitro addition
    tissue
    LDL lipid compartment

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

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

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

    Experimental context and source evidence
    dose
    Experimental betanin addition; concentration not specified in accessed abstract
    duration
    Oxidation time courses; duration not specified in accessed abstract
    evidence_access
    Primary PubMed abstract; detailed exposure for PMID 23931157 additionally checked in publisher results. No uninspected full text is claimed.
    evidence_scope
    literature_reviewed; source-derived curation, not universally established human effects
    experimental_model
    Isolated human LDL and MPO/nitrite biochemical system
    limitations
    Oxidation products were not chemically identified; clinical LDL lowering was not tested.
    nutrient_topic
    Betalains collection; each molecular form, species, exposure and preparation remains explicit. · Betalains
    organism
    Isolated human LDL and MPO/nitrite biochemical system
    plain_language
    Unidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay.
    primary_references
    Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
    route
    In vitro addition
    tissue
    LDL lipid compartment

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

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

    ## betalains-oxidation-products Unidentified products generated by MPO/nitrite oxidation of betanin also inhibited LDL oxidation in the assay. Model/species: Isolated human LDL and MPO/nitrite biochemical system Tissue: LDL lipid compartment Exposure: Experimental betanin addition; concentration not specified in accessed abstract Route: In vitro addition Duration: Oxidation time courses; duration not specified in accessed abstract Limits: Oxidation products were not chemically identified; clinical LDL lowering was not tested. Primary reference: Betanin inhibits the myeloperoxidase/nitrite-induced oxidation of human low-density lipoproteins. (2007). https://pubmed.ncbi.nlm.nih.gov/17364963/ DOI: 10.1080/10715760601038783
    Complete structured claim and evidence
  4. An uncontrolled 12-person nitrate/garlic combination study reported lower systolic pressure after two weeks, persisting at four weeks.

    Experimental context and source evidence
    acting_entity
    vascanox-hp-2023
    dose
    Vascanox HP combination; constituent doses not retrieved
    duration
    Four weeks
    evidence_access
    Primary abstract
    experimental_comparison
    Within-person baseline; no placebo or factorial comparison
    experimental_model
    Twelve participants completing an open-label combination study
    interpretation_status
    Source-derived research curation; not independent primary verification
    limitations
    No placebo or ingredient-factorial arms: cannot establish SAC contribution, nitrate contribution, interaction or synergy.
    nutrient_topic
    S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · S-allyl-L-cysteine / SAC
    organism
    Homo sapiens
    plain_language
    A cross-compound human lead remains available without assigning the effect to SAC.
    primary_references
    [37849591] Effects of S-Allylcysteine-Rich Garlic Extract and Dietary Inorganic Nitrate Formula on Blood Pressure and Salivary Nitric Oxide: An Open-Label Clinical Trial Among Hypertensive Subjects. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37849591/ · DOI 10.7759/cureus.45369
    route
    Oral
    tissue_or_cell_type
    Twelve participants completing an open-label combination study

    S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20) · lines 455–462

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Twelve participants completing an open-label combination study · source_derived_draft · unverified_draft

    ## s-allylcysteine-nitrate-combination A cross-compound human lead remains available without assigning the effect to SAC. An uncontrolled 12-person nitrate/garlic combination study reported lower systolic pressure after two weeks, persisting at four weeks. Model: Twelve participants completing an open-label combination study Limitations: No placebo or ingredient-factorial arms: cannot establish SAC contribution, nitrate contribution, interaction or synergy. Evidence access: Primary abstract [37849591] Effects of S-Allylcysteine-Rich Garlic Extract and Dietary Inorganic Nitrate Formula on Blood Pressure and Salivary Nitric Oxide: An Open-Label Clinical Trial Among Hypertensive Subjects. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37849591/ · DOI 10.7759/cureus.45369 Structured context: {"organism": "Homo sapiens", "tissue_or_cell_type": "Twelve participants completing an open-label combination study", "dose": "Vascanox HP combination; constituent doses not retrieved", "duration": "Four weeks", "route": "Oral", "experimental_comparison": "Within-person baseline; no placebo or factorial comparison", "acting_entity": "vascanox-hp-2023", "interpretation_status": "Source-derived research curation; not independent primary verification"}
    Complete structured claim and evidence
  5. Lowering assay pH from 7.5 to 6.5 increased the reported mARC NO-formation rate by nearly threefold.

    Experimental context and source evidence
    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
    Complete structured claim and evidence
  6. 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.

    Human sulfite oxidase / SUOX → NO source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence
  7. Adding CLA during labeled oral nitrite administration increased plasma 12-nitro-CLA formation.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Same five-person paired coadministration study.
    limitations
    Same dataset as the 9-nitro product, not an independent replication.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    A second nitrated product was detected separately.
    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 326–332

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same five-person paired coadministration study. · source_derived_draft · unverified_draft

    ## cla-human-nitro-12 A second nitrated product was detected separately. Adding CLA during labeled oral nitrite administration increased plasma 12-nitro-CLA formation. Model: Same five-person paired coadministration study. Limitations: Same dataset as the 9-nitro product, not an independent replication. 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
    Complete structured claim and evidence
  8. Adding CLA during labeled oral nitrite administration increased plasma 9-nitro-CLA formation.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Healthy-volunteer crossover; five returned for CLA coadministration.
    limitations
    Small acute study using investigational formulations; not a dosing recommendation.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Dietary lipid changed which nitrogen-oxide products formed.
    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 318–324

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Healthy-volunteer crossover; five returned for CLA coadministration. · source_derived_draft · unverified_draft

    ## cla-human-nitro-9 Dietary lipid changed which nitrogen-oxide products formed. Adding CLA during labeled oral nitrite administration increased plasma 9-nitro-CLA formation. Model: Healthy-volunteer crossover; five returned for CLA coadministration. Limitations: Small acute study using investigational formulations; not a dosing recommendation. 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
    Complete structured claim and evidence
  9. CLA yielded substantially more nitration products than nonconjugated linoleic acid under the tested nitrogen-oxide reactions.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Chemical, cellular and in-vivo nitration experiments.
    limitations
    This is formation of a different molecule, not evidence that plain CLA has every nitro-lipid action.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Its double-bond arrangement changes its chemical reactivity.
    primary_references
    Conjugated linoleic acid is a preferential substrate for fatty acid nitration. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23144452/ · DOI 10.1074/jbc.M112.401356

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 310–316

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chemical, cellular and in-vivo nitration experiments. · source_derived_draft · unverified_draft

    ## cla-nitration Its double-bond arrangement changes its chemical reactivity. CLA yielded substantially more nitration products than nonconjugated linoleic acid under the tested nitrogen-oxide reactions. Model: Chemical, cellular and in-vivo nitration experiments. Limitations: This is formation of a different molecule, not evidence that plain CLA has every nitro-lipid action. Evidence access: Primary abstract Conjugated linoleic acid is a preferential substrate for fatty acid nitration. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23144452/ · DOI 10.1074/jbc.M112.401356
    Complete structured claim and evidence
  10. CLA coadministration reduced labeled NO–deoxyhemoglobin formation and attenuated nitrite-associated vasodilation and platelet inhibition.

    Experimental context and source evidence
    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
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards