Component

Hypoxanthine

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

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

Read recorded mechanisms Open recursive mind map

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 it acts on

  1. Hypoxanthine plus thymidine attenuated EGCG growth inhibition, consistent with involvement of folate-dependent nucleotide supply.

    Hypoxanthine → Proliferation of EGCG-exposed lymphoma cells source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally.
    limitations
    Rescue supports pathway involvement but does not prove DHFR is the only target.
    nutrient_topic
    EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)
    plain_language
    Supplying salvage-pathway ingredients partly bypassed the growth effect.
    primary_references
    The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

    EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 148–154

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. · source_derived_draft · unverified_draft

    ## egcg-salvage Supplying salvage-pathway ingredients partly bypassed the growth effect. Hypoxanthine plus thymidine attenuated EGCG growth inhibition, consistent with involvement of folate-dependent nucleotide supply. Model: Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. Limitations: Rescue supports pathway involvement but does not prove DHFR is the only target. Evidence access: primary abstract. The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469
    Complete structured claim and evidence

What acts on it

  1. The primary article describes sequential XOR hydroxylation of hypoxanthine to xanthine and xanthine to urate.

    Human xanthine oxidoreductase / XDH → Hypoxanthine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/37713777.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8092b2aa7328b59f0275dd8a37d2a2dbb5abb2a32236d0cab5fffcc1ddc671d", "start_char": 1061, "end_char": 1244, "text_sha256": "45575621674b6b2e232b2e7b9605ad8e6acde4977d3f22e20abebfcbfa0b4dcb"}
    experimental_model
    Recombinant human XDH variants with urate, superoxide and NO assays
    exposure
    Xanthine, oxygen and inorganic nitrite assays
    limitations
    Established reaction summarized in the primary article background; this paper directly assayed xanthine-based activity rather than newly establishing the hypoxanthine step.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Homo sapiens protein
    plain_language
    Hypoxanthine enters the same two-step purine pathway.
    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 755–766

    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-xdh-hypoxanthine The primary article describes sequential XOR hydroxylation of hypoxanthine to xanthine and xanthine to urate. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Hypoxanthine enters the same two-step purine pathway. organism: Homo sapiens protein tissue_or_cell_type: Purified human enzyme experimental_model: Recombinant human XDH variants with urate, superoxide and NO assays limitations: Established reaction summarized in the primary article background; this paper directly assayed xanthine-based activity rather than newly establishing the hypoxanthine step. exposure: Xanthine, oxygen and inorganic nitrite assays evidence_span: {"source_cache": "artifacts/molybdenum-research/37713777.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8092b2aa7328b59f0275dd8a37d2a2dbb5abb2a32236d0cab5fffcc1ddc671d", "start_char": 1061, "end_char": 1244, "text_sha256": "45575621674b6b2e232b2e7b9605ad8e6acde4977d3f22e20abebfcbfa0b4dcb"} [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. Luteolin competitively inhibited purified bovine xanthine oxidase without time-dependent inhibition.

    Luteolin / 3′,4′,5,7-tetrahydroxyflavone → Bovine xanthine oxidoreductase / XDH source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Purified bovine enzyme steady-state kinetics.
    limitations
    Bovine enzyme evidence; not a clinical urate-lowering trial.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    It interfered with the purine-breakdown enzyme.
    primary_references
    Inhibition studies of bovine xanthine oxidase by luteolin, silibinin, quercetin, and curcumin. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19388706/ · DOI 10.1021/np8007123

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 284–290

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine enzyme steady-state kinetics. · source_derived_draft · unverified_draft

    ## luteolin-xo-inhibition It interfered with the purine-breakdown enzyme. Luteolin competitively inhibited purified bovine xanthine oxidase without time-dependent inhibition. Model: Purified bovine enzyme steady-state kinetics. Limitations: Bovine enzyme evidence; not a clinical urate-lowering trial. Evidence access: Primary abstract Inhibition studies of bovine xanthine oxidase by luteolin, silibinin, quercetin, and curcumin. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19388706/ · DOI 10.1021/np8007123
    Complete structured claim and evidence

  2. The same patient had low serum urate with increased urinary hypoxanthine and xanthine.

    Molybdenum → Serum urate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/6795919.publisher-abstract.txt", "locator": "Exact primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2838a46a598539818059c1a1f8295e283334afced15326a6b5ba1a6104cbfd7", "start_char": 0, "end_char": 1820, "text_sha256": "d2838a46a598539818059c1a1f8295e283334afced15326a6b5ba1a6104cbfd7"}
    experimental_model
    Single case during prolonged total parenteral nutrition
    exposure
    Prolonged parenteral nutrition followed by ammonium molybdate
    limitations
    Rare single case. The paper reports 300 micrograms/day ammonium molybdate, not 300 micrograms elemental molybdenum. Historical observation, not a general regimen.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Homo sapiens
    plain_language
    A second molybdenum-dependent pathway was also impaired.
    primary_references
    [mo-p6795919] Amino acid intolerance during prolonged total parenteral nutrition reversed by molybdate therapy. (1981). https://pubmed.ncbi.nlm.nih.gov/6795919/ DOI: 10.1093/ajcn/34.11.2551
    tissue_or_cell_type
    Systemic symptoms; plasma and urine
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1132–1143

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single case during prolonged total parenteral nutrition · source_derived_draft · unverified_draft

    ### mo-tpn-purines The same patient had low serum urate with increased urinary hypoxanthine and xanthine. Condition category: nutrient_deficiency nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second molybdenum-dependent pathway was also impaired. organism: Homo sapiens tissue_or_cell_type: Systemic symptoms; plasma and urine experimental_model: Single case during prolonged total parenteral nutrition limitations: Rare single case. The paper reports 300 micrograms/day ammonium molybdate, not 300 micrograms elemental molybdenum. Historical observation, not a general regimen. exposure: Prolonged parenteral nutrition followed by ammonium molybdate evidence_span: {"source_cache": "artifacts/molybdenum-research/6795919.publisher-abstract.txt", "locator": "Exact primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2838a46a598539818059c1a1f8295e283334afced15326a6b5ba1a6104cbfd7", "start_char": 0, "end_char": 1820, "text_sha256": "d2838a46a598539818059c1a1f8295e283334afced15326a6b5ba1a6104cbfd7"} [mo-p6795919] Amino acid intolerance during prolonged total parenteral nutrition reversed by molybdate therapy. (1981). https://pubmed.ncbi.nlm.nih.gov/6795919/ DOI: 10.1093/ajcn/34.11.2551
    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