Component

Ammonium metavanadate

Context-specific entity; species, compartment and exposure are stated on each claim.

2 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. Vanadium-exposed duck livers showed wider ER–mitochondrial gaps and altered abundance/association of the IP3R–GRP75–VDAC1 contact complex.

    Ammonium metavanadate → Mitochondria–ER contacts in vanadium-exposed duck liver source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Duck liver ultrastructure and MAM proteomics/co-association measurements.
    limitations
    No genetic or inhibitor rescue establishing this chain was extracted. Human orthologues are not substituted for duck measurements.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    A change at organelle contacts may link calcium handling, metabolism and injury.
    primary_references
    Dual-pathway mechanism of vanadium-induced hepatotoxicity in ducks: Synergistic crosstalk between glucose homeostasis disruption and NADH/FSP1/COQ10 axis-driven ferroptosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41362732/ · DOI 10.7150/ijbs.123482

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 366–372

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Duck liver ultrastructure and MAM proteomics/co-association measurements. · source_derived_draft · unverified_draft

    ## vanadium-duck-mam A change at organelle contacts may link calcium handling, metabolism and injury. Vanadium-exposed duck livers showed wider ER–mitochondrial gaps and altered abundance/association of the IP3R–GRP75–VDAC1 contact complex. Model: Duck liver ultrastructure and MAM proteomics/co-association measurements. Limitations: No genetic or inhibitor rescue establishing this chain was extracted. Human orthologues are not substituted for duck measurements. Evidence access: Primary full text Dual-pathway mechanism of vanadium-induced hepatotoxicity in ducks: Synergistic crosstalk between glucose homeostasis disruption and NADH/FSP1/COQ10 axis-driven ferroptosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41362732/ · DOI 10.7150/ijbs.123482
    Complete structured claim and evidence

  2. Dietary vanadium overexposure in ducks was associated with lower NADH/FSP1/CoQ10-axis measures and increased hepatic lipid peroxidation and Fe2+ accumulation.

    Ammonium metavanadate → Duck FSP1 / AIFM2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Ammonium metavanadate diets reported as 30 or 45 mg V/kg feed; 42-day duck study.
    limitations
    Observational pathway measurements after exposure, not direct enzyme inhibition or a human ferroptosis mechanism. Methods inconsistently say three and four groups while listing control plus two exposure groups.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    An animal toxicity study links the exposure to a lipid-defense pathway.
    primary_references
    Dual-pathway mechanism of vanadium-induced hepatotoxicity in ducks: Synergistic crosstalk between glucose homeostasis disruption and NADH/FSP1/COQ10 axis-driven ferroptosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41362732/ · DOI 10.7150/ijbs.123482

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 358–364

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ammonium metavanadate diets reported as 30 or 45 mg V/kg feed; 42-day duck study. · source_derived_draft · unverified_draft

    ## vanadium-duck-redox-axis An animal toxicity study links the exposure to a lipid-defense pathway. Dietary vanadium overexposure in ducks was associated with lower NADH/FSP1/CoQ10-axis measures and increased hepatic lipid peroxidation and Fe2+ accumulation. Model: Ammonium metavanadate diets reported as 30 or 45 mg V/kg feed; 42-day duck study. Limitations: Observational pathway measurements after exposure, not direct enzyme inhibition or a human ferroptosis mechanism. Methods inconsistently say three and four groups while listing control plus two exposure groups. Evidence access: Primary full text Dual-pathway mechanism of vanadium-induced hepatotoxicity in ducks: Synergistic crosstalk between glucose homeostasis disruption and NADH/FSP1/COQ10 axis-driven ferroptosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41362732/ · DOI 10.7150/ijbs.123482
    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