Component
Duck FSP1 / AIFM2
Context-specific entity; species, compartment and exposure are stated on each claim.
1 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Dietary vanadium overexposure in ducks was associated with lower NADH/FSP1/CoQ10-axis measures and increased hepatic lipid peroxidation and Fe2+ accumulation.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.