Component
FSP1
Ferroptosis suppressor protein 1; a CoQ oxidoreductase providing parallel lipid-radical defense.
2 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 it acts on
FSP1 can regenerate reduced CoQ as a parallel, glutathione-independent defense alongside GPX4.
Experimental context and source evidence
- availability_state
- Selenium restriction becomes severe enough to compromise GPX4 function in a susceptible context.
- experimental_scope
- Cell and cancer-model evidence for parallel defenses; GPX4 may be relatively preserved during nutritional restriction.
- limitations
- The source does not establish a nutritional dose or plasma value that disables GPX4. GPX4 deletion or drug inhibition is not equivalent to ordinary dietary deficiency; parallel protection is not guaranteed in every cell.
- trigger_kind
- nutrient_deficiency
Selenium deficiency: a mechanism-first reference · lines 123–123
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
But GPX4 is not the only barrier between a cell and ferroptosis. The FSP1–CoQ10 system provides a parallel, glutathione-independent defense by regenerating reduced CoQ, which can trap lipid radicals. Other systems also contribute. Evidence: cell and cancer-model experiments. [8,9]
Complete structured claim and evidenceFSP1 reduces CoQ and supplies a lipid-radical defense operating in parallel with GPX4.
Experimental context and source evidence
- cell_type
- Experimental cultured cells
- experimental_model
- Cell genetics and biochemical experiments
- limitations
- Capacity and dependence vary by cell; not a universal dietary threshold.
- organism
- Human cell models
Selenium: literature corrections and mechanism additions · lines 1492–1502
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Cell genetics and biochemical experiments · secondary_verified · secondary_verified
## fsp1-parallel Another defense changes how vulnerable cells are to GPX4 loss. FSP1 reduces CoQ and supplies a lipid-radical defense operating in parallel with GPX4. Organism: Human cell models Cell type: Experimental cultured cells Experimental model: Cell genetics and biochemical experiments Limitations: Capacity and dependence vary by cell; not a universal dietary threshold. Primary reference: [The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis](https://www.nature.com/articles/s41586-019-1705-2)
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.