Component
GPX4 Sec-to-Cys variant
Independent entity for contextual scientific-audit claims; no universal nutritional effect implied.
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 it acts on
GPX4 Sec-to-Cys substitution retains context-dependent residual function but increases peroxide-induced inactivation and ferroptosis susceptibility.
Experimental context and source evidence
- cell_type
- Knock-in tissues and derived/engineered cells
- experimental_model
- Gpx4 Sec-to-Cys knock-in mice, tissue assays and cell peroxide challenges
- limitations
- Tissue PCOOH activity was undetectable in reported brain/kidney assays; mutation is not nutritional deficiency.
- organism
- Mus musculus
Selenium: literature corrections and mechanism additions · lines 1263–1273
Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Gpx4 Sec-to-Cys knock-in mice, tissue assays and cell peroxide challenges · secondary_verified · secondary_verified
## gpx4-cys-vulnerability Replacing selenium with sulfur retains some function but weakens peroxide resistance. GPX4 Sec-to-Cys substitution retains context-dependent residual function but increases peroxide-induced inactivation and ferroptosis susceptibility. Organism: Mus musculus Cell type: Knock-in tissues and derived/engineered cells Experimental model: Gpx4 Sec-to-Cys knock-in mice, tissue assays and cell peroxide challenges Limitations: Tissue PCOOH activity was undetectable in reported brain/kidney assays; mutation is not nutritional deficiency. Primary reference: [Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis](https://pubmed.ncbi.nlm.nih.gov/29290465/)
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.