Component
Phospholipid hydroperoxides
Oxidized phospholipids reduced by GPX4 in membranes.
3 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
When GPX4 function is severely reduced, its direct control of membrane phospholipid hydroperoxides is compromised.
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 119–123
Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft
Why GPX4 is especially important GPX4 directly reduces phospholipid hydroperoxides in membranes and is a central suppressor of ferroptosis. Severe loss of GPX4 function can therefore have consequences very different from loss of a more dispensable peroxide-removing enzyme. 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 evidencePurified PHGPX (GPX4) with glutathione reduced phospholipid hydroperoxides within photooxidized human erythrocyte ghost membranes to alcohol products without prior phospholipase cleavage.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Primary abstract
- experimental_model
- Rose-bengal photoperoxidation followed by enzyme treatment
- exposure
- GSH/PHGPX after photooxidation.
- limitations
- Purified-enzyme preparation; distinguishes peroxide removal from vitamin E radical trapping.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Human-derived cell-free membranes
- plain_language
- GPX4 removed peroxide groups from membrane phospholipids using glutathione.
- primary_references
- [ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4
- tissue_or_cell_type
- Erythrocyte ghosts
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 550–562
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rose-bengal photoperoxidation followed by enzyme treatment · source_derived_draft · unverified_draft
### ver-gpx4-pl-hydroperoxide-reduction Purified PHGPX (GPX4) with glutathione reduced phospholipid hydroperoxides within photooxidized human erythrocyte ghost membranes to alcohol products without prior phospholipase cleavage. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: GPX4 removed peroxide groups from membrane phospholipids using glutathione. organism: Human-derived cell-free membranes tissue_or_cell_type: Erythrocyte ghosts experimental_model: Rose-bengal photoperoxidation followed by enzyme treatment limitations: Purified-enzyme preparation; distinguishes peroxide removal from vitamin E radical trapping. exposure: GSH/PHGPX after photooxidation. cross_nutrient: true evidence_location: Primary abstract [ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4
Complete structured claim and evidence
Where it participates (unsigned role)
GSH/PHGPX pretreatment completely suppressed the subsequent radical-peroxidation burst when photooxidized erythrocyte ghosts were challenged with ascorbate/iron or xanthine/xanthine-oxidase/iron.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Primary abstract
- experimental_model
- Sequential peroxide reduction and iron challenge
- exposure
- Photoperoxidation → GSH/PHGPX → iron-dependent challenge.
- limitations
- Ascorbate participates in this deliberately pro-oxidizing assay; this is not evidence that normal vitamin C intake damages membranes.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Human-derived cell-free membranes
- plain_language
- Removing membrane hydroperoxides prevented an iron-driven burst of further oxidation.
- primary_references
- [ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4
- tissue_or_cell_type
- Erythrocyte ghosts
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 578–590
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sequential peroxide reduction and iron challenge · source_derived_draft · unverified_draft
### ver-peroxide-removal-iron-burst GSH/PHGPX pretreatment completely suppressed the subsequent radical-peroxidation burst when photooxidized erythrocyte ghosts were challenged with ascorbate/iron or xanthine/xanthine-oxidase/iron. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing membrane hydroperoxides prevented an iron-driven burst of further oxidation. organism: Human-derived cell-free membranes tissue_or_cell_type: Erythrocyte ghosts experimental_model: Sequential peroxide reduction and iron challenge limitations: Ascorbate participates in this deliberately pro-oxidizing assay; this is not evidence that normal vitamin C intake damages membranes. exposure: Photoperoxidation → GSH/PHGPX → iron-dependent challenge. cross_nutrient: true evidence_location: Primary abstract [ver-thomas1990] Protective action of phospholipid hydroperoxide glutathione peroxidase against membrane-damaging lipid peroxidation. In situ reduction of phospholipid and cholesterol hydroperoxides. (1990). https://pubmed.ncbi.nlm.nih.gov/2294113/ DOI: 10.1016/s0021-9258(19)40252-4
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.