Component
Fibroblast GPX4 loss
Tamoxifen-inducible Gpx4 deletion in mouse embryonic fibroblasts; distinguish from selenium deprivation.
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.
Where it participates (unsigned role)
In Pfa1 mouse fibroblasts with inducible Gpx4 deletion, alpha-tocotrienol preserved viability at an EC50 of 0.12 µM compared with 2.0 µM for alpha-tocopherol over 72 hours.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Figure 3
- experimental_model
- Inducible Gpx4 deletion and resazurin viability assay
- exposure
- 1 µM 4-hydroxytamoxifen for 72 h; tocotrienol 0–10 µM and tocopherol 0–100 µM.
- limitations
- Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Mus musculus
- plain_language
- Alpha-tocotrienol was more potent than alpha-tocopherol in this GPX4-deletion cell-rescue assay.
- primary_references
- [ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1
- tissue_or_cell_type
- Pfa1 embryonic fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 774–786
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible Gpx4 deletion and resazurin viability assay · source_derived_draft · unverified_draft
### ver-alpha-t3-gpx4-rescue-potency In Pfa1 mouse fibroblasts with inducible Gpx4 deletion, alpha-tocotrienol preserved viability at an EC50 of 0.12 µM compared with 2.0 µM for alpha-tocopherol over 72 hours. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Alpha-tocotrienol was more potent than alpha-tocopherol in this GPX4-deletion cell-rescue assay. organism: Mus musculus tissue_or_cell_type: Pfa1 embryonic fibroblasts experimental_model: Inducible Gpx4 deletion and resazurin viability assay limitations: Potency in cell assays does not establish nutritional equivalence or human efficacy; the study also detected toxicity at higher concentrations, with tocotrienols toxic at lower concentrations than tocopherols. exposure: 1 µM 4-hydroxytamoxifen for 72 h; tocotrienol 0–10 µM and tocopherol 0–100 µM. cross_nutrient: true evidence_location: Figure 3 [ver-yang2026] Tocotrienols exhibit superior ferroptosis inhibition over tocopherols. (2026). https://pubmed.ncbi.nlm.nih.gov/41501350/ DOI: 10.1038/s41598-025-34673-1
Complete structured claim and evidenceIn mouse embryonic fibroblasts subjected to 48-hour inducible Gpx4 deletion, 200 µM alpha-tocopherol supplementation for the preceding 24 hours prevented the pronounced laser-wound repair defect.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Figure 4d; Methods
- experimental_model
- Tamoxifen-inducible Gpx4 deletion with re-expression controls
- exposure
- 1 µM tamoxifen for 48 h; 200 µM alpha-tocopherol for 24 h before repair assay.
- limitations
- Genetic GPX4 loss, not nutritional selenium deficiency; repair mechanism downstream of oxidation was not resolved.
- nutrient_topic
- Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
- organism
- Mus musculus
- plain_language
- Vitamin E loading rescued membrane resealing after GPX4 deletion in these fibroblasts.
- primary_references
- [ver-labazi2015] The antioxidant requirement for plasma membrane repair in skeletal muscle. (2015). https://pubmed.ncbi.nlm.nih.gov/25843658/ DOI: 10.1016/j.freeradbiomed.2015.03.016
- tissue_or_cell_type
- Embryonic fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 718–730
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tamoxifen-inducible Gpx4 deletion with re-expression controls · source_derived_draft · unverified_draft
### ver-gpx4-fibroblast-repair-rescue In mouse embryonic fibroblasts subjected to 48-hour inducible Gpx4 deletion, 200 µM alpha-tocopherol supplementation for the preceding 24 hours prevented the pronounced laser-wound repair defect. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E loading rescued membrane resealing after GPX4 deletion in these fibroblasts. organism: Mus musculus tissue_or_cell_type: Embryonic fibroblasts experimental_model: Tamoxifen-inducible Gpx4 deletion with re-expression controls limitations: Genetic GPX4 loss, not nutritional selenium deficiency; repair mechanism downstream of oxidation was not resolved. exposure: 1 µM tamoxifen for 48 h; 200 µM alpha-tocopherol for 24 h before repair assay. cross_nutrient: true evidence_location: Figure 4d; Methods [ver-labazi2015] The antioxidant requirement for plasma membrane repair in skeletal muscle. (2015). https://pubmed.ncbi.nlm.nih.gov/25843658/ DOI: 10.1016/j.freeradbiomed.2015.03.016
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.