Component
Mitochondrial membrane lipid peroxidation
Mitochondrial membrane lipid peroxidation. Species, exposure and limitations are retained in each linked claim.
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 acts on it
DHODH inactivation increased mitochondrial lipid peroxidation and ferroptosis in the reported GPX4-dependent experimental contexts.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/coq10-research/33981038.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1af5a97412b5ebf797083a069385c4ed98258e68845692732448bfe061a453b", "start_char": 0, "end_char": 1716, "text_sha256": "b1af5a97412b5ebf797083a069385c4ed98258e68845692732448bfe061a453b"}
- experimental_model
- Genetic and pharmacological cancer-cell studies
- exposure
- DHODH loss or brequinar, with GPX4 inhibition
- limitations
- Pharmacological attribution and relative DHODH contribution were directly challenged in 2023; preserve the dispute rather than generalizing to dietary CoQ effects.
- nutrient_topic
- Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
- organism
- Human cancer-cell and tumor models
- plain_language
- The effect depended on which other defense route remained available.
- primary_references
- [coq10-p33981038] DHODH-mediated ferroptosis defence is a targetable vulnerability in cancer. (2021). https://pubmed.ncbi.nlm.nih.gov/33981038/ DOI: 10.1038/s41586-021-03539-7
- tissue_or_cell_type
- Mitochondrial ferroptosis defense
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 827–838
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic and pharmacological cancer-cell studies · source_derived_draft · unverified_draft
### coq10-dhodh-loss DHODH inactivation increased mitochondrial lipid peroxidation and ferroptosis in the reported GPX4-dependent experimental contexts. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The effect depended on which other defense route remained available. organism: Human cancer-cell and tumor models tissue_or_cell_type: Mitochondrial ferroptosis defense experimental_model: Genetic and pharmacological cancer-cell studies limitations: Pharmacological attribution and relative DHODH contribution were directly challenged in 2023; preserve the dispute rather than generalizing to dietary CoQ effects. exposure: DHODH loss or brequinar, with GPX4 inhibition evidence_span: {"source_cache": "artifacts/coq10-research/33981038.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1af5a97412b5ebf797083a069385c4ed98258e68845692732448bfe061a453b", "start_char": 0, "end_char": 1716, "text_sha256": "b1af5a97412b5ebf797083a069385c4ed98258e68845692732448bfe061a453b"} [coq10-p33981038] DHODH-mediated ferroptosis defence is a targetable vulnerability in cancer. (2021). https://pubmed.ncbi.nlm.nih.gov/33981038/ DOI: 10.1038/s41586-021-03539-7
Complete structured claim and evidenceGPD2 deletion sensitized cancer cells to GPX4-inhibition-induced mitochondrial lipid peroxidation and ferroptosis.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/coq10-research/35749365.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d8219ff3cd63697715c88c25a9e558315bcd95c25bbc38f76987544bfee7581", "start_char": 0, "end_char": 1142, "text_sha256": "8d8219ff3cd63697715c88c25a9e558315bcd95c25bbc38f76987544bfee7581"}
- experimental_model
- Metabolomics, genetic deletion and tumor experiments
- exposure
- G3P supply and GPD2/GPX4 loss
- limitations
- Preclinical mechanism; no evidence that glycerol or CoQ supplements treat cancer.
- nutrient_topic
- Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
- organism
- Cancer-cell and tumor models
- plain_language
- Dependence on one pathway changed when the parallel defense was blocked.
- primary_references
- [coq10-p35749365] A ferroptosis defense mechanism mediated by glycerol-3-phosphate dehydrogenase 2 in mitochondria. (2022). https://pubmed.ncbi.nlm.nih.gov/35749365/ DOI: 10.1073/pnas.2121987119
- tissue_or_cell_type
- Mitochondrial glycerol-phosphate oxidation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 866–877
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolomics, genetic deletion and tumor experiments · source_derived_draft · unverified_draft
### coq10-gpd2-loss GPD2 deletion sensitized cancer cells to GPX4-inhibition-induced mitochondrial lipid peroxidation and ferroptosis. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Dependence on one pathway changed when the parallel defense was blocked. organism: Cancer-cell and tumor models tissue_or_cell_type: Mitochondrial glycerol-phosphate oxidation experimental_model: Metabolomics, genetic deletion and tumor experiments limitations: Preclinical mechanism; no evidence that glycerol or CoQ supplements treat cancer. exposure: G3P supply and GPD2/GPX4 loss evidence_span: {"source_cache": "artifacts/coq10-research/35749365.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8d8219ff3cd63697715c88c25a9e558315bcd95c25bbc38f76987544bfee7581", "start_char": 0, "end_char": 1142, "text_sha256": "8d8219ff3cd63697715c88c25a9e558315bcd95c25bbc38f76987544bfee7581"} [coq10-p35749365] A ferroptosis defense mechanism mediated by glycerol-3-phosphate dehydrogenase 2 in mitochondria. (2022). https://pubmed.ncbi.nlm.nih.gov/35749365/ DOI: 10.1073/pnas.2121987119
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.