Ferroptosis

cell_type

Studied cultures/tissue

experimental_model

Cultured cells and embryonic avian tissue

limitations

Does not validate all combustion analogies, numerical thresholds or dietary selenium effects.

organism

Mammalian cell cultures and embryonic avian tissue

Selenium: literature corrections and mechanism additions · lines 1480–1490

Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Cultured cells and embryonic avian tissue · secondary_verified · secondary_verified

## ferroptosis-waves Researchers have experimentally studied spreading ferroptotic death. Ferroptotic death propagated in the studied cell cultures and embryonic avian tissue. Organism: Mammalian cell cultures and embryonic avian tissue Cell type: Studied cultures/tissue Experimental model: Cultured cells and embryonic avian tissue Limitations: Does not validate all combustion analogies, numerical thresholds or dietary selenium effects. Primary reference: [Emergence of large-scale cell death through ferroptotic trigger waves](https://www.nature.com/articles/s41586-024-07623-6)

evidence_span

{"source_cache": "artifacts/dim-research/40100489.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0", "start_char": 0, "end_char": 1722, "text_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0"}

experimental_model

Cell perturbation and xenograft experiments

exposure

DIM; NRF2 overexpression and pharmacological rescue controls

limitations

Preclinical cancer context. Reduced defense here differs from Nrf2 induction in fibroblasts; neither result proves a universal antioxidant or prooxidant effect in people.

nutrient_topic

Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM

organism

Human non-small-cell lung-cancer cells and mouse xenografts

plain_language

Perturbation controls helped connect the response to specific defenses.

primary_references

[dim-p40100489] 3,3'-diindolylmethane induces ferroptosis and inhibits proliferation in non-small-cell lung cancer through the AHR/NRF2/GPX4 axis. (2025). https://pubmed.ncbi.nlm.nih.gov/40100489/ DOI: 10.1007/s12672-025-02096-z

tissue_or_cell_type

Ferroptosis and AHR/NRF2/GPX4

Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1351–1362

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell perturbation and xenograft experiments · source_derived_draft · unverified_draft

### dim-nsclc-ferroptosis DIM induced ferroptosis that could be reversed by ferrostatin-1, NAC or the tested AHR antagonist; NRF2 overexpression also reversed it. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Perturbation controls helped connect the response to specific defenses. organism: Human non-small-cell lung-cancer cells and mouse xenografts tissue_or_cell_type: Ferroptosis and AHR/NRF2/GPX4 experimental_model: Cell perturbation and xenograft experiments limitations: Preclinical cancer context. Reduced defense here differs from Nrf2 induction in fibroblasts; neither result proves a universal antioxidant or prooxidant effect in people. exposure: DIM; NRF2 overexpression and pharmacological rescue controls evidence_span: {"source_cache": "artifacts/dim-research/40100489.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0", "start_char": 0, "end_char": 1722, "text_sha256": "99bc986298e026c4bd40745004936bab65af37a931084f75634b89505f5b95d0"} [dim-p40100489] 3,3'-diindolylmethane induces ferroptosis and inhibits proliferation in non-small-cell lung cancer through the AHR/NRF2/GPX4 axis. (2025). https://pubmed.ncbi.nlm.nih.gov/40100489/ DOI: 10.1007/s12672-025-02096-z

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 15449, "end_char": 16082, "text_sha256": "689a74e99dd668d48baef5232109dbf2898ba3adca2999a83a7bb24b321420c0"}

experimental_model

Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice

exposure

MK-4/K1, NAD(P)H, FSP1 loss and inhibitors

limitations

Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human recombinant FSP1, mammalian cells and mice

plain_language

Providing the quinone did not fully substitute for an appropriately located working reductase.

primary_references

[k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3

tissue_or_cell_type

Lipid peroxidation and vitamin K reduction

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 799–810

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

### k2-fsp1-loss FSP1 knockout diminished MK-4 and K1 protection; wild-type FSP1 rescued protection while its myristoylation-defective G2A mutant did not. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the quinone did not fully substitute for an appropriately located working reductase. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 15449, "end_char": 16082, "text_sha256": "689a74e99dd668d48baef5232109dbf2898ba3adca2999a83a7bb24b321420c0"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3

access_level

abstract_only

compartment

Mitochondrial GSH versus intracellular GSH distinguished by authors

dose

Unknown: full methods unavailable

duration

Unknown: full methods unavailable

endpoint

ferroptosis

evidence_location

Primary indexed abstract; experiment-specific methods unavailable

experimental_model

Protein interaction/stability, knockdown and compound experiments reported in abstract

exposure

human-crc-dlat-knockdown

limitations

ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not identify each inducing exposure or rescue control.

nutrient_topic

Topical cross-reference only; no inheritance of another actor's effects. · GSH

organism

Human colorectal cancer models; individual experiments require full-text confirmation

plain_language

DLAT knockdown reportedly increased ferroptosis susceptibility.

primary_locator

[{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]

primary_references

https://doi.org/10.1016/j.freeradbiomed.2026.04.133

tissue_or_cell_type

Colorectal cancer models; claim-specific cell line not established from abstract

DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 801–815

AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

DLAT knockdown reportedly increased ferroptosis susceptibility. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: ferroptosis exposure: human-crc-dlat-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not identify each inducing exposure or rescue control. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: DLAT knockdown reportedly increased ferroptosis susceptibility.

access_level

abstract_only

compartment

Mitochondrial GSH versus intracellular GSH distinguished by authors

dose

Unknown: full methods unavailable

duration

Unknown: full methods unavailable

endpoint

ferroptosis

evidence_location

Primary indexed abstract; experiment-specific methods unavailable

experimental_model

Protein interaction/stability, knockdown and compound experiments reported in abstract

exposure

human-crc-slc25a39-knockdown

limitations

ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not identify each inducing exposure or rescue control.

nutrient_topic

Topical cross-reference only; no inheritance of another actor's effects. · GSH

organism

Human colorectal cancer models; individual experiments require full-text confirmation

plain_language

SLC25A39 knockdown reportedly increased ferroptosis susceptibility.

primary_locator

[{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]

primary_references

https://doi.org/10.1016/j.freeradbiomed.2026.04.133

tissue_or_cell_type

Colorectal cancer models; claim-specific cell line not established from abstract

DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 852–866

AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

SLC25A39 knockdown reportedly increased ferroptosis susceptibility. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: ferroptosis exposure: human-crc-slc25a39-knockdown limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not identify each inducing exposure or rescue control. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: SLC25A39 knockdown reportedly increased ferroptosis susceptibility.

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

evidence_span

{"source_cache": "artifacts/iron-research/24439385.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8d588af38ec5438fbec80971ead0764466237b3382492051aa3b3c297841703", "start_char": 0, "end_char": 957, "text_sha256": "f8d588af38ec5438fbec80971ead0764466237b3382492051aa3b3c297841703"}

experimental_model

Metabolomics, chemoproteomics, perturbation and cancer-cell sensitivity profiling

exposure

Two classes of ferroptosis-inducing compounds

limitations

Preclinical drug-response mechanism; selenium or vitamin E supplementation is not established as a universal treatment.

nutrient_topic

Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron

organism

Human cancer-cell lines and mouse xenografts

plain_language

The protective enzyme specifically controlled this iron-linked death pathway in the tested cells.

primary_references

[iron-p24439385] Regulation of ferroptotic cancer cell death by GPX4. (2014). https://pubmed.ncbi.nlm.nih.gov/24439385/ DOI: 10.1016/j.cell.2013.12.010

tissue_or_cell_type

Glutathione/GPX4 antioxidant system

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 1265–1276

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolomics, chemoproteomics, perturbation and cancer-cell sensitivity profiling · source_derived_draft · unverified_draft

### iron-gpx4-ferroptosis GPX4 overexpression or knockdown altered lethality of all 12 tested ferroptosis inducers, but not 11 compounds with other lethal mechanisms. Condition category: normal nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protective enzyme specifically controlled this iron-linked death pathway in the tested cells. organism: Human cancer-cell lines and mouse xenografts tissue_or_cell_type: Glutathione/GPX4 antioxidant system experimental_model: Metabolomics, chemoproteomics, perturbation and cancer-cell sensitivity profiling limitations: Preclinical drug-response mechanism; selenium or vitamin E supplementation is not established as a universal treatment. exposure: Two classes of ferroptosis-inducing compounds evidence_span: {"source_cache": "artifacts/iron-research/24439385.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8d588af38ec5438fbec80971ead0764466237b3382492051aa3b3c297841703", "start_char": 0, "end_char": 957, "text_sha256": "f8d588af38ec5438fbec80971ead0764466237b3382492051aa3b3c297841703"} [iron-p24439385] Regulation of ferroptotic cancer cell death by GPX4. (2014). https://pubmed.ncbi.nlm.nih.gov/24439385/ DOI: 10.1016/j.cell.2013.12.010

evidence_span

{"source_cache": "artifacts/iron-research/22632970.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0", "start_char": 0, "end_char": 1089, "text_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0"}

experimental_model

Chemical and genetic characterization of nonapoptotic cell death

exposure

Erastin and ferrostatin-1 experiments

limitations

Experimental ferroptosis; dietary iron is not equated with a cancer-cell-death drug exposure.

nutrient_topic

Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron

organism

Cancer-cell systems and rat brain slices

plain_language

Usable iron is essential, but under particular conditions it also enables oxidative cell death.

primary_references

[iron-p22632970] Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012). https://pubmed.ncbi.nlm.nih.gov/22632970/ DOI: 10.1016/j.cell.2012.03.042

tissue_or_cell_type

Cellular iron, cystine transport and oxidative injury

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 1226–1237

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemical and genetic characterization of nonapoptotic cell death · source_derived_draft · unverified_draft

### iron-iron-ferroptosis Erastin-induced ferroptosis depended on intracellular iron and was distinct from apoptosis, necrosis and autophagy in the study. Condition category: normal nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Usable iron is essential, but under particular conditions it also enables oxidative cell death. organism: Cancer-cell systems and rat brain slices tissue_or_cell_type: Cellular iron, cystine transport and oxidative injury experimental_model: Chemical and genetic characterization of nonapoptotic cell death limitations: Experimental ferroptosis; dietary iron is not equated with a cancer-cell-death drug exposure. exposure: Erastin and ferrostatin-1 experiments evidence_span: {"source_cache": "artifacts/iron-research/22632970.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0", "start_char": 0, "end_char": 1089, "text_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0"} [iron-p22632970] Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012). https://pubmed.ncbi.nlm.nih.gov/22632970/ DOI: 10.1016/j.cell.2012.03.042

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/)

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/coq10-research/36658222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8cd5c486ecb31ad03ea06a817eb5bc56e60abdfa8ae8d50a46502974be2898ce", "start_char": 0, "end_char": 1410, "text_sha256": "8cd5c486ecb31ad03ea06a817eb5bc56e60abdfa8ae8d50a46502974be2898ce"}

experimental_model

Protein processing, localization, transport and cell-growth experiments

exposure

PARL processing and compartment-specific STARD7 expression

limitations

Intracellular distribution mechanism; increasing oral dose does not prove delivery to a particular organelle.

nutrient_topic

Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system

organism

Mammalian cell models

plain_language

Total supply and the location of that supply are different questions.

primary_references

[coq10-p36658222] Mitochondria regulate intracellular coenzyme Q transport and ferroptotic resistance via STARD7. (2023). https://pubmed.ncbi.nlm.nih.gov/36658222/ DOI: 10.1038/s41556-022-01071-y

tissue_or_cell_type

Mitochondria and plasma membrane

trigger_kind

machinery_impairment Imported condition classification; unverified.

Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 515–526

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein processing, localization, transport and cell-growth experiments · source_derived_draft · unverified_draft

### coq10-stard7-tradeoff Cytosolic STARD7 overexpression increased ferroptosis resistance while reducing mitochondrial CoQ abundance and respiratory growth. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Total supply and the location of that supply are different questions. organism: Mammalian cell models tissue_or_cell_type: Mitochondria and plasma membrane experimental_model: Protein processing, localization, transport and cell-growth experiments limitations: Intracellular distribution mechanism; increasing oral dose does not prove delivery to a particular organelle. exposure: PARL processing and compartment-specific STARD7 expression evidence_span: {"source_cache": "artifacts/coq10-research/36658222.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8cd5c486ecb31ad03ea06a817eb5bc56e60abdfa8ae8d50a46502974be2898ce", "start_char": 0, "end_char": 1410, "text_sha256": "8cd5c486ecb31ad03ea06a817eb5bc56e60abdfa8ae8d50a46502974be2898ce"} [coq10-p36658222] Mitochondria regulate intracellular coenzyme Q transport and ferroptotic resistance via STARD7. (2023). https://pubmed.ncbi.nlm.nih.gov/36658222/ DOI: 10.1038/s41556-022-01071-y

evidence_span

{"source_cache": "artifacts/k2-research/35922516.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a", "start_char": 0, "end_char": 1403, "text_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a"}

experimental_model

Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice

exposure

MK-4/K1, NAD(P)H, FSP1 loss and inhibitors

limitations

Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human recombinant FSP1, mammalian cells and mice

plain_language

The antioxidant action belongs to the reduced chemical form, not just the name on a supplement bottle.

primary_references

[k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3

tissue_or_cell_type

Lipid peroxidation and vitamin K reduction

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 786–797

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

### k2-kh2-lipid-protection Reduced vitamin K forms trapped radicals and inhibited phospholipid peroxidation in the tested systems. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The antioxidant action belongs to the reduced chemical form, not just the name on a supplement bottle. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a", "start_char": 0, "end_char": 1403, "text_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3

experimental_model

Cell-free assay and cell lines.

limitations

ATRA direct activity was not reproduced in the 2024 assays; no clinical or nutrient-replacement inference.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Homo sapiens

plain_language

Different vitamin A forms were protective in the tested systems.

primary_references

[va-jakaria2023] Vitamin A metabolites inhibit ferroptosis (2023). https://pubmed.ncbi.nlm.nih.gov/37236031/ DOI: 10.1016/j.biopha.2023.114930

tissue_or_cell_type

Cell-free chemistry and cell cultures

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1789–1798

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free assay and cell lines. · source_derived_draft · unverified_draft

### va-atra-direct-radical-trapping2023 The 2023 study reported direct radical-trapping activity for retinol, retinal and ATRA alongside ferroptosis protection. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different vitamin A forms were protective in the tested systems. organism: Homo sapiens tissue_or_cell_type: Cell-free chemistry and cell cultures experimental_model: Cell-free assay and cell lines. limitations: ATRA direct activity was not reproduced in the 2024 assays; no clinical or nutrient-replacement inference. [va-jakaria2023] Vitamin A metabolites inhibit ferroptosis (2023). https://pubmed.ncbi.nlm.nih.gov/37236031/ DOI: 10.1016/j.biopha.2023.114930

experimental_model

Human stem-cell neurons/organoids.

limitations

No dietary recommendation or evidence that vitamin A replaces vitamin E in humans.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Homo sapiens

plain_language

Suppressing ferroptosis supported this developmental model.

primary_references

[va-berndt2024] Suppression of ferroptosis by vitamin A or radical-trapping antioxidants is essential for neuronal development (2024). https://pubmed.ncbi.nlm.nih.gov/39218970/ DOI: 10.1038/s41467-024-51996-1

tissue_or_cell_type

Human neural cultures

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1823–1832

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human stem-cell neurons/organoids. · source_derived_draft · unverified_draft

### va-atra-neuronal-ferroptosis-rescue ATRA or ferrostatin-1 rescued differentiation under antioxidant-deprived neuronal culture conditions. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suppressing ferroptosis supported this developmental model. organism: Homo sapiens tissue_or_cell_type: Human neural cultures experimental_model: Human stem-cell neurons/organoids. limitations: No dietary recommendation or evidence that vitamin A replaces vitamin E in humans. [va-berndt2024] Suppression of ferroptosis by vitamin A or radical-trapping antioxidants is essential for neuronal development (2024). https://pubmed.ncbi.nlm.nih.gov/39218970/ DOI: 10.1038/s41467-024-51996-1

evidence_span

{"source_cache": "artifacts/iron-research/22632970.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0", "start_char": 0, "end_char": 1089, "text_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0"}

experimental_model

Chemical and genetic characterization of nonapoptotic cell death

exposure

Erastin and ferrostatin-1 experiments

limitations

Experimental ferroptosis; dietary iron is not equated with a cancer-cell-death drug exposure.

nutrient_topic

Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron

organism

Cancer-cell systems and rat brain slices

plain_language

The death pathway connected iron with the supply of material needed for glutathione.

primary_references

[iron-p22632970] Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012). https://pubmed.ncbi.nlm.nih.gov/22632970/ DOI: 10.1016/j.cell.2012.03.042

tissue_or_cell_type

Cellular iron, cystine transport and oxidative injury

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 1239–1250

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemical and genetic characterization of nonapoptotic cell death · source_derived_draft · unverified_draft

### iron-cystine-ferroptosis Erastin inhibited cystine uptake through system xc-minus, weakening antioxidant defenses before iron-dependent oxidative death. Condition category: normal nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The death pathway connected iron with the supply of material needed for glutathione. organism: Cancer-cell systems and rat brain slices tissue_or_cell_type: Cellular iron, cystine transport and oxidative injury experimental_model: Chemical and genetic characterization of nonapoptotic cell death limitations: Experimental ferroptosis; dietary iron is not equated with a cancer-cell-death drug exposure. exposure: Erastin and ferrostatin-1 experiments evidence_span: {"source_cache": "artifacts/iron-research/22632970.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0", "start_char": 0, "end_char": 1089, "text_sha256": "c0137d17ae5942c8904ece05ab6513f4fad588149ed0d7167e49f01a63b36cb0"} [iron-p22632970] Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012). https://pubmed.ncbi.nlm.nih.gov/22632970/ DOI: 10.1016/j.cell.2012.03.042