Component

Reduced CoQ10

Reduced coenzyme Q, a lipid-radical-trapping antioxidant regenerated by FSP1.

16 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Ubiquinol did not reduce pain severity or interference versus placebo in confirmed simvastatin myalgia.

    Reduced CoQ10 → Statin-associated muscle pain source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/25545331.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837", "start_char": 0, "end_char": 1976, "text_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837"}
    experimental_model
    Randomized double-blind trial after blinded symptom confirmation
    exposure
    600 mg/day ubiquinol with simvastatin 20 mg/day for eight weeks
    limitations
    Small confirmed-myalgia sample; null outcome is not proof that every other regimen is ineffective.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    41 subjects with confirmed simvastatin myalgia
    plain_language
    A more strictly selected trial did not reproduce the pain benefit.
    primary_references
    [coq10-p25545331] A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. (2015). https://pubmed.ncbi.nlm.nih.gov/25545331/ DOI: 10.1016/j.atherosclerosis.2014.12.016
    tissue_or_cell_type
    Pain, muscle performance and serum CoQ

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1165–1176

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind trial after blinded symptom confirmation · source_derived_draft · unverified_draft

    ### coq10-statin-pain-null Ubiquinol did not reduce pain severity or interference versus placebo in confirmed simvastatin myalgia. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A more strictly selected trial did not reproduce the pain benefit. organism: 41 subjects with confirmed simvastatin myalgia tissue_or_cell_type: Pain, muscle performance and serum CoQ experimental_model: Randomized double-blind trial after blinded symptom confirmation limitations: Small confirmed-myalgia sample; null outcome is not proof that every other regimen is ineffective. exposure: 600 mg/day ubiquinol with simvastatin 20 mg/day for eight weeks evidence_span: {"source_cache": "artifacts/coq10-research/25545331.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837", "start_char": 0, "end_char": 1976, "text_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837"} [coq10-p25545331] A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. (2015). https://pubmed.ncbi.nlm.nih.gov/25545331/ DOI: 10.1016/j.atherosclerosis.2014.12.016
    Complete structured claim and evidence

  2. Serum CoQ increased from 1.3 to 5.2 micrograms/mL with ubiquinol, without improved muscle strength or aerobic performance.

    Reduced CoQ10 → Plasma coenzyme Q10 concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/25545331.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837", "start_char": 0, "end_char": 1976, "text_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837"}
    experimental_model
    Randomized double-blind trial after blinded symptom confirmation
    exposure
    600 mg/day ubiquinol with simvastatin 20 mg/day for eight weeks
    limitations
    Small confirmed-myalgia sample; null outcome is not proof that every other regimen is ineffective.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    41 subjects with confirmed simvastatin myalgia
    plain_language
    A larger blood pool did not guarantee a functional response.
    primary_references
    [coq10-p25545331] A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. (2015). https://pubmed.ncbi.nlm.nih.gov/25545331/ DOI: 10.1016/j.atherosclerosis.2014.12.016
    tissue_or_cell_type
    Pain, muscle performance and serum CoQ

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1178–1189

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind trial after blinded symptom confirmation · source_derived_draft · unverified_draft

    ### coq10-statin-plasma-not-function Serum CoQ increased from 1.3 to 5.2 micrograms/mL with ubiquinol, without improved muscle strength or aerobic performance. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A larger blood pool did not guarantee a functional response. organism: 41 subjects with confirmed simvastatin myalgia tissue_or_cell_type: Pain, muscle performance and serum CoQ experimental_model: Randomized double-blind trial after blinded symptom confirmation limitations: Small confirmed-myalgia sample; null outcome is not proof that every other regimen is ineffective. exposure: 600 mg/day ubiquinol with simvastatin 20 mg/day for eight weeks evidence_span: {"source_cache": "artifacts/coq10-research/25545331.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837", "start_char": 0, "end_char": 1976, "text_sha256": "2aad217d0053cae8ea41f5be8ee7e0be0fa83f83d779f34e30fabe2a0b29c837"} [coq10-p25545331] A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. (2015). https://pubmed.ncbi.nlm.nih.gov/25545331/ DOI: 10.1016/j.atherosclerosis.2014.12.016
    Complete structured claim and evidence

  3. Reduced CoQ can trap lipid radicals and contribute to resistance against lipid-peroxidation-driven ferroptosis.

    Reduced CoQ10 → Lipid peroxidation source_derived_draftsource_reported: Cell/biochemical and animal cancer models; supplied-source synthesis with a narrow FSP1 primary-study spot check.
    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 123–123

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    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 evidence

  4. Ubiquinol-10 reduced alpha-tocopheroxyl to alpha-tocopherol in stopped-flow solution experiments, with second-order rate constants of 3.74 × 10^5 M^-1 s^-1 in benzene and 2.15 × 10^5 M^-1 s^-1 in ethanol at 25 °C.

    Reduced CoQ10 → Alpha-tocopherol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Primary abstract
    experimental_model
    Stopped-flow spectrophotometry
    exposure
    25 °C; reduced CoQ10.
    limitations
    No direct tissue flux or oral CoQ10 effect was measured.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Cell-free
    plain_language
    Reduced CoQ10 recycled the vitamin E radical in these chemical assays.
    primary_references
    [ver-mukai1990] Stopped-flow kinetic study of the regeneration reaction of tocopheroxyl radical by reduced ubiquinone-10 in solution. (1990). https://pubmed.ncbi.nlm.nih.gov/2383582/ DOI: 10.1016/0304-4165(90)90176-w
    tissue_or_cell_type
    Benzene or ethanol solution

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 508–520

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stopped-flow spectrophotometry · source_derived_draft · unverified_draft

    ### ver-ubiquinol-regeneration Ubiquinol-10 reduced alpha-tocopheroxyl to alpha-tocopherol in stopped-flow solution experiments, with second-order rate constants of 3.74 × 10^5 M^-1 s^-1 in benzene and 2.15 × 10^5 M^-1 s^-1 in ethanol at 25 °C. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced CoQ10 recycled the vitamin E radical in these chemical assays. organism: Cell-free tissue_or_cell_type: Benzene or ethanol solution experimental_model: Stopped-flow spectrophotometry limitations: No direct tissue flux or oral CoQ10 effect was measured. exposure: 25 °C; reduced CoQ10. cross_nutrient: true evidence_location: Primary abstract [ver-mukai1990] Stopped-flow kinetic study of the regeneration reaction of tocopheroxyl radical by reduced ubiquinone-10 in solution. (1990). https://pubmed.ncbi.nlm.nih.gov/2383582/ DOI: 10.1016/0304-4165(90)90176-w
    Complete structured claim and evidence

What acts on it

  1. Complex III oxidizes reduced CoQ as part of respiratory electron flow examined in this study.

    Mitochondrial respiratory complex III → Reduced CoQ10 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/38243131.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "de9afaeca8a144d79c9f0d0d3b3faafaa4560af2292b8624d1a04ed45ee5d136", "start_char": 0, "end_char": 1039, "text_sha256": "de9afaeca8a144d79c9f0d0d3b3faafaa4560af2292b8624d1a04ed45ee5d136"}
    experimental_model
    Muscle-specific knockout and protein-complex analyses
    exposure
    Etfdh deletion and metabolon characterization
    limitations
    Skeletal-muscle context; does not establish identical complex organization in every human tissue.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Mouse skeletal muscle and biochemical systems
    plain_language
    The carrier must release its electrons before it can accept more.
    primary_references
    [coq10-p38243131] An ETFDH-driven metabolon supports OXPHOS efficiency in skeletal muscle by regulating coenzyme Q homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38243131/ DOI: 10.1038/s42255-023-00956-y
    tissue_or_cell_type
    ETFDH-complex III-COQ2 assembly

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 424–435

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Muscle-specific knockout and protein-complex analyses · source_derived_draft · unverified_draft

    ### coq10-complex-iii-q Complex III oxidizes reduced CoQ as part of respiratory electron flow examined in this study. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carrier must release its electrons before it can accept more. organism: Mouse skeletal muscle and biochemical systems tissue_or_cell_type: ETFDH-complex III-COQ2 assembly experimental_model: Muscle-specific knockout and protein-complex analyses limitations: Skeletal-muscle context; does not establish identical complex organization in every human tissue. exposure: Etfdh deletion and metabolon characterization evidence_span: {"source_cache": "artifacts/coq10-research/38243131.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "de9afaeca8a144d79c9f0d0d3b3faafaa4560af2292b8624d1a04ed45ee5d136", "start_char": 0, "end_char": 1039, "text_sha256": "de9afaeca8a144d79c9f0d0d3b3faafaa4560af2292b8624d1a04ed45ee5d136"} [coq10-p38243131] An ETFDH-driven metabolon supports OXPHOS efficiency in skeletal muscle by regulating coenzyme Q homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38243131/ DOI: 10.1038/s42255-023-00956-y
    Complete structured claim and evidence

  2. CoQ appeared in blood predominantly as ubiquinol regardless of which of the tested redox forms was consumed.

    Ubiquinone-10 → Reduced CoQ10 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/32188111.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6", "start_char": 0, "end_char": 1662, "text_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6"}
    experimental_model
    Randomized three-period crossover pharmacokinetic study
    exposure
    Single equivalent 100-mg doses in three formulations
    limitations
    Small single-dose formulation comparison; plasma exposure is not tissue delivery or clinical efficacy. Product-specific findings cannot rank every ubiquinone or ubiquinol product.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    21 healthy adults aged 65-74
    plain_language
    The form swallowed and the form circulating are not necessarily the same.
    primary_references
    [coq10-p32188111] Comparative Bioavailability of Different Coenzyme Q10 Formulations in Healthy Elderly Individuals. (2020). https://pubmed.ncbi.nlm.nih.gov/32188111/ DOI: 10.3390/nu12030784
    tissue_or_cell_type
    Plasma total CoQ and redox state over 48 hours

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 892–903

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-period crossover pharmacokinetic study · source_derived_draft · unverified_draft

    ### coq10-oral-redox CoQ appeared in blood predominantly as ubiquinol regardless of which of the tested redox forms was consumed. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The form swallowed and the form circulating are not necessarily the same. organism: 21 healthy adults aged 65-74 tissue_or_cell_type: Plasma total CoQ and redox state over 48 hours experimental_model: Randomized three-period crossover pharmacokinetic study limitations: Small single-dose formulation comparison; plasma exposure is not tissue delivery or clinical efficacy. Product-specific findings cannot rank every ubiquinone or ubiquinol product. exposure: Single equivalent 100-mg doses in three formulations evidence_span: {"source_cache": "artifacts/coq10-research/32188111.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6", "start_char": 0, "end_char": 1662, "text_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6"} [coq10-p32188111] Comparative Bioavailability of Different Coenzyme Q10 Formulations in Healthy Elderly Individuals. (2020). https://pubmed.ncbi.nlm.nih.gov/32188111/ DOI: 10.3390/nu12030784
    Complete structured claim and evidence

  3. FSP1 can regenerate reduced CoQ as a parallel, glutathione-independent defense alongside GPX4.

    FSP1 → Reduced CoQ10 source_derived_draftsource_reported: Cell/biochemical and animal cancer models; supplied-source synthesis with a narrow FSP1 primary-study spot check.
    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 123–123

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    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 evidence

  4. FSP1 reduces CoQ and supplies a lipid-radical defense operating in parallel with GPX4.

    FSP1 → Reduced CoQ10 source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    Experimental cultured cells
    experimental_model
    Cell genetics and biochemical experiments
    limitations
    Capacity and dependence vary by cell; not a universal dietary threshold.
    organism
    Human cell models

    Selenium: literature corrections and mechanism additions · lines 1492–1502

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Cell genetics and biochemical experiments · secondary_verified · secondary_verified

    ## fsp1-parallel Another defense changes how vulnerable cells are to GPX4 loss. FSP1 reduces CoQ and supplies a lipid-radical defense operating in parallel with GPX4. Organism: Human cell models Cell type: Experimental cultured cells Experimental model: Cell genetics and biochemical experiments Limitations: Capacity and dependence vary by cell; not a universal dietary threshold. Primary reference: [The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis](https://www.nature.com/articles/s41586-019-1705-2)
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Complex I transferred electrons from NADH to ubiquinone-10 in reconstituted membranes.

    Mitochondrial respiratory complex I → Ubiquinone-10 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/29133414.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d", "start_char": 0, "end_char": 1770, "text_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d"}
    experimental_model
    Proteoliposome enzyme kinetics
    exposure
    Ubiquinones with one to ten isoprenoid units
    limitations
    Purified enzyme system; short-chain analogues do not have identical binding and release kinetics to Q10.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Mammalian complex I preparation
    plain_language
    CoQ receives electrons from the first respiratory complex.
    primary_references
    [coq10-p29133414] Correlating kinetic and structural data on ubiquinone binding and reduction by respiratory complex I. (2017). https://pubmed.ncbi.nlm.nih.gov/29133414/ DOI: 10.1073/pnas.1714074114
    tissue_or_cell_type
    Membrane quinone channel

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 385–396

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proteoliposome enzyme kinetics · source_derived_draft · unverified_draft

    ### coq10-complex-i-q Complex I transferred electrons from NADH to ubiquinone-10 in reconstituted membranes. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CoQ receives electrons from the first respiratory complex. organism: Mammalian complex I preparation tissue_or_cell_type: Membrane quinone channel experimental_model: Proteoliposome enzyme kinetics limitations: Purified enzyme system; short-chain analogues do not have identical binding and release kinetics to Q10. exposure: Ubiquinones with one to ten isoprenoid units evidence_span: {"source_cache": "artifacts/coq10-research/29133414.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d", "start_char": 0, "end_char": 1770, "text_sha256": "139122e8a567596e6ec1b4bd361567d0e5cd4e3329fec72d47b949a86d29610d"} [coq10-p29133414] Correlating kinetic and structural data on ubiquinone binding and reduction by respiratory complex I. (2017). https://pubmed.ncbi.nlm.nih.gov/29133414/ DOI: 10.1073/pnas.1714074114
    Complete structured claim and evidence

  2. The study reported DHODH-dependent ubiquinol generation as a mitochondrial ferroptosis-defense pathway.

    Human dihydroorotate dehydrogenase / DHODH → Ubiquinone source_derived_draftungraded
    Experimental context and source evidence
    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
    A pyrimidine-synthesis enzyme can also contribute reduced CoQ in the studied system.
    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

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 814–825

    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-quinol The study reported DHODH-dependent ubiquinol generation as a mitochondrial ferroptosis-defense pathway. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pyrimidine-synthesis enzyme can also contribute reduced CoQ in the studied system. 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 evidence

  3. The tested water-soluble formulation had 2.4-fold higher baseline-corrected exposure than standard ubiquinone capsules; the ubiquinol-capsule comparison was not statistically significant.

    Coenzyme Q10 / CoQ10 redox system → Plasma coenzyme Q10 concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/32188111.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6", "start_char": 0, "end_char": 1662, "text_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6"}
    experimental_model
    Randomized three-period crossover pharmacokinetic study
    exposure
    Single equivalent 100-mg doses in three formulations
    limitations
    Small single-dose formulation comparison; plasma exposure is not tissue delivery or clinical efficacy. Product-specific findings cannot rank every ubiquinone or ubiquinol product.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    21 healthy adults aged 65-74
    plain_language
    The formulation mattered; the redox-form label alone did not establish superiority.
    primary_references
    [coq10-p32188111] Comparative Bioavailability of Different Coenzyme Q10 Formulations in Healthy Elderly Individuals. (2020). https://pubmed.ncbi.nlm.nih.gov/32188111/ DOI: 10.3390/nu12030784
    tissue_or_cell_type
    Plasma total CoQ and redox state over 48 hours

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 879–890

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-period crossover pharmacokinetic study · source_derived_draft · unverified_draft

    ### coq10-formulation-exposure The tested water-soluble formulation had 2.4-fold higher baseline-corrected exposure than standard ubiquinone capsules; the ubiquinol-capsule comparison was not statistically significant. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The formulation mattered; the redox-form label alone did not establish superiority. organism: 21 healthy adults aged 65-74 tissue_or_cell_type: Plasma total CoQ and redox state over 48 hours experimental_model: Randomized three-period crossover pharmacokinetic study limitations: Small single-dose formulation comparison; plasma exposure is not tissue delivery or clinical efficacy. Product-specific findings cannot rank every ubiquinone or ubiquinol product. exposure: Single equivalent 100-mg doses in three formulations evidence_span: {"source_cache": "artifacts/coq10-research/32188111.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6", "start_char": 0, "end_char": 1662, "text_sha256": "651570863e9a81a09c85040d74da26366d5b9f94145d97cac6aad48378597ce6"} [coq10-p32188111] Comparative Bioavailability of Different Coenzyme Q10 Formulations in Healthy Elderly Individuals. (2020). https://pubmed.ncbi.nlm.nih.gov/32188111/ DOI: 10.3390/nu12030784
    Complete structured claim and evidence

  4. FSP1 used NAD(P)H to regenerate the reduced CoQ pool that traps lipid peroxyl radicals.

    NADPH → FSP1 / AIFM2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/31634899.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e96f6d5aed6def29533d907cd9ae90bc287d3f7beb6b9447aec3308d57a0dfe", "start_char": 0, "end_char": 1818, "text_sha256": "1e96f6d5aed6def29533d907cd9ae90bc287d3f7beb6b9447aec3308d57a0dfe"}
    experimental_model
    Expression cloning and cell-death experiments
    exposure
    GPX4 deletion or inhibitors and FSP1 manipulation
    limitations
    Cancer-cell defense mechanism; preventing ferroptosis is not always a desirable disease outcome and oral CoQ benefit is not tested.
    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 models
    plain_language
    The antioxidant form must be regenerated using reducing power.
    primary_references
    [coq10-p31634899] FSP1 is a glutathione-independent ferroptosis suppressor. (2019). https://pubmed.ncbi.nlm.nih.gov/31634899/ DOI: 10.1038/s41586-019-1707-0
    tissue_or_cell_type
    FSP1-CoQ antioxidant pathway

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 801–812

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Expression cloning and cell-death experiments · source_derived_draft · unverified_draft

    ### coq10-fsp1-nadph FSP1 used NAD(P)H to regenerate the reduced CoQ pool that traps lipid peroxyl radicals. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The antioxidant form must be regenerated using reducing power. organism: Human cancer-cell models tissue_or_cell_type: FSP1-CoQ antioxidant pathway experimental_model: Expression cloning and cell-death experiments limitations: Cancer-cell defense mechanism; preventing ferroptosis is not always a desirable disease outcome and oral CoQ benefit is not tested. exposure: GPX4 deletion or inhibitors and FSP1 manipulation evidence_span: {"source_cache": "artifacts/coq10-research/31634899.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e96f6d5aed6def29533d907cd9ae90bc287d3f7beb6b9447aec3308d57a0dfe", "start_char": 0, "end_char": 1818, "text_sha256": "1e96f6d5aed6def29533d907cd9ae90bc287d3f7beb6b9447aec3308d57a0dfe"} [coq10-p31634899] FSP1 is a glutathione-independent ferroptosis suppressor. (2019). https://pubmed.ncbi.nlm.nih.gov/31634899/ DOI: 10.1038/s41586-019-1707-0
    Complete structured claim and evidence

  5. GPD2 coupled glycerol-3-phosphate oxidation to ubiquinol formation.

    Human mitochondrial glycerol-3-phosphate dehydrogenase / GPD2 → Ubiquinone source_derived_draftungraded
    Experimental context and source evidence
    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
    Another metabolic input feeds the same reduced CoQ pool.
    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

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 853–864

    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-quinol GPD2 coupled glycerol-3-phosphate oxidation to ubiquinol formation. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another metabolic input feeds the same reduced CoQ pool. 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

  6. Mammalian TrxR1 reduced ubiquinone-10 to ubiquinol-10.

    TXNRD1 → Ubiquinone-10 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/12435734.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "929e8de2bc15ea62eb4a3814995fd289de759d721f16b848174ad65f95847c55", "start_char": 0, "end_char": 1340, "text_sha256": "929e8de2bc15ea62eb4a3814995fd289de759d721f16b848174ad65f95847c55"}
    experimental_model
    Enzyme kinetics, mutants and overexpressing-cell homogenates
    exposure
    NADPH or NADH; selenite and selenium-deprived enzyme variants
    limitations
    Biochemical selenium dependence; not proof that all CoQ recycling stops with low selenium or that combined supplements are synergistic clinically.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Mammalian TrxR1 and human HEK293 cells
    plain_language
    A selenium-dependent enzyme can regenerate the antioxidant form of CoQ.
    primary_references
    [coq10-p12435734] The mammalian cytosolic selenoenzyme thioredoxin reductase reduces ubiquinone. A novel mechanism for defense against oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/12435734/ DOI: 10.1074/jbc.m210456200
    tissue_or_cell_type
    Ubiquinone reduction

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 762–773

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme kinetics, mutants and overexpressing-cell homogenates · source_derived_draft · unverified_draft

    ### coq10-txnrd1-coq Mammalian TrxR1 reduced ubiquinone-10 to ubiquinol-10. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A selenium-dependent enzyme can regenerate the antioxidant form of CoQ. organism: Mammalian TrxR1 and human HEK293 cells tissue_or_cell_type: Ubiquinone reduction experimental_model: Enzyme kinetics, mutants and overexpressing-cell homogenates limitations: Biochemical selenium dependence; not proof that all CoQ recycling stops with low selenium or that combined supplements are synergistic clinically. exposure: NADPH or NADH; selenite and selenium-deprived enzyme variants evidence_span: {"source_cache": "artifacts/coq10-research/12435734.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "929e8de2bc15ea62eb4a3814995fd289de759d721f16b848174ad65f95847c55", "start_char": 0, "end_char": 1340, "text_sha256": "929e8de2bc15ea62eb4a3814995fd289de759d721f16b848174ad65f95847c55"} [coq10-p12435734] The mammalian cytosolic selenoenzyme thioredoxin reductase reduces ubiquinone. A novel mechanism for defense against oxidative stress. (2003). https://pubmed.ncbi.nlm.nih.gov/12435734/ DOI: 10.1074/jbc.m210456200
    Complete structured claim and evidence

  7. The same solution study detected no reaction of oxidized ubiquinone-10 with tocopheroxyl radicals, distinguishing it from the active reduced ubiquinol-10 form.

    Ubiquinone-10 → Alpha-tocopherol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Primary abstract
    experimental_model
    Stopped-flow comparison of CoQ10 redox states
    exposure
    Oxidized ubiquinone-10 comparator.
    limitations
    A non-detected reaction under these assay conditions is not an assertion that cellular CoQ cannot first be reduced.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Cell-free
    plain_language
    CoQ10 needed to be in its reduced state for the measured recycling reaction.
    primary_references
    [ver-mukai1990] Stopped-flow kinetic study of the regeneration reaction of tocopheroxyl radical by reduced ubiquinone-10 in solution. (1990). https://pubmed.ncbi.nlm.nih.gov/2383582/ DOI: 10.1016/0304-4165(90)90176-w
    tissue_or_cell_type
    Chemical solution

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 522–534

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stopped-flow comparison of CoQ10 redox states · source_derived_draft · unverified_draft

    ### ver-oxidized-coq-no-regeneration The same solution study detected no reaction of oxidized ubiquinone-10 with tocopheroxyl radicals, distinguishing it from the active reduced ubiquinol-10 form. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: CoQ10 needed to be in its reduced state for the measured recycling reaction. organism: Cell-free tissue_or_cell_type: Chemical solution experimental_model: Stopped-flow comparison of CoQ10 redox states limitations: A non-detected reaction under these assay conditions is not an assertion that cellular CoQ cannot first be reduced. exposure: Oxidized ubiquinone-10 comparator. cross_nutrient: true evidence_location: Primary abstract [ver-mukai1990] Stopped-flow kinetic study of the regeneration reaction of tocopheroxyl radical by reduced ubiquinone-10 in solution. (1990). https://pubmed.ncbi.nlm.nih.gov/2383582/ DOI: 10.1016/0304-4165(90)90176-w
    Complete structured claim and evidence

  8. Vitamin K1 hydroquinone reacted with alpha-tocopheroxyl in stopped-flow assays; it regenerated vitamin E more rapidly than ubiquinol-10 across the tested ethanol, benzene and isopropanol/water solvent systems.

    Phylloquinol / vitamin K1 hydroquinone → Alpha-tocopherol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Primary abstract
    experimental_model
    Biological hydroquinone comparison
    exposure
    Reduced K1; isopropanol/water 5:1 v/v and separate organic solvents.
    limitations
    Does not establish dietary K/E synergy, clinical benefit or competition in coagulation.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Cell-free
    plain_language
    The reduced form of vitamin K1 recycled vitamin E in solution.
    primary_references
    [ver-mukai1992] Stopped-flow kinetic study of vitamin E regeneration reaction with biological hydroquinones (reduced forms of ubiquinone, vitamin K, and tocopherolquinone) in solution. (1992). https://pubmed.ncbi.nlm.nih.gov/1429580/ DOI: 10.1016/s0021-9258(18)41666-3
    tissue_or_cell_type
    Chemical solutions

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 536–548

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biological hydroquinone comparison · source_derived_draft · unverified_draft

    ### ver-phylloquinol-regeneration Vitamin K1 hydroquinone reacted with alpha-tocopheroxyl in stopped-flow assays; it regenerated vitamin E more rapidly than ubiquinol-10 across the tested ethanol, benzene and isopropanol/water solvent systems. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The reduced form of vitamin K1 recycled vitamin E in solution. organism: Cell-free tissue_or_cell_type: Chemical solutions experimental_model: Biological hydroquinone comparison limitations: Does not establish dietary K/E synergy, clinical benefit or competition in coagulation. exposure: Reduced K1; isopropanol/water 5:1 v/v and separate organic solvents. cross_nutrient: true evidence_location: Primary abstract [ver-mukai1992] Stopped-flow kinetic study of vitamin E regeneration reaction with biological hydroquinones (reduced forms of ubiquinone, vitamin K, and tocopherolquinone) in solution. (1992). https://pubmed.ncbi.nlm.nih.gov/1429580/ DOI: 10.1016/s0021-9258(18)41666-3
    Complete structured claim and evidence

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