Component

Coenzyme Q10 / CoQ10 redox system

Coenzyme Q10 is an endogenously synthesized lipid redox carrier. Oxidized ubiquinone-10 and reduced ubiquinol-10 support electron transfer and membrane protection; their location, regeneration and availability matter.

25 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.

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. CoQ-deficient human fibroblasts had impaired sulfide oxidation proportional to their residual CoQ.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/coq10-research/27856618.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485", "start_char": 0, "end_char": 1261, "text_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485"}
    experimental_model
    Patient fibroblasts, biosynthesis inhibition and mouse genetics
    exposure
    Genetic or pharmacological CoQ depletion and in-vitro repletion
    limitations
    Tissue-specific disease models; mouse residual percentages are not diagnostic human thresholds.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Human fibroblasts/HeLa cells and Pdss2 mutant mice
    plain_language
    A low CoQ pool can disrupt another pathway before considering ATP alone.
    primary_references
    [coq10-p27856618] Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/27856618/ DOI: 10.15252/emmm.201606356
    tissue_or_cell_type
    Sulfide oxidation and tissue CoQ
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 541–552

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient fibroblasts, biosynthesis inhibition and mouse genetics · source_derived_draft · unverified_draft

    ### coq10-coq-sulfide-loss CoQ-deficient human fibroblasts had impaired sulfide oxidation proportional to their residual CoQ. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low CoQ pool can disrupt another pathway before considering ATP alone. organism: Human fibroblasts/HeLa cells and Pdss2 mutant mice tissue_or_cell_type: Sulfide oxidation and tissue CoQ experimental_model: Patient fibroblasts, biosynthesis inhibition and mouse genetics limitations: Tissue-specific disease models; mouse residual percentages are not diagnostic human thresholds. exposure: Genetic or pharmacological CoQ depletion and in-vitro repletion evidence_span: {"source_cache": "artifacts/coq10-research/27856618.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485", "start_char": 0, "end_char": 1261, "text_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485"} [coq10-p27856618] Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/27856618/ DOI: 10.15252/emmm.201606356
    Complete structured claim and evidence
  2. CoQ supplementation rescued sulfide-pathway biochemical abnormalities in deficient fibroblasts.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/27856618.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485", "start_char": 0, "end_char": 1261, "text_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485"}
    experimental_model
    Patient fibroblasts, biosynthesis inhibition and mouse genetics
    exposure
    Genetic or pharmacological CoQ depletion and in-vitro repletion
    limitations
    Tissue-specific disease models; mouse residual percentages are not diagnostic human thresholds.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Human fibroblasts/HeLa cells and Pdss2 mutant mice
    plain_language
    Supplying the missing carrier improved the tested disposal pathway in cells.
    primary_references
    [coq10-p27856618] Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/27856618/ DOI: 10.15252/emmm.201606356
    tissue_or_cell_type
    Sulfide oxidation and tissue CoQ

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 554–565

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient fibroblasts, biosynthesis inhibition and mouse genetics · source_derived_draft · unverified_draft

    ### coq10-coq-sulfide-rescue CoQ supplementation rescued sulfide-pathway biochemical abnormalities in deficient fibroblasts. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplying the missing carrier improved the tested disposal pathway in cells. organism: Human fibroblasts/HeLa cells and Pdss2 mutant mice tissue_or_cell_type: Sulfide oxidation and tissue CoQ experimental_model: Patient fibroblasts, biosynthesis inhibition and mouse genetics limitations: Tissue-specific disease models; mouse residual percentages are not diagnostic human thresholds. exposure: Genetic or pharmacological CoQ depletion and in-vitro repletion evidence_span: {"source_cache": "artifacts/coq10-research/27856618.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485", "start_char": 0, "end_char": 1261, "text_sha256": "a8b98767d3bed9661c05c7b82b55817b6d9912abd8bfc9dd9d59ca9763025485"} [coq10-p27856618] Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/27856618/ DOI: 10.15252/emmm.201606356
    Complete structured claim and evidence
  3. CoQ treatment partly reversed apoptosis after Coq6 knockdown in podocyte and zebrafish models.

    Coenzyme Q10 / CoQ10 redox system → Podocyte apoptosis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/21540551.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f01d7d237328376c3eb1ed5a3c2c1ee7561d78fb3890101ab5e8eb678c64def", "start_char": 0, "end_char": 1142, "text_sha256": "3f01d7d237328376c3eb1ed5a3c2c1ee7561d78fb3890101ab5e8eb678c64def"}
    experimental_model
    Human pedigrees, yeast validation, podocyte and zebrafish knockdown
    exposure
    COQ6 variants; cell/embryo knockdown and CoQ treatment
    limitations
    The canonical podocyte process is the cell endpoint; zebrafish apoptosis was also studied. Partial model rescue is not universal clinical reversal.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    13 humans from seven families plus model systems
    plain_language
    Replacing the carrier helped in models of a specific synthesis defect.
    primary_references
    [coq10-p21540551] COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness. (2011). https://pubmed.ncbi.nlm.nih.gov/21540551/ DOI: 10.1172/jci45693
    tissue_or_cell_type
    Renal podocytes and inner-ear disease

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1022–1033

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pedigrees, yeast validation, podocyte and zebrafish knockdown · source_derived_draft · unverified_draft

    ### coq10-coq6-model-rescue CoQ treatment partly reversed apoptosis after Coq6 knockdown in podocyte and zebrafish models. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing the carrier helped in models of a specific synthesis defect. organism: 13 humans from seven families plus model systems tissue_or_cell_type: Renal podocytes and inner-ear disease experimental_model: Human pedigrees, yeast validation, podocyte and zebrafish knockdown limitations: The canonical podocyte process is the cell endpoint; zebrafish apoptosis was also studied. Partial model rescue is not universal clinical reversal. exposure: COQ6 variants; cell/embryo knockdown and CoQ treatment evidence_span: {"source_cache": "artifacts/coq10-research/21540551.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3f01d7d237328376c3eb1ed5a3c2c1ee7561d78fb3890101ab5e8eb678c64def", "start_char": 0, "end_char": 1142, "text_sha256": "3f01d7d237328376c3eb1ed5a3c2c1ee7561d78fb3890101ab5e8eb678c64def"} [coq10-p21540551] COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness. (2011). https://pubmed.ncbi.nlm.nih.gov/21540551/ DOI: 10.1172/jci45693
    Complete structured claim and evidence
  4. 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.

    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
  5. Two-year major adverse events occurred in 15% on CoQ versus 26% on placebo, hazard ratio 0.50 (95% CI 0.32-0.80).

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/25282031.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65", "start_char": 0, "end_char": 2024, "text_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65"}
    experimental_model
    Q-SYMBIO randomized double-blind multicenter trial
    exposure
    100 mg CoQ10 three times daily added to standard therapy
    limitations
    One adjunctive-treatment trial; recruitment preceded current heart-failure regimens. Does not show universal benefit or replacement of standard treatment.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    420 patients with moderate-to-severe chronic heart failure
    plain_language
    This trial found a benefit on clinical events when CoQ was added to usual care.
    primary_references
    [coq10-p25282031] The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. (2014). https://pubmed.ncbi.nlm.nih.gov/25282031/ DOI: 10.1016/j.jchf.2014.06.008
    tissue_or_cell_type
    Short-term function and two-year clinical events

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1087–1098

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Q-SYMBIO randomized double-blind multicenter trial · source_derived_draft · unverified_draft

    ### coq10-heart-failure-events Two-year major adverse events occurred in 15% on CoQ versus 26% on placebo, hazard ratio 0.50 (95% CI 0.32-0.80). Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This trial found a benefit on clinical events when CoQ was added to usual care. organism: 420 patients with moderate-to-severe chronic heart failure tissue_or_cell_type: Short-term function and two-year clinical events experimental_model: Q-SYMBIO randomized double-blind multicenter trial limitations: One adjunctive-treatment trial; recruitment preceded current heart-failure regimens. Does not show universal benefit or replacement of standard treatment. exposure: 100 mg CoQ10 three times daily added to standard therapy evidence_span: {"source_cache": "artifacts/coq10-research/25282031.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65", "start_char": 0, "end_char": 2024, "text_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65"} [coq10-p25282031] The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. (2014). https://pubmed.ncbi.nlm.nih.gov/25282031/ DOI: 10.1016/j.jchf.2014.06.008
    Complete structured claim and evidence
  6. All-cause mortality was 10% versus 18%, and cardiovascular mortality was 9% versus 16%, favoring CoQ in Q-SYMBIO.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/25282031.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65", "start_char": 0, "end_char": 2024, "text_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65"}
    experimental_model
    Q-SYMBIO randomized double-blind multicenter trial
    exposure
    100 mg CoQ10 three times daily added to standard therapy
    limitations
    One adjunctive-treatment trial; recruitment preceded current heart-failure regimens. Does not show universal benefit or replacement of standard treatment.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    420 patients with moderate-to-severe chronic heart failure
    plain_language
    Mortality was a reported secondary outcome, separate from symptom markers.
    primary_references
    [coq10-p25282031] The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. (2014). https://pubmed.ncbi.nlm.nih.gov/25282031/ DOI: 10.1016/j.jchf.2014.06.008
    tissue_or_cell_type
    Short-term function and two-year clinical events

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1100–1111

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Q-SYMBIO randomized double-blind multicenter trial · source_derived_draft · unverified_draft

    ### coq10-heart-failure-mortality All-cause mortality was 10% versus 18%, and cardiovascular mortality was 9% versus 16%, favoring CoQ in Q-SYMBIO. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mortality was a reported secondary outcome, separate from symptom markers. organism: 420 patients with moderate-to-severe chronic heart failure tissue_or_cell_type: Short-term function and two-year clinical events experimental_model: Q-SYMBIO randomized double-blind multicenter trial limitations: One adjunctive-treatment trial; recruitment preceded current heart-failure regimens. Does not show universal benefit or replacement of standard treatment. exposure: 100 mg CoQ10 three times daily added to standard therapy evidence_span: {"source_cache": "artifacts/coq10-research/25282031.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65", "start_char": 0, "end_char": 2024, "text_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65"} [coq10-p25282031] The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. (2014). https://pubmed.ncbi.nlm.nih.gov/25282031/ DOI: 10.1016/j.jchf.2014.06.008
    Complete structured claim and evidence
  7. The 16-week NT-proBNP, NYHA-class and six-minute-walk endpoints did not significantly change between trial groups.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/25282031.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65", "start_char": 0, "end_char": 2024, "text_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65"}
    experimental_model
    Q-SYMBIO randomized double-blind multicenter trial
    exposure
    100 mg CoQ10 three times daily added to standard therapy
    limitations
    One adjunctive-treatment trial; recruitment preceded current heart-failure regimens. Does not show universal benefit or replacement of standard treatment.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    420 patients with moderate-to-severe chronic heart failure
    plain_language
    The early markers did not mirror the later event finding.
    primary_references
    [coq10-p25282031] The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. (2014). https://pubmed.ncbi.nlm.nih.gov/25282031/ DOI: 10.1016/j.jchf.2014.06.008
    tissue_or_cell_type
    Short-term function and two-year clinical events

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1113–1124

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Q-SYMBIO randomized double-blind multicenter trial · source_derived_draft · unverified_draft

    ### coq10-heart-failure-short The 16-week NT-proBNP, NYHA-class and six-minute-walk endpoints did not significantly change between trial groups. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The early markers did not mirror the later event finding. organism: 420 patients with moderate-to-severe chronic heart failure tissue_or_cell_type: Short-term function and two-year clinical events experimental_model: Q-SYMBIO randomized double-blind multicenter trial limitations: One adjunctive-treatment trial; recruitment preceded current heart-failure regimens. Does not show universal benefit or replacement of standard treatment. exposure: 100 mg CoQ10 three times daily added to standard therapy evidence_span: {"source_cache": "artifacts/coq10-research/25282031.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65", "start_char": 0, "end_char": 2024, "text_sha256": "20ff9f86de1fab16a33ecadfb2c4e09e9017860f01854cfecf490d473fb8fb65"} [coq10-p25282031] The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. (2014). https://pubmed.ncbi.nlm.nih.gov/25282031/ DOI: 10.1016/j.jchf.2014.06.008
    Complete structured claim and evidence
  8. The 50% responder rate for attack frequency was 47.6% with CoQ versus 14.4% with placebo in the third treatment month.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/15728298.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "efc7a89a0f36fb7248716b6a3e951d719b4e7f2c1051cd8ea50b61a1f4e4941f", "start_char": 0, "end_char": 533, "text_sha256": "efc7a89a0f36fb7248716b6a3e951d719b4e7f2c1051cd8ea50b61a1f4e4941f"}
    experimental_model
    Double-blind randomized placebo-controlled trial
    exposure
    CoQ10 100 mg three times daily
    limitations
    Small preventive trial; third-month endpoint, not proof of correction of a diagnosed CoQ deficiency.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    42 migraine patients
    plain_language
    A small migraine trial reported fewer attacks.
    primary_references
    [coq10-p15728298] Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. (2005). https://pubmed.ncbi.nlm.nih.gov/15728298/ DOI: 10.1212/01.wnl.0000151975.03598.ed
    tissue_or_cell_type
    Attack frequency and headache days

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1191–1202

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial · source_derived_draft · unverified_draft

    ### coq10-migraine-adult The 50% responder rate for attack frequency was 47.6% with CoQ versus 14.4% with placebo in the third treatment month. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A small migraine trial reported fewer attacks. organism: 42 migraine patients tissue_or_cell_type: Attack frequency and headache days experimental_model: Double-blind randomized placebo-controlled trial limitations: Small preventive trial; third-month endpoint, not proof of correction of a diagnosed CoQ deficiency. exposure: CoQ10 100 mg three times daily evidence_span: {"source_cache": "artifacts/coq10-research/15728298.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "efc7a89a0f36fb7248716b6a3e951d719b4e7f2c1051cd8ea50b61a1f4e4941f", "start_char": 0, "end_char": 533, "text_sha256": "efc7a89a0f36fb7248716b6a3e951d719b4e7f2c1051cd8ea50b61a1f4e4941f"} [coq10-p15728298] Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. (2005). https://pubmed.ncbi.nlm.nih.gov/15728298/ DOI: 10.1212/01.wnl.0000151975.03598.ed
    Complete structured claim and evidence
  9. At day 224, headache outcomes did not differ between CoQ and placebo; both groups improved over time.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/21586650.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f3500b1c0ad9329d8b4f4c4cc7bdadb07c8cae55e8d336dccf0265620aa25292", "start_char": 0, "end_char": 2235, "text_sha256": "f3500b1c0ad9329d8b4f4c4cc7bdadb07c8cae55e8d336dccf0265620aa25292"}
    experimental_model
    Randomized double-blind crossover add-on trial
    exposure
    CoQ10 100 mg with standardized multidisciplinary care
    limitations
    Substantial attrition; early improvement and final between-group outcome are different analyses.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    120 children/adolescents randomized; 50 analyzed at final endpoint
    plain_language
    A pediatric study did not establish a lasting added benefit beyond the background care.
    primary_references
    [coq10-p21586650] A randomized, double-blinded, placebo-controlled, crossover, add-on study of CoEnzyme Q10 in the prevention of pediatric and adolescent migraine. (2011). https://pubmed.ncbi.nlm.nih.gov/21586650/ DOI: 10.1177/0333102411406755
    tissue_or_cell_type
    Migraine outcomes

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1204–1215

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

    ### coq10-migraine-child At day 224, headache outcomes did not differ between CoQ and placebo; both groups improved over time. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pediatric study did not establish a lasting added benefit beyond the background care. organism: 120 children/adolescents randomized; 50 analyzed at final endpoint tissue_or_cell_type: Migraine outcomes experimental_model: Randomized double-blind crossover add-on trial limitations: Substantial attrition; early improvement and final between-group outcome are different analyses. exposure: CoQ10 100 mg with standardized multidisciplinary care evidence_span: {"source_cache": "artifacts/coq10-research/21586650.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f3500b1c0ad9329d8b4f4c4cc7bdadb07c8cae55e8d336dccf0265620aa25292", "start_char": 0, "end_char": 2235, "text_sha256": "f3500b1c0ad9329d8b4f4c4cc7bdadb07c8cae55e8d336dccf0265620aa25292"} [coq10-p21586650] A randomized, double-blinded, placebo-controlled, crossover, add-on study of CoEnzyme Q10 in the prevention of pediatric and adolescent migraine. (2011). https://pubmed.ncbi.nlm.nih.gov/21586650/ DOI: 10.1177/0333102411406755
    Complete structured claim and evidence
  10. CoQ modestly attenuated exercise-related lactate rise and improved one cycling oxygen-consumption measure.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/20886510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e", "start_char": 0, "end_char": 1053, "text_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e"}
    experimental_model
    Randomized double-blind crossover trial
    exposure
    CoQ10 1200 mg/day for 60 days
    limitations
    Heterogeneous mitochondrial disease, not exclusively genetically proven primary CoQ deficiency; small short study.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    30 mitochondrial-cytopathy patients
    plain_language
    Some exercise measurements changed in this heterogeneous group.
    primary_references
    [coq10-p20886510] A randomized trial of coenzyme Q10 in mitochondrial disorders. (2010). https://pubmed.ncbi.nlm.nih.gov/20886510/ DOI: 10.1002/mus.21758
    tissue_or_cell_type
    Exercise and clinical function

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1230–1241

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

    ### coq10-mitochondrial-exercise CoQ modestly attenuated exercise-related lactate rise and improved one cycling oxygen-consumption measure. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some exercise measurements changed in this heterogeneous group. organism: 30 mitochondrial-cytopathy patients tissue_or_cell_type: Exercise and clinical function experimental_model: Randomized double-blind crossover trial limitations: Heterogeneous mitochondrial disease, not exclusively genetically proven primary CoQ deficiency; small short study. exposure: CoQ10 1200 mg/day for 60 days evidence_span: {"source_cache": "artifacts/coq10-research/20886510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e", "start_char": 0, "end_char": 1053, "text_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e"} [coq10-p20886510] A randomized trial of coenzyme Q10 in mitochondrial disorders. (2010). https://pubmed.ncbi.nlm.nih.gov/20886510/ DOI: 10.1002/mus.21758
    Complete structured claim and evidence
  11. The trial found no improvement in strength or other major clinical variables despite minor exercise effects.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/20886510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e", "start_char": 0, "end_char": 1053, "text_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e"}
    experimental_model
    Randomized double-blind crossover trial
    exposure
    CoQ10 1200 mg/day for 60 days
    limitations
    Heterogeneous mitochondrial disease, not exclusively genetically proven primary CoQ deficiency; small short study.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    30 mitochondrial-cytopathy patients
    plain_language
    Mitochondrial disease does not automatically imply a broad response to CoQ.
    primary_references
    [coq10-p20886510] A randomized trial of coenzyme Q10 in mitochondrial disorders. (2010). https://pubmed.ncbi.nlm.nih.gov/20886510/ DOI: 10.1002/mus.21758
    tissue_or_cell_type
    Exercise and clinical function

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1243–1254

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

    ### coq10-mitochondrial-strength-null The trial found no improvement in strength or other major clinical variables despite minor exercise effects. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mitochondrial disease does not automatically imply a broad response to CoQ. organism: 30 mitochondrial-cytopathy patients tissue_or_cell_type: Exercise and clinical function experimental_model: Randomized double-blind crossover trial limitations: Heterogeneous mitochondrial disease, not exclusively genetically proven primary CoQ deficiency; small short study. exposure: CoQ10 1200 mg/day for 60 days evidence_span: {"source_cache": "artifacts/coq10-research/20886510.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e", "start_char": 0, "end_char": 1053, "text_sha256": "7df48f2e8cf3da738d09c37cb1e96cb62a3eceae213ff722b49855ea174f863e"} [coq10-p20886510] A randomized trial of coenzyme Q10 in mitochondrial disorders. (2010). https://pubmed.ncbi.nlm.nih.gov/20886510/ DOI: 10.1002/mus.21758
    Complete structured claim and evidence
  12. Median protein-to-creatinine ratio fell from 1.66 to 0.19 g/gCr at 12 months; six of seven patients with 12-month data had at least a 50% reduction.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/coq10-research/42435122.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59862dedc0e8ce5d72cf95f5f04a1d16e447cc16e9f2310fac81d15fb1fa9aa4", "start_char": 0, "end_char": 1715, "text_sha256": "59862dedc0e8ce5d72cf95f5f04a1d16e447cc16e9f2310fac81d15fb1fa9aa4"}
    experimental_model
    Retrospective longitudinal clinical cohort
    exposure
    CoQ supplementation; median initial dose 10 mg/kg/day
    limitations
    2026 observational cohort without untreated randomization; incomplete 12-month data and genotype-specific context.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    12 Japanese patients: 11 COQ8B and one COQ6
    plain_language
    The treatment signal was in a genetically defined disease, not routine tiredness.
    primary_references
    [coq10-p42435122] Kidney outcomes of coenzyme Q10 supplementation in patients with genetically confirmed CoQ10 nephropathy in Japan. (2026). https://pubmed.ncbi.nlm.nih.gov/42435122/ DOI: 10.1007/s10157-026-02917-7
    tissue_or_cell_type
    Genetically confirmed CoQ nephropathy
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1048–1059

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective longitudinal clinical cohort · source_derived_draft · unverified_draft

    ### coq10-nephropathy-proteinuria Median protein-to-creatinine ratio fell from 1.66 to 0.19 g/gCr at 12 months; six of seven patients with 12-month data had at least a 50% reduction. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The treatment signal was in a genetically defined disease, not routine tiredness. organism: 12 Japanese patients: 11 COQ8B and one COQ6 tissue_or_cell_type: Genetically confirmed CoQ nephropathy experimental_model: Retrospective longitudinal clinical cohort limitations: 2026 observational cohort without untreated randomization; incomplete 12-month data and genotype-specific context. exposure: CoQ supplementation; median initial dose 10 mg/kg/day evidence_span: {"source_cache": "artifacts/coq10-research/42435122.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59862dedc0e8ce5d72cf95f5f04a1d16e447cc16e9f2310fac81d15fb1fa9aa4", "start_char": 0, "end_char": 1715, "text_sha256": "59862dedc0e8ce5d72cf95f5f04a1d16e447cc16e9f2310fac81d15fb1fa9aa4"} [coq10-p42435122] Kidney outcomes of coenzyme Q10 supplementation in patients with genetically confirmed CoQ10 nephropathy in Japan. (2026). https://pubmed.ncbi.nlm.nih.gov/42435122/ DOI: 10.1007/s10157-026-02917-7
    Complete structured claim and evidence
  13. Neither CoQ dose slowed UPDRS worsening versus placebo; the trial stopped for futility.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/24664227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b", "start_char": 0, "end_char": 3023, "text_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b"}
    experimental_model
    Randomized double-blind phase III trial
    exposure
    CoQ10 1200 or 2400 mg/day; all groups received 1200 IU/day vitamin E
    limitations
    Vitamin E was a common background intervention; this comparison cannot identify its independent effect.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    600 early-Parkinson patients
    plain_language
    A plausible mitochondrial mechanism did not translate into slower Parkinson progression in this trial.
    primary_references
    [coq10-p24664227] A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. (2014). https://pubmed.ncbi.nlm.nih.gov/24664227/ DOI: 10.1001/jamaneurol.2014.131
    tissue_or_cell_type
    UPDRS progression

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1217–1228

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

    ### coq10-parkinson-null Neither CoQ dose slowed UPDRS worsening versus placebo; the trial stopped for futility. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A plausible mitochondrial mechanism did not translate into slower Parkinson progression in this trial. organism: 600 early-Parkinson patients tissue_or_cell_type: UPDRS progression experimental_model: Randomized double-blind phase III trial limitations: Vitamin E was a common background intervention; this comparison cannot identify its independent effect. exposure: CoQ10 1200 or 2400 mg/day; all groups received 1200 IU/day vitamin E evidence_span: {"source_cache": "artifacts/coq10-research/24664227.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b", "start_char": 0, "end_char": 3023, "text_sha256": "b1f301e82d4650432dab586db0be51f96e131f3c6084af9aebde932e8072676b"} [coq10-p24664227] A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. (2014). https://pubmed.ncbi.nlm.nih.gov/24664227/ DOI: 10.1001/jamaneurol.2014.131
    Complete structured claim and evidence
  14. Mean NT-proBNP at 48 months was 214 ng/L in the combined-treatment group versus 302 ng/L with placebo.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/22626835.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587", "start_char": 0, "end_char": 1797, "text_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587"}
    experimental_model
    Randomized double-blind combined-supplement trial
    exposure
    Selenium plus CoQ10 versus placebo; 5.2-year follow-up
    limitations
    Combined intervention without selenium-only and CoQ-only arms; no independent CoQ effect or statistical nutrient synergy can be identified.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    443 Swedish adults aged 70-88
    plain_language
    A heart-stress marker also differed; this was the same trial, not an independent replication.
    primary_references
    [coq10-p22626835] Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: a 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. (2013). https://pubmed.ncbi.nlm.nih.gov/22626835/ DOI: 10.1016/j.ijcard.2012.04.156
    tissue_or_cell_type
    Cardiovascular mortality and cardiac measurements

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1139–1150

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

    ### coq10-selenium-combination-marker Mean NT-proBNP at 48 months was 214 ng/L in the combined-treatment group versus 302 ng/L with placebo. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A heart-stress marker also differed; this was the same trial, not an independent replication. organism: 443 Swedish adults aged 70-88 tissue_or_cell_type: Cardiovascular mortality and cardiac measurements experimental_model: Randomized double-blind combined-supplement trial limitations: Combined intervention without selenium-only and CoQ-only arms; no independent CoQ effect or statistical nutrient synergy can be identified. exposure: Selenium plus CoQ10 versus placebo; 5.2-year follow-up evidence_span: {"source_cache": "artifacts/coq10-research/22626835.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587", "start_char": 0, "end_char": 1797, "text_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587"} [coq10-p22626835] Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: a 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. (2013). https://pubmed.ncbi.nlm.nih.gov/22626835/ DOI: 10.1016/j.ijcard.2012.04.156
    Complete structured claim and evidence
  15. Cardiovascular mortality was 5.9% with combined selenium/CoQ versus 12.6% with placebo in the Swedish trial.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/22626835.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587", "start_char": 0, "end_char": 1797, "text_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587"}
    experimental_model
    Randomized double-blind combined-supplement trial
    exposure
    Selenium plus CoQ10 versus placebo; 5.2-year follow-up
    limitations
    Combined intervention without selenium-only and CoQ-only arms; no independent CoQ effect or statistical nutrient synergy can be identified.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    443 Swedish adults aged 70-88
    plain_language
    The combination had a favorable result, but the design cannot tell how much came from each component.
    primary_references
    [coq10-p22626835] Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: a 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. (2013). https://pubmed.ncbi.nlm.nih.gov/22626835/ DOI: 10.1016/j.ijcard.2012.04.156
    tissue_or_cell_type
    Cardiovascular mortality and cardiac measurements

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1126–1137

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

    ### coq10-selenium-combination-mortality Cardiovascular mortality was 5.9% with combined selenium/CoQ versus 12.6% with placebo in the Swedish trial. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination had a favorable result, but the design cannot tell how much came from each component. organism: 443 Swedish adults aged 70-88 tissue_or_cell_type: Cardiovascular mortality and cardiac measurements experimental_model: Randomized double-blind combined-supplement trial limitations: Combined intervention without selenium-only and CoQ-only arms; no independent CoQ effect or statistical nutrient synergy can be identified. exposure: Selenium plus CoQ10 versus placebo; 5.2-year follow-up evidence_span: {"source_cache": "artifacts/coq10-research/22626835.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587", "start_char": 0, "end_char": 1797, "text_sha256": "68f71b162945240d48d14b42d132856ad242c2cc57640eae3a60a3aaa2706587"} [coq10-p22626835] Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: a 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. (2013). https://pubmed.ncbi.nlm.nih.gov/22626835/ DOI: 10.1016/j.ijcard.2012.04.156
    Complete structured claim and evidence
  16. The 2022 trial found no effect on myalgia; individual changes in muscle CoQ did not correlate with changes in symptom intensity.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/36139772.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992", "start_char": 0, "end_char": 1370, "text_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992"}
    experimental_model
    Randomized placebo-controlled muscle-biopsy supplementation trial
    exposure
    CoQ10 400 mg/day for eight weeks
    limitations
    One formulation/regimen and a small sample; a failed tissue or clinical response cannot establish universal nonresponse.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    37 simvastatin-treated adults with or without myalgia
    plain_language
    A measured muscle pool and the pain outcome must be assessed separately.
    primary_references
    [coq10-p36139772] Coenzyme Q10 Supplementation in Statin Treated Patients: A Double-Blinded Randomized Placebo-Controlled Trial. (2022). https://pubmed.ncbi.nlm.nih.gov/36139772/ DOI: 10.3390/antiox11091698
    tissue_or_cell_type
    Muscle CoQ, mitochondrial function and symptoms

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 996–1007

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized placebo-controlled muscle-biopsy supplementation trial · source_derived_draft · unverified_draft

    ### coq10-statin-2022-pain-null The 2022 trial found no effect on myalgia; individual changes in muscle CoQ did not correlate with changes in symptom intensity. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A measured muscle pool and the pain outcome must be assessed separately. organism: 37 simvastatin-treated adults with or without myalgia tissue_or_cell_type: Muscle CoQ, mitochondrial function and symptoms experimental_model: Randomized placebo-controlled muscle-biopsy supplementation trial limitations: One formulation/regimen and a small sample; a failed tissue or clinical response cannot establish universal nonresponse. exposure: CoQ10 400 mg/day for eight weeks evidence_span: {"source_cache": "artifacts/coq10-research/36139772.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992", "start_char": 0, "end_char": 1370, "text_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992"} [coq10-p36139772] Coenzyme Q10 Supplementation in Statin Treated Patients: A Double-Blinded Randomized Placebo-Controlled Trial. (2022). https://pubmed.ncbi.nlm.nih.gov/36139772/ DOI: 10.3390/antiox11091698
    Complete structured claim and evidence
  17. CoQ supplementation did not increase muscle CoQ or alter measured mitochondrial respiratory function, content or reactive-oxygen-species production.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/36139772.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992", "start_char": 0, "end_char": 1370, "text_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992"}
    experimental_model
    Randomized placebo-controlled muscle-biopsy supplementation trial
    exposure
    CoQ10 400 mg/day for eight weeks
    limitations
    One formulation/regimen and a small sample; a failed tissue or clinical response cannot establish universal nonresponse.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    37 simvastatin-treated adults with or without myalgia
    plain_language
    Taking more did not ensure delivery or functional change in the sampled muscle.
    primary_references
    [coq10-p36139772] Coenzyme Q10 Supplementation in Statin Treated Patients: A Double-Blinded Randomized Placebo-Controlled Trial. (2022). https://pubmed.ncbi.nlm.nih.gov/36139772/ DOI: 10.3390/antiox11091698
    tissue_or_cell_type
    Muscle CoQ, mitochondrial function and symptoms

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 983–994

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized placebo-controlled muscle-biopsy supplementation trial · source_derived_draft · unverified_draft

    ### coq10-statin-muscle-repletion-null CoQ supplementation did not increase muscle CoQ or alter measured mitochondrial respiratory function, content or reactive-oxygen-species production. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Taking more did not ensure delivery or functional change in the sampled muscle. organism: 37 simvastatin-treated adults with or without myalgia tissue_or_cell_type: Muscle CoQ, mitochondrial function and symptoms experimental_model: Randomized placebo-controlled muscle-biopsy supplementation trial limitations: One formulation/regimen and a small sample; a failed tissue or clinical response cannot establish universal nonresponse. exposure: CoQ10 400 mg/day for eight weeks evidence_span: {"source_cache": "artifacts/coq10-research/36139772.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992", "start_char": 0, "end_char": 1370, "text_sha256": "07baaf957ba2b166fce6e23f157e7d2123c92bea20032628c332c0a40639b992"} [coq10-p36139772] Coenzyme Q10 Supplementation in Statin Treated Patients: A Double-Blinded Randomized Placebo-Controlled Trial. (2022). https://pubmed.ncbi.nlm.nih.gov/36139772/ DOI: 10.3390/antiox11091698
    Complete structured claim and evidence
  18. Pain severity and interference improved relative to placebo after 30 days of CoQ in the 50-patient study.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/25375075.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4", "start_char": 0, "end_char": 1622, "text_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4"}
    experimental_model
    Randomized placebo-controlled study
    exposure
    CoQ10 50 mg twice daily for 30 days
    limitations
    Small short study; symptoms were not confirmed by a blinded statin-placebo lead-in as in the later trial.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    50 statin-treated patients reporting mild-to-moderate muscle symptoms
    plain_language
    One trial found less muscle pain with added CoQ.
    primary_references
    [coq10-p25375075] Coenzyme Q10 supplementation decreases statin-related mild-to-moderate muscle symptoms: a randomized clinical study. (2014). https://pubmed.ncbi.nlm.nih.gov/25375075/ DOI: 10.12659/msm.890777
    tissue_or_cell_type
    Brief Pain Inventory scores

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1152–1163

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

    ### coq10-statin-pain-positive Pain severity and interference improved relative to placebo after 30 days of CoQ in the 50-patient study. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: One trial found less muscle pain with added CoQ. organism: 50 statin-treated patients reporting mild-to-moderate muscle symptoms tissue_or_cell_type: Brief Pain Inventory scores experimental_model: Randomized placebo-controlled study limitations: Small short study; symptoms were not confirmed by a blinded statin-placebo lead-in as in the later trial. exposure: CoQ10 50 mg twice daily for 30 days evidence_span: {"source_cache": "artifacts/coq10-research/25375075.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4", "start_char": 0, "end_char": 1622, "text_sha256": "c1b3bae22ef80093dd226d2bebbc1791ac08e3952c694f801a72f308fd7258e4"} [coq10-p25375075] Coenzyme Q10 supplementation decreases statin-related mild-to-moderate muscle symptoms: a randomized clinical study. (2014). https://pubmed.ncbi.nlm.nih.gov/25375075/ DOI: 10.12659/msm.890777
    Complete structured claim and evidence
  19. The case report described reduced warfarin responsiveness during CoQ use and recovery after withdrawal.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/9621803.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498", "start_char": 0, "end_char": 752, "text_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498"}
    experimental_model
    Case report with supplement withdrawal
    exposure
    CoQ10 exposure then discontinuation
    limitations
    Single case; temporal association is not proof of mechanism or interaction frequency. Chemical similarity does not establish vitamin K activity.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    72-year-old woman taking warfarin
    plain_language
    A possible drug interaction was reported, but one case cannot determine how often it occurs.
    primary_references
    [coq10-p9621803] [Interaction between warfarin and coenzyme Q10]. (1998). https://pubmed.ncbi.nlm.nih.gov/9621803/
    tissue_or_cell_type
    Anticoagulant response

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1256–1267

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case report with supplement withdrawal · source_derived_draft · unverified_draft

    ### coq10-warfarin-case The case report described reduced warfarin responsiveness during CoQ use and recovery after withdrawal. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A possible drug interaction was reported, but one case cannot determine how often it occurs. organism: 72-year-old woman taking warfarin tissue_or_cell_type: Anticoagulant response experimental_model: Case report with supplement withdrawal limitations: Single case; temporal association is not proof of mechanism or interaction frequency. Chemical similarity does not establish vitamin K activity. exposure: CoQ10 exposure then discontinuation evidence_span: {"source_cache": "artifacts/coq10-research/9621803.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498", "start_char": 0, "end_char": 752, "text_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498"} [coq10-p9621803] [Interaction between warfarin and coenzyme Q10]. (1998). https://pubmed.ncbi.nlm.nih.gov/9621803/
    Complete structured claim and evidence
  20. INR remained stable and mean warfarin dose did not change significantly during CoQ versus placebo periods.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coq10-research/12772396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14", "start_char": 0, "end_char": 1260, "text_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14"}
    experimental_model
    Randomized double-blind placebo-controlled crossover trial
    exposure
    CoQ10 100 mg/day for four weeks; separate ginkgo and placebo periods
    limitations
    Small short trial with dose adjustment to maintain INR. Same trial was reported in a 2002 letter; not independent replication.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    24 stable warfarin-treated outpatients; three withdrawals
    plain_language
    A small controlled study did not demonstrate the interaction reported in cases.
    primary_references
    [coq10-p12772396] [Effect of Coenzyme Q10 and Ginkgo biloba on warfarin dosage in patients on long-term warfarin treatment. A randomized, double-blind, placebo-controlled cross-over trial]. (2003). https://pubmed.ncbi.nlm.nih.gov/12772396/
    tissue_or_cell_type
    INR and adjusted weekly warfarin dose

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1269–1280

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

    ### coq10-warfarin-trial INR remained stable and mean warfarin dose did not change significantly during CoQ versus placebo periods. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A small controlled study did not demonstrate the interaction reported in cases. organism: 24 stable warfarin-treated outpatients; three withdrawals tissue_or_cell_type: INR and adjusted weekly warfarin dose experimental_model: Randomized double-blind placebo-controlled crossover trial limitations: Small short trial with dose adjustment to maintain INR. Same trial was reported in a 2002 letter; not independent replication. exposure: CoQ10 100 mg/day for four weeks; separate ginkgo and placebo periods evidence_span: {"source_cache": "artifacts/coq10-research/12772396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14", "start_char": 0, "end_char": 1260, "text_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14"} [coq10-p12772396] [Effect of Coenzyme Q10 and Ginkgo biloba on warfarin dosage in patients on long-term warfarin treatment. A randomized, double-blind, placebo-controlled cross-over trial]. (2003). https://pubmed.ncbi.nlm.nih.gov/12772396/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Dietary vanadium overexposure in ducks was associated with lower NADH/FSP1/CoQ10-axis measures and increased hepatic lipid peroxidation and Fe2+ accumulation.

    Ammonium metavanadate → Duck FSP1 / AIFM2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Ammonium metavanadate diets reported as 30 or 45 mg V/kg feed; 42-day duck study.
    limitations
    Observational pathway measurements after exposure, not direct enzyme inhibition or a human ferroptosis mechanism. Methods inconsistently say three and four groups while listing control plus two exposure groups.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    An animal toxicity study links the exposure to a lipid-defense pathway.
    primary_references
    Dual-pathway mechanism of vanadium-induced hepatotoxicity in ducks: Synergistic crosstalk between glucose homeostasis disruption and NADH/FSP1/COQ10 axis-driven ferroptosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41362732/ · DOI 10.7150/ijbs.123482

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 358–364

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ammonium metavanadate diets reported as 30 or 45 mg V/kg feed; 42-day duck study. · source_derived_draft · unverified_draft

    ## vanadium-duck-redox-axis An animal toxicity study links the exposure to a lipid-defense pathway. Dietary vanadium overexposure in ducks was associated with lower NADH/FSP1/CoQ10-axis measures and increased hepatic lipid peroxidation and Fe2+ accumulation. Model: Ammonium metavanadate diets reported as 30 or 45 mg V/kg feed; 42-day duck study. Limitations: Observational pathway measurements after exposure, not direct enzyme inhibition or a human ferroptosis mechanism. Methods inconsistently say three and four groups while listing control plus two exposure groups. Evidence access: Primary full text Dual-pathway mechanism of vanadium-induced hepatotoxicity in ducks: Synergistic crosstalk between glucose homeostasis disruption and NADH/FSP1/COQ10 axis-driven ferroptosis. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41362732/ · DOI 10.7150/ijbs.123482
    Complete structured claim and evidence
  2. SLC25A26 mutations were associated with impaired CoQ10 and lipoic-acid biosynthesis in the functional study.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human mitochondrial disease study and functional models.
    limitations
    This does not demonstrate that oral methionine, SAM, CoQ10 or lipoate repairs the transporter.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    One transport gate connects methyl-donor supply with other cofactors.
    primary_references
    Intra-mitochondrial Methylation Deficiency Due to Mutations in SLC25A26. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26522469/ · DOI 10.1016/j.ajhg.2015.09.013
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 124–130

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human mitochondrial disease study and functional models. · source_derived_draft · unverified_draft

    ## methionine-mitochondrial-cofactor-products One transport gate connects methyl-donor supply with other cofactors. SLC25A26 mutations were associated with impaired CoQ10 and lipoic-acid biosynthesis in the functional study. Model: Human mitochondrial disease study and functional models. Limitations: This does not demonstrate that oral methionine, SAM, CoQ10 or lipoate repairs the transporter. Evidence access: Primary abstract Intra-mitochondrial Methylation Deficiency Due to Mutations in SLC25A26. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26522469/ · DOI 10.1016/j.ajhg.2015.09.013
    Complete structured claim and evidence
  3. The 1990 human lovastatin report observed reductions in circulating CoQ10 during drug exposure in five hospitalized patients and a separately monitored volunteer.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Small uncontrolled clinical series, including pre-existing cardiac disease.
    limitations
    Does not establish causal cardiomyopathy, tissue deficiency or the same effect from a specified red yeast rice product.
    nutrient_topic
    Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
    plain_language
    A constituent has human CoQ observations, with major study limitations.
    primary_references
    [2247468] Lovastatin decreases coenzyme Q levels in humans. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2247468/ · DOI 10.1073/pnas.87.22.8931

    Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 84–90

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Small uncontrolled clinical series, including pre-existing cardiac disease. · source_derived_draft · unverified_draft

    ## red-yeast-rice-human-lovastatin-coq A constituent has human CoQ observations, with major study limitations. The 1990 human lovastatin report observed reductions in circulating CoQ10 during drug exposure in five hospitalized patients and a separately monitored volunteer. Model: Small uncontrolled clinical series, including pre-existing cardiac disease. Limitations: Does not establish causal cardiomyopathy, tissue deficiency or the same effect from a specified red yeast rice product. Evidence access: Primary abstract [2247468] Lovastatin decreases coenzyme Q levels in humans. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2247468/ · DOI 10.1073/pnas.87.22.8931
    Complete structured claim and evidence
  4. The same acute mouse study reported lower cardiac CoQ10 after red yeast rice gavage, with greater suppression at the higher dose.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Male ICR mice, 1 or 5 g/kg oral gavage.
    limitations
    The abstract repeats the heart label in its time-course description; precise tissue-specific onset is not reconstructed from that ambiguous wording.
    nutrient_topic
    Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
    plain_language
    A second tissue showed a measured change.
    primary_references
    [15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 100–106

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Male ICR mice, 1 or 5 g/kg oral gavage. · source_derived_draft · unverified_draft

    ## red-yeast-rice-mouse-ryr-heart-coq A second tissue showed a measured change. The same acute mouse study reported lower cardiac CoQ10 after red yeast rice gavage, with greater suppression at the higher dose. Model: Male ICR mice, 1 or 5 g/kg oral gavage. Limitations: The abstract repeats the heart label in its time-course description; precise tissue-specific onset is not reconstructed from that ambiguous wording. Evidence access: Primary abstract [15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
    Complete structured claim and evidence
  5. Acute red yeast rice gavage at 1 or 5 g/kg reduced hepatic CoQ10 in male ICR mice, with suppression still reported at 24 hours.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Soybean-oil preparation; eight mice per experimental subgroup, sampled from 0.5 to 24 hours.
    limitations
    High-dose rodent exposure; the abstract describes controls killed immediately, so time and feeding controls limit interpretation. No human dose equivalence is inferred.
    nutrient_topic
    Red yeast rice collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Red yeast rice
    plain_language
    The mixture itself was tested in mice at high doses.
    primary_references
    [15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Red yeast rice: constituents, mevalonate, CoQ and product-specific interactions (2026-09-20) · lines 92–98

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Soybean-oil preparation; eight mice per experimental subgroup, sampled from 0.5 to 24 hours. · source_derived_draft · unverified_draft

    ## red-yeast-rice-mouse-ryr-liver-coq The mixture itself was tested in mice at high doses. Acute red yeast rice gavage at 1 or 5 g/kg reduced hepatic CoQ10 in male ICR mice, with suppression still reported at 24 hours. Model: Soybean-oil preparation; eight mice per experimental subgroup, sampled from 0.5 to 24 hours. Limitations: High-dose rodent exposure; the abstract describes controls killed immediately, so time and feeding controls limit interpretation. No human dose equivalence is inferred. Evidence access: Primary abstract [15705235] Acute administration of red yeast rice (Monascus purpureus) depletes tissue coenzyme Q(10) levels in ICR mice. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15705235/ · DOI 10.1079/bjn20041285
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards