Effect of Coenzyme Q10 Intake on Endogenous Coenzyme Q Content, Mitochondrial Electron Transport Chain, Antioxidative Defenses, and Life Span of Mice
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The main purpose of this study was to determine whether intake of coenzyme Q10, which can potentially act as both an antioxidant and a prooxidant, has an impact on indicators of oxidative stress and the aging process. Mice were fed diets providing daily supplements of 0, 93, or 371 mg CoQ10 /kg body weight, starting at 3.5 months of age. Effects on mitochondrial superoxide generation, activities of oxidoreductases, protein oxidative damage, glutathione redox state, and life span of male mice were determined. Amounts of CoQ9 and CoQ10, measured after 3.5 or 17.5 months of intake, in homogenates and mitochondria of liver, heart, kidney, skeletal muscle, and brain increased with the dosage and duration of CoQ10 intake in all the tissues except brain. Activities of mitochondrial electron transport chain oxidoreductases, rates of mitochondrial O2-* generation, state 3 respiration, carbonyl content, glutathione redox state of tissues, and activities of superoxide dismutase, catalase, and glutathione peroxidase, determined at 19 or 25 months of age, were unaffected by CoQ10 administration. Life span studies, conducted on 50 mice in each group, showed that CoQ10 administration had no effect on mortality. Altogether, the results indicated that contrary to the historical view, supplemental intake of CoQ10 elevates the endogenous content of both CoQ9 and CoQ10, but has no discernable effect on the main antioxidant defenses or prooxidant generation in most tissues, and has no impact on the life span of mice.
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Although beneficial, lifelong supplementation with CoQ10 may also be deleterious.
“Although beneficial, lifelong supplementation with CoQ10 may also be deleterious [92,93,94].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [92]
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- Authors
- Sohal, R. S., Kamzalov, S., Sumien, N., Ferguson, M., Rebrin, I., Heinrich, K. R., & Forster, M. J.
- Affiliations
- University of Southern California (US)
- University of North Texas Health Science Center (US)
- Corresponding author
- Sohal, Rajindar S.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2006-02
- Volume
- 40
- Issue
- 3
- Pages
- 480-487
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC2834650
- OpenAlex
- W2071820285
- Cited by
- 131
- References
- 44
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 5 · 2023: 3 · 2022: 4 · 2021: 8 · 2020: 5 · 2019: 9 · 2018: 7 · 2017: 1 · 2016: 7 · 2015: 5 · 2014: 4 · 2013: 6 · 2012: 6
- FWCI
- 2.52
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01 AG17526, R01AG007657, R01AG017526)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- coenzyme Q10, dietary supplementation, mitochondrial electron transport chain, oxidative stress, antioxidant defense, protein carbonylation, glutathione redox state, superoxide dismutase, catalase, glutathione peroxidase, aging, lifespan, pro-oxidant activity
- MeSH terms
- Aging, Animals, Antioxidants, Catalase, Coenzymes, Electron Transport, Glutathione, Glutathione Peroxidase, Male, Mice, Inbred C57BL, Mitochondria, Oxidation-Reduction, Oxidoreductases, Superoxides, Superoxide Dismutase, Ubiquinone, Oxidative Stress, Dietary Supplements, Mice
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