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Reduced Coenzyme Q10 Decelerates Senescence and Age-Related Hearing Loss in Senescence-Accelerated Mice by Activating Mitochondrial Functions.

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Coenzyme Q in Aging

Abstract

Coenzyme Q (CoQ) is present in all cellular and organelle membranes, in organisms ranging from yeast to humans. CoQ is synthesized exclusively in the mitochondrial inner membrane from farnesyl pyrophosphate via the mevalonate pathway. Meanwhile, CoQ in foods or medicines is converted to the reduced form (CoQH2: ubiquinol) in small intestine epithelia before absorption. Previous studies in humans and rodents suggest that coenzyme Q10 (CoQ10) supplementation mitigates cardiomyopathies, age-related declines in myocardial and arterial function, and some neurodegenerative disorders. CoQ10 also has beneficial effects in the aging process and lessens age-related hearing loss in animal models. Using Senescence-Accelerated Mouse Prone 1 (SAMP1) mice, we demonstrated that the reduced form of CoQ10 (CoQ10H2: ubiquinol-10) has more potent anti-aging effects than the oxidized form of CoQ10 (CoQ10: ubiquinone-10). SAMP1 mice receiving lifelong supplementation with either 0.2 or 0.5% CoQ10H2 had lower senescence grading scores than untreated control mice. Microarrays containing 45,100 probe sets identified several peroxisome proliferator-activated receptor-α (PPAR-α)-associated genes that were upregulated in the livers of the SAMP1 mice given CoQ10H2. Our recent results show that CoQ10H2 may enhance mitochondrial activity by increasing levels of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor c coactivator 1α (PGC-1α), and SIRT3 that protect against the progression of aging and age-related diseases.

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Correspondence to Jinko Sawashita .

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Sawashita, J., Zhe, X., Higuchi, K. (2020). Reduced Coenzyme Q10 Decelerates Senescence and Age-Related Hearing Loss in Senescence-Accelerated Mice by Activating Mitochondrial Functions.. In: López Lluch, G. (eds) Coenzyme Q in Aging. Springer, Cham. https://doi.org/10.1007/978-3-030-45642-9_9

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