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Supplementation with ubiquinol 10 has been shown to improve the health of experimental animals and elderly individuals. The present study investigated the effects of lifetime supplementation with ubiquinol 10 on the progression of aging and lifespan in C57BL/6 mice, a standard strain for biomedical and aging research. A diet containing ubiquinol 10 (0.3 % w/w) and a control diet were fed to female C57BL/6J mice from 8 weeks of age until death, and the progression of senescence, lifespan, and physiological and pathological findings were examined. Body weights increased until 72 weeks of age and then decreased gradually in both groups. Food intake was significantly higher in the ubiquinol 10 group until 56 weeks of age. The median, 10th decile (10 % survivors), and maximum lifespans and survival curves did not significantly differ between the ubiquinol 10 and control groups. The grading score of senescence improved only at the age of 48 weeks in ubiquinol 10 group. No significant differences were observed in major physiological markers, such as the glucose tolerance test, serum triglycerides, and cholesterol concentrations. The expression levels of genes regulating aging in the liver markedly decreased with age in both groups. Organ weights did not significantly differ, except for significantly lighter brown adipose tissue in the ubiquinol 10 group. Senile AApoAII amyloidosis was noted in old mice; however, the degree of amyloid deposition was similar in the two groups. The degree of senescence only improved in middle-aged mice (48 weeks of age), and no apparent anti-aging or lifespan-extending effects were observed with lifetime supplementation with ubiquinol 10 in female C57BL/6J mice, which are standard laboratory mice considered to exhibit normal aging processes. • In this study, we investigated the long-term effects of dietary supplementation with ubiquinol 10, the reduced form of coenzyme Q10, on aging progression and lifespan in C57BL/6J mice. • In our previous research, we demonstrated the anti-aging effects of ubiquinol-10 and clarified its molecular mechanisms through studies using senescence-accelerated mice (SAMP1) and obese mice with type 2 diabetes (KK-Ay). These studies demonstrated that ubiquinol 10 improved mitochondrial function, reduced oxidative stress, activated AMP-activated protein kinase (AMPK), and increased the expression of genes regulating aging, such as Sirt1, Ppargc1a, and Ppara (Tian et al., 2014; Xu et al., 2017). Although ubiquinol 10 has demonstrated promising anti-aging effects in accelerated aging and metabolic disorder models, our results show that it did not significantly alter the lifespan or progression of aging in normal-aging and most commonly used laboratory mice. However, we observed a significant improvement in senescence grading scores during middle age, suggesting partial anti-aging effects under physiological aging conditions. • We believe that our findings provide meaningful insights into the context-dependent efficacy of ubiquinol 10 and its potential limitations in healthy aging models. This study contributes to the understanding of age-related interventions and may be of interest to the readers of Experimental Gerontology.
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Igarashi et al. (2025) studied this question.
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