Abstract
Increasing evidence shows that melatonin protected against age-related mitochondrial oxidative damage. However, the protective effects of melatonin against ovarian aging has not been explored. Young Kunming females (aged 2–3 months) were fed with melatonin added to drinking water for 6 or 12 months (mo). We found that long-term (12 mo) melatonin treatment significantly reduced ovarian aging, as indicated by substantial increases in litter size, pool of follicles, and telomere length as well as oocyte quantity and quality. Melatonin treatment suppressed ovarian mitochondrial oxidative damage by decreasing mitochondrial reactive oxygen species (mROS) generation, inhibiting apoptosis, repressing collapse of mitochondrial membrane potential and preserving respiratory chain complex activities. Female mice fed with melatonin had enhanced mitochondrial antioxidant activities, thus reducing the risk of mitochondrial oxidative damage cause by free radicals. Notably, melatonin treatment enhanced SIRT3 activity but not the protein expression level, and increased the binding affinity of FoxO3a to the promoters of both superoxide dismutase 2 (SOD2) and catalase (CAT). In conclusion, melatonin exerted protection against aging-induced fertility decline and maintenance of mitochondrial redox balance.
Highlights
Increasing evidence shows that melatonin protected against age-related mitochondrial oxidative damage
In the ovarian mitochondria from female mice treated with melatonin for 12 mo, adenosine triphosphate (ATP) content (Fig. 5a) and membrane potential (MMP) (Fig. 5b) were significantly higher than in age-matched untreated females
In Chromatin immunoprecipitation (ChIP) assay, we found that sirtuin 3 (SIRT3) promoted the binding of FoxO3a to the promoter of superoxide dismutase 2 (SOD2) and CAT (Fig. 7d)
Summary
Increasing evidence shows that melatonin protected against age-related mitochondrial oxidative damage. We found that long-term (12 mo) melatonin treatment significantly reduced ovarian aging, as indicated by substantial increases in litter size, pool of follicles, and telomere length as well as oocyte quantity and quality. Female mice fed with melatonin had enhanced mitochondrial antioxidant activities, reducing the risk of mitochondrial oxidative damage cause by free radicals. Melatonin modulates mitochondria-related functions and strengthens its antioxidant defense systems, effects facilitated by its amphiphilic nature, enabling it to penetrate all morphophysiological barriers and enter all subcellular compartments. Melatonin and its metabolites were powerful antioxidants and free radical scavengers[13,14] This property enabled them to protect cellular membranes, the electron transport chain and mitochondria from oxidative injury. The use of melatonin to improve age-related mitochondrial oxidative stress in the ovaries seems feasible
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