Open AccessMelatonin improves age-induced fertility decline and attenuates ovarian mitochondrial oxidative stress in mice
Author(s) -
Chao Song,
Wei Peng,
Shutao Yin,
Jiamin Zhao,
Binying Fu,
Jingcheng Zhang,
Tingchao Mao,
Haibo Wu,
Yong Zhang
Publication year - 2016
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/srep35165
Subject(s) - melatonin , oxidative stress , sod2 , sirt3 , reactive oxygen species , superoxide dismutase , catalase , medicine , oxidative phosphorylation , endocrinology , mitochondrion , mitochondrial ros , biology , andrology , microbiology and biotechnology , biochemistry , enzyme , sirtuin , nad+ kinase
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.