earticle

영어

Melatonin has antioxidant and scavenger effects in the cellular antioxidant system. It acts by protecting cells from oxidative injury via superoxide-free radicals and hydrogen peroxide (H2O2). Recent studies have shown that treatment with melatonin improves somatic cell nuclear transfer (SCNT) embryo development and increases the success of somatic cell reprogramming. However, the mechanisms for this remain unclear. This research investigated the protective effects and underlying mechanisms of action for melatonin in porcine SCNT embryos under oxidative stress. The results suggested that the developmental competence of porcine SCNT embryos was significantly enhanced after melatonin treatment. In addition, melatonin attenuated the H2O2-induced increase in reactive oxygen species levels, decrease in glutathione levels, and mitochondrial dysfunction. Importantly, melatonin also inhibited phospho-histone γH2A.X expression and comet tail formation, suggesting that it prevents H2O2-induced DNA damage. Meanwhile, the expression of genes involved in homologous recombination (MRE11a, BRAC1, and RAD51) and non-homologous end-joining (PRKDC, XRCC6, and TP53BP1) pathways for the repair of double-stranded breaks was reduced upon melatonin treatment in porcine SCNT embryos on day 5 of development under H2O2-induced oxidative stress. Taken together, these results indicated that melatonin promotes porcine SCNT embryo development by preventing oxidative stress-induced DNA damage via quenching of free radical formation. Our results reveal a previously unrecognized regulatory effect of melatonin in response to oxidative stress and DNA damage. This provides a novel mechanism for the improvements in SCNT embryo development that were reported to be associated with exposure to this hormone.