Melatonin prevents oocyte deterioration due to cotinine exposure in mice†

Cotinine, the major metabolite of nicotine and a key component in cigarette smoke, causes poor oocyte quality, which could be rescued by melatonin supplementation during meiotic maturation in mouse oocytes. Levels of cotinine, a major metabolite of nicotine, have been positively correlated with risks of cigarette smoking-related diseases. Melatonin is synthesized by the pineal gland and has been demonstrated to be beneficial to oocyte maturation due to its antioxidative activity. In this study, we investigated the effects of cotinine on mouse oocyte meiosis and the protective roles of melatonin in vitro and in vivo. The results showed that cotinine exposure caused defects in the first polar body extrusion and reduced parthenogenetic activation in in vitro-matured oocytes. Additionally, cotinine exposure increased the level of oxidative stress, which resulted in aberrant actin distribution, abnormal spindle morphology, chromosome misalignment, and even oocyte aneuploidy. Simultaneously, cotinine exposure decreased the mitochondrial membrane potential and antioxidant gene expression and increased apoptosis-related gene expression. However, all these toxic effects of cotinine could be reversed after the addition of melatonin, and the mechanism may be a decrease in reactive oxygen species production. In conclusion, cotinine causes poor oocyte quality, which could be rescued by melatonin supplementation during meiotic maturation in mouse oocytes.

Automated summary

The major nicotine metabolite cotinine negatively affects mouse oocyte meiosis, leading to poor quality, while supplementation with melatonin can protect oocytes by reducing oxidative stress levels and abnormal occurrences.