Melatonin protects bovine oocyte from βHB-induced oxidative stress through the Nrf2 pathway.

Abstract

Accumulation of ketone bodies in the blood or tissues can trigger ketosis, exerting detrimental effects on bovine oocytes maturation. Exposure to its primary component, β-hydroxybutyric acid (βHB), disrupts mitochondrial function, culminating in the excessive buildup of reactive oxygen species (ROS) and subsequent initiation of apoptosis in oocytes. These ultimately result in poor oocyte quality. Melatonin, recognized for its endogenous antioxidant properties, is capable of mitigating ROS levels and enhancing the expression of antioxidant enzymes. In this study, we explored the protective effects of melatonin on the damages induced by βHB. Melatonin was added at a concentration of 10^-9 M to the culture medium on bovine oocytes. Parameters including first polar body extrusion rate, mitochondrial membrane potential, ROS, cell apoptosis were assessed. Results showed that melatonin could restore bovine oocyte maturation rate, enhance mitochondrial function, reduce cell apoptosis rate, and mitigate oxidative stress levels. Notably, Nrf2 signaling pathway inhibitor ML385 significantly attenuated the protective effects of melatonin on oxidative stress induced by βHB exposure. In summary, our study demonstrates that melatonin can protect oocytes from oxidative stress induced by βHB exposure, with indications that this protective mechanism may be mediated through the Nrf2 pathway.