Oxidative-stress-mediated apoptosis triggered by microplastics disrupts bovine oocyte maturation

With the extensive use of plastic products, microplastics (MPs) have become environmental contaminants distributed worldwide. Although MPs have been reported to exert toxic effects on oocytes in rodents and pigs, their impact on ruminant oocytes and the underlying mechanisms remain unclear. In this study, bovine oocytes were exposed to MPs (0-200 μg/mL) during in vitro maturation to evaluate their toxic effects and mechanisms. MP exposure markedly impaired cumulus expansion, reduced the first polar body (PB1) extrusion rate, and decreased both cleavage and blastocyst formation rates. Moreover, MPs induced mitochondrial dysfunction, as evidenced by abnormal mitochondrial morphology, decreased mitochondrial membrane potential (MMP), and reduced ATP production. These alterations were accompanied by the excessive accumulation of reactive oxygen species (ROS), leading to oxidative stress and apoptosis. Mechanistically, MPs increased the expression of the proapoptotic proteins BAX and cleaved CASP-3 and increased the proportion of Annexin V-positive oocytes. Importantly, supplementation with 0.5 μM melatonin significantly alleviated MPs-induced damage by restoring mitochondrial function, reducing ROS accumulation, and suppressing apoptosis, thereby improving oocyte maturation and subsequent embryonic development. Collectively, these findings demonstrate that MPs impair bovine oocyte quality by inducing mitochondrial dysfunction-mediated oxidative stress and apoptosis. Melatonin, as a potent endogenous antioxidant, effectively mitigates MP-induced cytotoxicity, highlighting its protective role in improving oocyte developmental competence under environmental stress.