Spermidine alleviates heat stress-induced deterioration of porcine oocytes.

Increased global warming is associated with a wide range of risks to human and animal health, including the reproductive disorders. However, the strategies to improve the heat stress (HS)-induced female germ cell defects are still underexplored. Here, we report that spermidine (SPD) treatment is a feasible approach to ameliorate the quality of porcine oocytes under HS. We found that SPD treatment during HS exposure promoted the oocyte maturation as indicated by the increased polar body extrusion rate and cumulus cell expansion area. In the meantime, SPD treatment also restored the spindle/chromosome structure, actin polymerization, and cortical granule dynamics to enhance the oocyte quality. Notably, transcriptome analysis revealed that the favorable effects of SPD treatment against HS exposure was involved in the pathways related to the translation activity and mitochondrial function. We further validated that SPD treatment mitigated translation defects and mitochondrial dysfunction present in HS-exposed oocytes, and hence reducing levels of reactive oxygen species and DNA damage to inhibit the occurrence of apoptosis. In conclusion, our findings demonstrate that SPD can be used to alleviated HS-induced meiotic defects in oocytes, which holds potential applications in improving human and animal reproductive health, and optimizing in vitro reproductive technologies.