Short-term heat stress induces mitochondrial degradation and biogenesis and enhances mitochondrial quality in porcine oocytes.

Mitochondria in oocytes play important roles in many processes, including early embryo development. Promotion of mitochondrial degradation and biogenesis through Sirtuin 1 (SIRT1) activation enhances mitochondrial function and oocyte quality. Previous studies that used somatic cells have shown that short-term heat stress (SHS) induces SIRT1-regulated mitochondrial biogenesis. In this study, we examined whether SHS can induce mitochondrial degradation and biogenesis in porcine oocytes. We collected cumulus cell-oocyte complexes (COCs) from prepubertal gilt ovaries acquired from a slaughterhouse. COCs were treated at 41.5 °C (vehicle: 38.5 °C) for the first one hour of in vitro maturation, and the mitochondrial kinetics, oocyte function, and developmental competence of oocytes were examined. SHS increased the expression level of heat shock protein 72, which induced the high expression of SIRT1 and the phosphorylation of AMP-activated protein kinase. SHS did not alter the mitochondrial DNA copy number in oocytes, but induced mitochondrial degradation and biogenesis, which enhanced the mitochondrial membrane potential and ATP content in oocytes, and improved the ability of the oocytes to develop into blastocysts.