Heat stress during maturation of bovine oocytes profoundly impacts the mitochondrial bioenergetic profile and causes endoplasmic reticulum stress in subsequent blastocysts†.

Abstract

In dairy cows, detrimental effects of global warming and intensive genetic selection for high milk yield on reproductive performance have become increasingly relevant in cooler regions. Based on the current knowledge, we hypothesized that elevated temperature during oocyte maturation affects mitochondria and endoplasmic reticulum in parallel with mitochondrial dysfunction, representing the mechanistic link between reactive oxygen species and endoplasmic reticulum stress. To prove that the present study aimed to uncover the consequences of heat stress during oocyte maturation on mitochondrial health, cellular oxidative stress response, and its implications for endoplasmic reticulum stress. Immature bovine oocytes were matured either under routine temperatures (38.8°C, Control) or exposed to elevated temperatures (41°C, heat stress). Metaphase II (MII) oocytes and subsequent blastocysts were analyzed in terms of developmental capacity, mitochondrial membrane potential, the bioenergetic profile, reactive oxygen species level, and expression of candidate genes playing a role in oxidative stress, endoplasmic reticulum stress, and apoptosis. While no effect on matured oocytes became obvious, heat stress embryos demonstrated typical alterations of the mitochondrial bioenergetic profile in terms of higher mitochondrial membrane potentials not going along with higher ATP-linked oxygen consumption, significantly lower maximum respiration, and spare capacity rates, implicating less efficient mitochondria accompanied with significantly higher reactive oxygen species levels. Moreover, gene expression of heat stress embryos supported the assumption that mitochondria are the mechanistic link between oxidative stress and endoplasmic reticulum stress, impairing early embryo development by promoting apoptosis.