Abstract #503

# 503
Reduction in oocyte developmental competence by stress is associated with alterations in mitochondrial function.
Z. Roth*1, 1Department of Animal Sciences, Robert H. Smith Faculty of Agriculture, Food and Environment, the Hebrew University, Rehovot, Israel.

Stress can impact reproductive performance of lactating cows by targeting the ovarian pool of follicles and their enclosed oocyte. Among the documented stressors are heat, environmental and food toxins, metabolic stress and pathogens. Oocytes collected during the hot season are of lower quality than those collected in the winter, as expressed by reduced cleavage rate and lower blastocyst formation. A similar pattern has been reported for oocytes exposed to endocrine-disrupting chemicals or those collected from cows with mastitis or metritis. While the underlying mechanism might differ, accumulating evidence suggests that various stressors impair oocyte mitochondrial functioning. Within the oocyte, mitochondria are involved in ATP generation, calcium homeostasis, regulation of cytoplasmic redox, signal transduction and apoptosis. Summer heat stress is strongly associated with alterations in mitochondrial distribution, an increased proportion of highly polarized mitochondria, and impaired expression of mitochondrion-associated genes, in particular those encoding oxidative phosphorylation complexes for ATP production. Thus, it is proposed that stress reduces ATP levels below the required threshold, compromising the progression of oocyte maturation. Oxidative phosphorylation in mitochondria is the major source of reactive oxygen species (ROS). Under physiological conditions, ROS are essential for nuclear maturation; however, disequilibrium between ROS production and antioxidative capacity might lead to DNA damage and apoptosis, as documented for oocytes exposed to heat stress or environmental toxicants. The review provides new insights into the cellular and molecular responses of the oocyte to stress with an emphasis on the mitochondria. It discusses some strategies to mitigate the effects of stress on the mitochondria, such as incorporation of coenzyme Q10—a key component of the mitochondrial respiratory chain, administration of antioxidants and microinjection of healthy mitochondria. Exploring the oocyte's cellular and molecular responses to a specific stress might enable the development of new strategies to mitigate its effects on fertility.

Key Words: stress, mitochondria, oocyte developmental competence

Speaker Bio
The decline in dairy cattle reproductive performance over the past few decades has caused large economic losses, slowed genetic progress, and impaired efficiency and sustainability of the dairy industry. The phenomenon has been amply described but the underlying causes are only partially understood, and possible solutions are few and limited. The research in my laboratory focuses on stressors that deleteriously affect cow reproduction, with a particular emphasis on the female and male gametes. The two main disrupting stressors include seasonal thermal stress and environmental pollutants. These have global implications, taking into consideration global climate changes (warming) and the increasing awareness of pollutants as biologically active molecules. Another studied stressor is mastitis— a pathogenic stress that is associated with environmental pathogens. The work Roths' laboratory makes use of in-vivo and in-vitro experimental approaches to explore physiological, cellular and molecular alterations. The problem-solving components are based on basic studies and consist of hormonal administration targeted to improving fertility in stressed animals.