Thermotolerance for Physiological and Endocrine Regulation of Embryo-Uterine Development

Abstract

Hyperthermia affects most aspects of reproductive performance in mammals by compromising the physiology of reproductive tract, through hormonal imbalance, disrupting the development and maturation of oocyte, causing embryonic mortality, abortion, growth retardation, and major developmental defects. Heat stress reduces the steroidogenic capacity of its theca and granulosa cells by altering the efficiency of follicular selection resulting in drop of luteinizing hormone and estradiol secretions from the dominant follicle in the plasma, reduced intensity, and duration of estrus expression. The mechanism for the developmental stage-dependent change in heat tolerance is considered to be the accumulation of antioxidants in embryos in response to heat-inducible production of reactive oxygen species. Morula or blastocysts can repair heat-induced misfolded or unfolded proteins or facilitate DNA damage induced apoptosis. Therefore, embryo transfer (ET) that can bypass the heat-sensitive stage could be a good solution to improve the conception rate under heat stress. However, further research is required to improve the reduction in pregnancy rates due to summer heat stress.