Impact of Heat Stress on Embryonic Implantation

Abstract

One of the expected effects of mammalian developmental defects is a rise in air temperature. Heat stress adversely affects embryo oogenesis, oocyte maturation, fertilization, and implantation. The number of defects caused by heat stress in all mammals is almost identical, but each species has its own particular sensitivity to specific defects. It suggests that genotype may have a significant effect on the type of defect, its occurrence, and its extent. By heat output and loss, the body temperature is usually preserved in a restricted range, but the equilibrium can be disrupted by illness, inadequate nutrition, and severe environmental temperature. Elevated maternal temperature during pregnancy, either by fever or any other means of heating, may result in embryo death, retarded development, abortion, and many embryonic defects such as cell proliferation, migration, differentiation and apoptosis or programmed cell death, structural and functional defects, and changes in maternal physiology. Maternal heat stress also reduces the levels of placental hormones. This chapter deals with the heat stress effect on reduction of reproductive function, implantation defects, etc. of different animals and humans.