abstract
- Elevated temperature can reduce developmental competence of the preimplantation embryo. Whether an embryo survives elevated temperature depends on its genotype, stage of development, exposure to regulatory molecules and redox status. Following fertilization, the embryo is very sensitive to heat shock. By Days 4-5 after insemination, however, the embryo has acquired increased resistance to elevated temperature. One system that may potentiate embryonic survival at later stages of embryonic development is the apoptosis response-inhibition of apoptosis responses at Day 4 exacerbated effects of heat shock on development. Embryo responses to heat shock at Days 4-5 also depend upon genotype because Bos indicus embryos are more resistant than embryos from non-adapted B. taurus. Some experiments (although not all) indicate that survival following heat shock can be increased by reducing oxygen tension, suggesting involvement of reactive oxygen species or hypoxia-induced factors. Embryonic responses to heat shock are also affected by regulatory molecules that act to modify cellular physiology and improve cell survival. The best characterized of these is insulin-like growth factor-1 (IGF-1). Actions of IGF-1 to allow development following heat shock are independent of its anti-apoptotic actions because inhibition of the phosphatidylinositol-3 kinase pathway through which IGF-1 blocks apoptosis does not prevent thermoprotective effects of IGF-1 on development. Identification of specific determinants of embryonic survival creates the opportunity for new strategies to improve pregnancy rates in animals exposed to heat stress. Many environmental perturbations activate similar cellular responses. Therefore, molecular and cellular systems that improve embryonic survival to heat shock may confer protection from other embryotoxic conditions.