High environmental temperatures observed during the hot months of the year reduce fertility in lactating dairy cows. Summer heat stress depression in fertility is a multifactorial problem that affects physiological and cellular functions in several tissues. It has been shown that in addition to compromise follicular development, hormonal secretion, endometrial and embryonic function, heat stress also markedly reduces oocyte developmental ability. Oocyte susceptibility to elevated temperature can be detected during the germinal vesicle (GV) and oocyte maturation periods. In vivo (heat stress) and in vitro (heat shock) experiments indicated that exposure of bovine oocytes to elevated temperature affects the events required for successful oocyte maturation, fertilization and preimplantation embryonic development. This heatinduced decrease in oocyte function occurs due to a series of cellular alterations that affects nuclear and cytoplasmic compartments of the bovine oocyte. However, thermoprotective molecules such as growth factors and apoptosis inhibitors, which rescue heatinduced oocyte damage and developmental competence, can reverse these cellular changes. Therefore, identification of thermoprotective molecules can be considered as an alternative to modulate the effects of elevated temperature in reproductive function.