RESUMEN
Global warming has negatively influenced animal production performance, in addition to animal well-being and welfare, consequently impairing the economic sustainability of the livestock industry. Heat stress impact on male fertility is complex and multifactorial, with the fertilizing ability of spermatozoa affected by several pathways. Among the most significative changes are the increase in and accumulation of reactive oxygen species (ROS) causing lipid peroxidation and motility impairment. The exposure of DNA during the cell division of spermatogenesis makes it vulnerable to both ROS and apoptotic enzymes, while the subsequent post-meiotic DNA condensation makes restoration impossible, harming later embryonic development. Mitochondria are also susceptible to the loss of membrane potential and electron leakage during oxidative phosphorylation, lowering their energy production capacity under heat stress. Although cells are equipped with defense mechanisms against heat stress, heat insults that are too intense lead to cell death. Heat shock proteins (HSP) belong to a thermostable and stress-induced protein family, which eliminate protein clusters and are essential to proteostasis under heat stress. This review focuses on effects of heat stress on sperm quality and on the mechanisms leading to defective sperm under heat stress.
