LAUSR

Heat stress can compromise most productive functions of mammals and birds raised for agricultural purposes. Many of the deleterious effects of heat stress are a result of physiological adaptations to maintain constant body temperature. These adaptations include reduction in physical activity, reduced feed intake, nutrient repartitioning, redistribution of blood flow from the body core to the periphery, and increased evaporative heat loss. When heat stress becomes greater than can be compensated for physiologically, hyperthermia results and cellular function becomes at risk because of free radical damage, membrane instability, and changes in protein structure. It is well established that effects of heat stress on fertility involve disruption of function of the oocyte and early embryo by direct effects of elevated temperature. It is likely that other physiological systems are also compromised because of cellular damage. There are a variety of molecular systems to limit cellular damage caused by hyperthermia, including antioxidant systems, the endoplasmic reticulum stress response, and heat shock proteins. There has been limited success in mitigating effects of heat stress by manipulating antioxidant status. Cellular resistance to heat stress is subject to genetic variation, and it may be possible to select genetically for cellular resistance to hyperthermia.