Nutritional regulation of mitochondrial ROS production of chickens exposed to acute and chronic heat stress

Harmful effects of heat stress on organisms are a matter of concern for environmental health and global warming. High ambient temperature, whether it is ‘acute' or ‘chronic' in nature, constitutes a significant hindrance to the growth of animals. Heat-induced reactive oxygen species (ROS) formation may be a factor that causes molecular changes in DNA, proteins, lipids and other biological molecules. To create a method for nutritional regulation of ROS production and protein degradation of skeletal muscle in heat-stressed chickens, we focused on elucidating underlying effects of heat stress on ROS production of skeletal muscle with two models to identify conditions for making broiler chickens more tolerant to heat stress. ‘Acute' heat stress in broiler chickens under 34 °C conditions induces increased mitochondrial ROS production via increased β-oxidation and downregulation of the avian form of mitochondrial uncoupling protein (avUCP), resulting in higher oxidative damage to mitochondrial proteins and lipids. Similarly, ‘chronic' heat stress induces increased ROS production in skeletal muscle mitochondria, probably via elevation of the membrane potential DY in state 4, resulting from enhanced oxygen consumption in the initial stage of heat exposure. However, animals can become acclimatized to environmental heat stress. Muscle protein degradation can occur after a short time (3 d) after heat exposure and this may be due to the activation of ubiquitination by atrogin-1 involved with mitochondrial ROS production. Nutritional regulation of ROS production and protein degradation, such as via enhanced avUCP gene expression, are important for making broiler chickens more tolerant to heat stress.