Oxidative metabolism and efficiency: the delicate balancing act of mitochondria

Mitochondria are responsible for roughly 90% of the ATP produced in a cell. A consequence of aerobic metabolism is oxidative stress that results from production of mitochondrial reactive oxygen species (ROS) due to inefficiency of electron transport. Several antioxidant-redox coupled reactions in the mitochondria help minimize oxidative damage in the mitochondria. These redox reactions not only protect mitochondria from oxidative damage but also are important in regulating cellular redox status. Oxidative stress from mitochondrial ROS occurs in broilers in pulmonary hypertension syndrome, heat stress, and in the phenotypic expression of feed efficiency. Low levels of mitochondrial ROS are now recognized to play important roles in signal transduction mechanisms. A topology of ROS production has been reported that indicates that ROS derived from Complex I primarily cause oxidative damage, whereas ROS generated from Complex III are primarily involved in cell signaling. Reverse electron transport, once considered an artifact of in vitro conditions, now plays significant roles in physiological conditions including inflammation, ischemia-reperfusion, muscle differentiation, and energy utilization. Understanding the balancing act that mitochondria play in health and disease will continue to be vital biological component of improving efficiency in animal production.