367 Oxidative stress and efficiency: The tightrope act of mitochondria in health and disease.

Abstract

Oxidative stress from mitochondrial reactive oxygen species (ROS) production is an unavoidable consequence of aerobic metabolism. High amounts of ROS can cause oxidation but low levels of mitochondrial ROS are now recognized to play important roles in signal transduction. In a pedigree male (PedM) broiler model of feed efficiency (FE), increased ROS production was observed in low FE along with a pervasive protein oxidation. Subsequent proteogenomic studies in muscle have revealed evidence of enhanced mitoproteome abundance, enhanced mechanisms for mitochondrial phosphocreatine shuttling, and enhanced ribosome assembly in the high FE phenotype. In addition, there appears to be enhanced infrastructure that would foster greater repair of damaged proteins or organelles through the autophagy and proteosome pathways in the high FE phenotype. Although protein and organelle degradation, recycling, and reconstruction would be energetically expensive, it is possible energy invested into maintaining optimal function of proteins and organelles contributes to cellular efficiency in the high FE phenotype. In the last 5 years, new findings in mitochondrial physiology have been reported. Reverse electron transport (RET), once considered an artifact of in vitro conditions, has now been demonstrated to play significant roles in inflammation, ischemia-reperfusion, muscle differentiation, and energy utilization. A topology of ROS production indicates that ROS derived from Complex I of the respiratory chain primarily cause oxidative damage, whereas ROS generated from Complex III are primarily involved in cell signaling. Understanding the balancing act that mitochondria play in health and disease will continue to be a vital biological component in health-production efficiency and disease in commercial poultry and livestock production.