Mitochondrial Physiology, Oxidative Stress, and Animal Production Efficiency

Mitochondria produce ~90% of the ATP in a cell and a major source of oxidative stress due to generation of reactive oxygen species (ROS). Mitochondrial ROS are produced when electrons leak from the electron transport chain (ETC) causing univalent reduction of oxygen to superoxide that leads to additional ROS (e.g. hydroxyl radical, hydrogen peroxide) as well as reactive nitrogen species. If not metabolized by antioxidants, these reactive molecules can oxidize membranes, proteins, and DNA. For decades, site-specific defects in electron transport were attributed to electron leak primarily from Complexes I and III of the ETC due to electon movement in the forward direction (towards the terminal electron acceptor, oxygen); observations of reverse electron flow were thought to only occur in vitro. Recent research, however, indicates that reverse electron flow contributes to physiologically relevant conditions; e.g. aging, inflammation, ischemia-reperfusion injury, chemoreception, and muscle differentiation. Furthermore, ROS produced at Complex I appears to be responsible for most of the ROS-mediated oxidative damage, whereas ROS produced at Complex III may be primarily involved in signal transduction. We reported elevated mitochondrial ROS production due to site-specific defects in electron transport in Complex I and III in Pedigree Male (PedM) broilers exhibiting low feed efficiency (FE) compared to a high FE phenotype. Higher mitochondrial ROS production was likely responsible for the pervasive protein oxidation present in the low FE PedM phenotype. As ROS can stimulate signal transduction in addition to oxidation, we hypothesized that gene expression in the low FE phenotype gene expression was the product of inherent gene expression modulated by mitochondrial ROS. With this in mind, proteogenomic studies were conducted on breast muscle from PedM broilers exhibiting high and low FE phenotypes. These studies have provided insight into the cellular basis of FE that include progesterone signaling, ribosomal assembly, mitochondrial phosphocreatine and ADP-ATP shuttling, proteosome expression, and the autophagy pathway that were enhanced in the high FE phenotype. While these findings are interesting academically, we hope that they may provide clues for genetic markers or for emerging technologies to continue to make improvements in poultry and livestock production efficiency.