Meeting Abstract
Mitochondria are central to energy transformation in animals but the cascade of electron transfer from oxidative fuels to the terminal formation of water is not completely efficient: some electrons can prematurely escape. As these electrons ‘leak’ from the canonical electron transfer pathways they contribute to the formation of reactive oxygen species (ROS) such as superoxide and H2O2. These mitochondrial ROS have been implicated with growth and performance trade-offs, signalling, as well as with aging and senescence related declines in function; although, the latter relationship has become somewhat beleaguered. However, relatively few studies have delved deeply into comparing and explaining differences in mitochondrial electron leak across species. Complicating such comparisons, there are > 10 potential sites of significant electron leak in mitochondria. The many candidate sites of ROS formation, combined with differential reliance on intramitochondrial antioxidant systems, makes it complex to derive straightforward comparisons across or within species. But the magnitude and nature of mitochondrial superoxide/H2O2 formation is intrinsically linked to mitochondrial energetics. Therefore this complex system can often be best understood by assessing multiple levels of mitochondrial function. Here the convoluted interrelationships mitochondrial ROS metabolism has with respiration rate, membrane potential, and electron carrier reduction state are examined. In doing so the importance of tissue type, assay condition and the means of normalizing data for comparison across muscle mitochondria from endotherm and ectotherm vertebrates will be considered.
