Du 2017 Evolution
|Du SNN, Khajali F, Dawson NJ, Scott GR (2017) Hybridization increases mitochondrial production of reactive oxygen species in sunfish. Evolution 71:1643-52.|
Abstract: Mitochondrial dysfunction and oxidative stress have been suggested to be possible mechanisms underlying hybrid breakdown, as a result of mito-nuclear incompatibilities in respiratory complexes of the electron transport system. However, it remains unclear whether hybridization increases the production of reactive oxygen species (ROS) by mitochondria. We used high-resolution respirometry and fluorometry on isolated liver mitochondria to examine mitochondrial physiology and ROS emission in naturally occurring hybrids of pumpkinseed (Lepomis gibbosus) and bluegill (L. macrochirus). ROS emission was greater in hybrids than in both parent species when respiration was supported by complex I (but not complex II) substrates, and was associated with increases in lipid peroxidation. However, respiratory capacities for oxidative phosphorylation, phosphorylation efficiency, and O2 kinetics in hybrids were intermediate between those in parental species. Flux control ratios of capacities for electron transport (measured in uncoupled mitochondria) relative to oxidative phosphorylation suggested that the limiting influence of the phosphorylation system is reduced in hybrids. This likely helped offset impairments in electron transport capacity and complex III activity, but contributed to augmenting ROS production. Therefore, hybridization can increase mitochondrial ROS production, in support of previous suggestions that mitochondrial dysfunction can induce oxidative stress and thus contribute to hybrid breakdown.
© 2017 The Author(s). Evolution © 2017 The Society for the Study of Evolution.
• Keywords: Energy metabolism, Oxidative stress, Post-zygotic isolation, Speciation, Temperature, Thermal sensitivity, Ampliflu Red • Bioblast editor: Kandolf G • O2k-Network Lab: CA Hamilton Scott GR
Labels: MiParea: Respiration, Comparative MiP;environmental MiP
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Fishes Tissue;cell: Liver Preparation: Isolated mitochondria
Regulation: Oxygen kinetics Coupling state: LEAK, OXPHOS, ET Pathway: N, S, NS, ROX HRR: Oxygraph-2k, O2k-Fluorometer