Data from: Hybridization increases mitochondrial production of reactive oxygen species in sunfish

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.线粒体功能障碍与氧化应激被认为是杂种衰败的潜在机制，其根源在于电子传递系统呼吸复合体中的核质不相容性。然而，杂交是否会提升线粒体活性氧（reactive oxygen species, ROS）的生成量，目前仍不明确。本研究采用高分辨率呼吸测定法与荧光光度法，对分离的肝脏线粒体进行实验，以探究南瓜籽太阳鱼（*Lepomis gibbosus*）与蓝鳃太阳鱼（*L. macrochirus*）的天然杂交个体的线粒体生理状态及ROS释放情况。当以复合体I（complex I）而非复合体II（complex II）底物支撑呼吸作用时，杂交个体的ROS释放量高于两个亲本物种，且该现象与脂质过氧化水平升高相关。不过，杂交个体的氧化磷酸化（oxidative phosphorylation）呼吸能力、磷酸化效率及氧气动力学参数均介于亲本物种之间。以解偶联线粒体（uncoupled mitochondria）中测得的电子传递能力相对于氧化磷酸化能力的通量控制比分析可知，杂交个体的磷酸化系统所起到的限制作用有所减弱。这一变化或有助于抵消电子传递能力与复合体III（complex III）活性的损伤，但同时加剧了ROS的生成。综上，杂交可提升线粒体ROS的生成量，这支持了此前的假说：线粒体功能障碍可诱导氧化应激，进而参与杂种衰败的发生过程。