Division of Life Science, Graduate School of Agricultural Science, Tohoku University, Aoba-ku, Sendai, Japan.
FEBS Lett. 2010 Jul 16;584(14):3143-8. doi: 10.1016/j.febslet.2010.05.057. Epub 2010 May 31.
We previously showed that heat stress stimulates reactive oxygen species (ROS) production in skeletal muscle mitochondria of birds, probably via an elevation in mitochondrial membrane potential (DeltaPsi). To clarify the mechanism underlying the elevation of DeltaPsi, modular kinetic analysis was applied to oxidative phosphorylation in skeletal muscle mitochondria of heat-stressed birds (34 degrees C for 12h). In the birds exposed to heat stress, 'substrate oxidation' (a DeltaPsi-producer) was increased compared to control (24 degrees C) birds, although there was little difference in 'proton leak' (a DeltaPsi-consumer), suggesting that an elevation in the DeltaPsi at state 4 may be due to enhanced substrate oxidation. It thus appears that enhanced substrate oxidation plays a crucial role in the overproduction of ROS for heat-stressed birds, probably via elevated DeltaPsi.
我们之前曾表明，热应激会刺激鸟类骨骼肌线粒体中活性氧（ROS）的产生，这可能是通过提高线粒体膜电位（DeltaPsi）实现的。为了阐明导致 DeltaPsi 升高的机制，我们对热应激鸟类（34°C 12 小时）的骨骼肌线粒体氧化磷酸化进行了模块化动力学分析。在暴露于热应激的鸟类中，与对照组（24°C）相比，“底物氧化”（DeltaPsi 产生者）增加，尽管“质子泄漏”（DeltaPsi 消耗者）差异不大，这表明状态 4 下 DeltaPsi 的升高可能是由于底物氧化增强所致。因此，增强的底物氧化似乎在热应激鸟类中 ROS 的过度产生中起着关键作用，可能是通过升高的 DeltaPsi 实现的。
