Protons overproduction

Heat stress is an environmental factor responsible for oxidative stress. We reported that reactive oxygen species (ROS) production by mitochondria was significantly increased in skeletal muscle of birds after exposure to heat stress (Mujahid et al., 2007), and that muscle mitochondria from heat-stressed birds also had the higher mitochondrial membrane potential (AT) (M. Kikusato, unpublished data). These results implied that the overproduction of ROS may depend on AT. We also found that heat stress significantly decreased avian uncoupling protein (avUCP) in muscle mitochondria (Mujahid et al., 2009). Therefore, this decrease may contribute to excess ROS production, possibly via a depression of inducible proton leak. To elucidate more precisely the mechanism involved in the overproduction of mitochondrial ROS under heat stress conditions, we have attempted to clarify how heat stress-induced ROS production depends on AT, and to evaluate the effect of avUCP downregulation on the inducible proton leak. 

In conclusion, heat stress increased AT due to enhanced substrate oxidation and deereased proton leak, thereby leading to the overproduction of mitochondrial ROS in muscle mitochondria of birds. The downregulation of avUCP content (data not shown) imder heat-stress conditions could also contribute to the overproduction of ROS via a depression in FFA-inducible proton leak. 

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