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 (ΔΨ). To clarify the mechanism underlying the elevation of ΔΨ, modular kinetic analysis was applied to oxidative phosphorylation in skeletal muscle mitochondria of heat-stressed birds (34°C for 12. h). In the birds exposed to heat stress, 'substrate oxidation' (a ΔΨ-producer) was increased compared to control (24°C) birds, although there was little difference in 'proton leak' (a ΔΨ-consumer), suggesting that an elevation in the ΔΨ 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 ΔΨ.
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