This study was conducted to determine if dietary supplementation with coenzyme Q10 (CoQ10), which can act as a potent antioxidant and is an obligatory cofactor of mitochondrial uncoupling protein, suppresses the heat stress (HS)-induced overproduction of mitochondrial reactive oxygen species (ROS) and oxidative damage in the skeletal muscle of birds. The carbonyl protein content of skeletal muscle was significantly higher in birds exposed to HS treatment (34°C, 12 h) than in thermoneutral birds (25°C). This increase was suppressed by CoQ10 supplementation (40 mg/kg diet). Succinate-supported mitochondrial ROS production was increased by HS treatment, and this increase was also suppressed by CoQ10 supplementation. In contrast, CoQ10 supplementation did not affect the HS-induced decrease in mitochondrial proton leak. The mitochondrial membrane potential (ΔΨ), to which HS-induced ROS production was previously shown to be sensitive, tended to be increased by HS treatment, but this rise in ΔΨ was not affected by CoQ10 supplementation. Taken together, these results suggest that dietary CoQ10 supplementation attenuates HS-induced oxidative damage to skeletal muscle, by preventing the overproduction of succinate-supported mitochondrial ROS in a manner that is independent of ΔΨ.
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