Heat stress impairs mitochondria functions and induces oxidative injury in broiler chickens

The objective of this study was to explore the linkage of oxidative stress occurring in mitochondria, skeletal muscles, and plasma in heat stress-challenged broilers. At d 35, 24 broilers were randomly assigned to 2 treatments: rearing at high temperature (32 +/- 1 degrees C; heat stress group) or normal temperature (21 +/- 1.2 degrees C; control) for 7 d. The oxidative damage of lipid, DNA, and protein and the activities of antioxidative enzymes were measured, respectively, in plasma, skeletal muscles (breast and thigh muscles), and skeletal muscle mitochondria. The result showed that heat exposure increased (P < 0.01) plasma concentrations of thiobarbituric acid reacting substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) whereas it deceased total antioxidant capacity (P < 0.05) and ability to inhibit hydroxyl radicals (AIHR; P < 0.001). Protein carbonyl and TBARS levels were increased (P < 0.001) by heat stress in breast and thigh muscles. In skeletal muscle mitochondria, heat stress increased (P < 0.05) 8-OHdG and suppressed AIHR. Plasma activity of superoxide dismutase (SOD) was increased (P < 0.001) whereas glutathione peroxidase (GSH-Px) was suppressed by heat stress (P < 0.001). Heat exposure increased SOD and catalase activities in breast muscle (P < 0.01) but the reverse was true in thigh muscle (P < 0.05). Glutathione peroxidase was increased in thigh muscle (P < 0.001) but was not changed in breast muscle (P > 0.05). Heat stress increased SOD (P < 0.05) and decreased GSH-Px activities (P < 0.05) of mitochondria regardless of muscle types. Plasma allantoin level increased (P < 0.01) correspondingly with urate (P < 0.001) in heat-stressed broilers, indicating that urate could serve as an antioxidant to enhance the antioxidative capacity during stress in a concentration-dependent manner. The activities of respiratory chain complexes I and III were estimated in skeletal muscle mitochondria. Mitochondrial complex I activity was suppressed (P < 0.01) by heat exposure in breast and thigh muscles but complex III activity was elevated only in breast muscle (P < 0.01) of heat-stressed broiler. The fatty acid composition in skeletal muscle was not influenced by heat stress. In conclusion, suppressed mitochondrial complex I activity is associated with oxidative stress induced by heat exposure, which, in turn, is linked with the oxidative damages in muscle tissues and plasma.