In vivo effects of high dietary copper levels on hepatocellular mitochondrial respiration and electron transport chain enzymes in broilers.

The diet of broiler chickens supplemented with increasing concentrations of copper (Cu) was assessed for the effect of Cu on liver mitochondrial function. A total of 160, 1-d-old Cobb 500 broilers (Gallus domesticus) were randomly assigned in equal numbers into 4 groups, which differed in the concentration of copper supplements in the diet; 11 (control), 110, 220 and 330 mg of Cu/kg dry matter. Liver mitochondrial function was recorded at 12, 24, 36, 48 and 60 d of age. Supplementation with 110 mg Cu/kg dry matter enhanced mitochondrial function and activities of complexes I-V, and this was significant at 36 d of age compared with the other diets (P < 0.05). Supplementation with 220 mg Cu/kg dry matter and 330 mg Cu/kg dry matter enhanced mitochondrial function and activities of complexes I-V at 12, 24 and 36 d of age, but displayed reduced function (P < 0.05) at 48 and 60 d of age except in complex IV (P > 0.05). Mitochondrial hydrogen peroxide (H2O2) production was also increased (P < 0.05) with an increase of copper supplementation in the diet. The results indicate that appropriate dietary copper supplements are sufficient for improving mitochondrial function and activities of the respiratory complexes. Higher concentrations of copper, on the other hand, lead to copper toxicity by affecting certain respiratory complexes.