文摘
This study is to examine if Cu2+ can act directly on mitochondria or indirectly by producing reactive oxygen species (ROS), isolated broiler hepatic mitochondria were exposed to different concentrations of Cu2+ (10, 30, 50?μM). Respiratory chain complex activities, ROS generation, respiratory control ratio (RCR) and mitochondrial membrane potential were investigated. Dose-dependent inhibition of respiratory chain complexes and induction of ROS were observed, which coincided with decreasing RCR both with glutamate-?malate or succinate. Further investigation indicated that the membrane potential determined by rhodamine 123 release decreased after CuCl2 exposure at 30 and 50?μM. In addition, the effects of the antioxidants NAC (200?μM) and GSH (200?μM) were studied at 50?μM Cu2+. The results indicate that Cu can induce mitochondrial dysfunction in excessive dose and the effect of Cu2+ exposure on respiratory chain is not site-specific, and antioxidants can protect the mitochondrial function by reducing the formation of free radicals.