Efficacy of catalpol as protectant against oxidative stress and mitochondrial dysfunction on rotenone-induced toxicity in mice brain.

Abstract Rotenone, a specific inhibitor of mitochondrial complex I, reproduces many features of Parkinson's disease. The aim of the study was carried out to investigate how rotenone affected the mitochondrial function and antioxidant/oxidant parameters of mouse striatum, and secondly, to evaluate the ameliorating effects of catalpol against rotenone-induced damage. Our results showed that rotenone induced significant changes in mitochondrial function such as complex I activity and mitochondrial membrane potential decreased, and enhanced antioxidant status as glutathione depletion, enzymatic (glutathione peroxidase and superoxide dismutase) disorders, and increased lipid peroxidation. Catalpol increased complex I, superoxide dismutase and glutathione peroxidase activities, reduced lipid peroxidation and loss of mitochondrial membrane potential in rotenone-treated mice. These in vivo data indicated that catalpol might have protection against deleterious mouse damage caused by rotenone.