Mitochondria-produced reactive oxygen species (ROS) are thought to contribute to cell death caused by a multitude of pathological conditions. However, low physiologically relevant concentration of reactive oxygen species could be useful and essential to regulate a variety of key molecular mechanisms. Rotenone exposure has been reported to produce an in- vivo experimental model of Parkinson’s disease by inhibiting the mitochondrial function and eliciting oxidative stress. Thus, this study was conducted to evaluate the probable preventive