Acute exposure to moderately high concentrations of freshly generated cadmium oxide fumes (200-500 µg cadmium/m 3 ) may cause symptoms like the metal fume fever. The present study addressed the effect of Cadmium (Cd) on Oxidative Stress in rat brain. The three months rats were exposed to Cd intraperitonially at concentrations of low dose (1.5mg/kg bw) and high dose (3mg/kg bw) for a period of three weeks. A separate batch of low dose and high dose of Cd exposed rats received Vitamin-E intraperitonially for a week. In this study, we have examined the Glutathione peroxidase (GPX) activity, Glutathione reductase (GR) activity, Glutathione-stransferase (GST) activity, Xanthine oxidase (XO) activity levels and Lipid peroxidation (LP) in three brain regions, Cerebral Cortex, Cerebellum, and Hippocampus. We assessed the biochemical end points indicative of oxidative Stress in these three brain regions. The GPX, GR, and XO activity levels showed significant decrease and the GST activity, LP levels showed significant increase over control rats in dose dependent manner. The exposure to Vitamin-E however to low and high dose of Cd showed recovery, the GPX, GR, and XO activity levels were increased and decreased GST activity, Lipid Peroxidation were observed. The results may be attributed to the reason that the Cd exposure disrupts the functioning of brain which resulted in oxidative deficits. The Vitamin-E lessened the Cd burden in the brain as effective chelating agent decreasing the oxidative stress.