Free oxygen radicals which are toxic to the central nervous system are called as neurotoxic agents. Oxidative stress is seen as a result of several pathophysiological events including subarachnoid hemorrhage, edema, ischemia, hypertension, inflammatory reaction and trauma, leading to the production of lipid peroxidation products. In the present study, the malondialdehyde (MDA) level which is a lipid peroxidation product induced by traumatic brain injury as well the reduced glutathione (GSH) levels and glutathione peroxidase (GPx) enzyme activity which are indicators of antioxidant defense system were measured. Moreover, neuroprotective effects of alpha – tocopherol were investigated.             A total of 28 male Wistar rats were used in the present study. First group of rats underwent craniotomy with no trauma and accepted as sham group. The second group underwent craniotomi followed by trauma. The third group received intraperitoneal (i.p) injection of vehicle 8 hours before the craniotomy and trauma. The fourth group treated with i.p. alpha–tocopherol 8 hours before the craniotomy and trauma. All animals were decapitated 12 hours after the end of the treatment.              In the trauma group, MDA levels were significantly higher than the sham and alpha–tocopherol groups (p<0.05). GSH levels were significantly higher in alpha–tocopherol and sham groups compared to the trauma+ vehicle group (p<0.05). However, there was no significant difference between the sham and alpha–tocopherol groups (p>0.05). Although mean GPx activity was slightly higher in sham and alpha–tocopherol groups, there was no statistical difference between the groups.             In conclusion, MDA levels increase and GSH levels decrease in traumatized brain tissue. The results of present study suggest that trauma induces peroxidative cell injury by increasing the oxidative stress. Alpha–tocopherol may have neuroprotective effect by preventing the oxidative stress and related peroxidation.