Electroconvulsive therapy has been used in the treatment of psychiatric disorders since the 1930s, but little progress has been made in understanding the cellular mechanisms underlying its therapeutic and adverse effects. Electroconvulsive shock (ECS) in animals provides a common experimental model for studying the effects of electroconvulsive therapy in humans. In order to examine the changes of the brain oxidative stress parameters in several brain structures in the early time period after ECS-induced seizures, the levels of lipid peroxidation as well as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the rat hippocampus, cerebellum, frontal cortex and the pons/medulla region were determined at different time points during the first 24 h after single ECS-induced seizures. In the hippocampus and cerebellum the levels of lipid peroxidation were unchanged, while the SOD and GSH-Px activities were significantly increased. Levels of lipid peroxidation and the activities of SOD and GSH-Px were not statistically changed in the pons/medulla region. Levels of lipid peroxidation in the frontal cortex were significantly higher in comparison to the control group at all time points examined while the SOD and GSH-Px activities were not statistically changed. In conclusion, the results of the present study indicate that single ECS causes the rat brain structure-specific alterations in the levels of lipid peroxidation as well as in the SOD and GSH-Px activities at different time points within the first 24 h after the seizures induction. Oxidative lipid damage was evident only in the frontal cortex, while the hippocampus, cerebellum and the pons/medulla region remained oxidatively unaffected in our experimental conditions.