Status epilepticus (SE) is a neurological emergency with an associated mortality of 10-12% [1]. Pilocarpine-induced seizure models have provided information on the behavioral and neurochemical characteristics associated with seizure activity [2,3]. Other studies suggest permanent changes in different biochemical systems during SE. An increase in lipid peroxidation, a decrease in GSH content, and excessive free radical formation may occur during SE induced by pilocarpine [4,5].This model can be used to investigate the development of neuropathology in SE [6]. Despite numerous studies clearly indicating the importance of enzyme activity in the epileptic phenomenon, the mechanisms by which these enzymes influence SE are not completely understood [7,8]. Therefore, we decided to study enzymatic activity related to oxidative stress mechanisms during SE [9].Oxidative stress, which is defined as the over-production of free radicals, can dramatically alter neuronal function and has been related to SE [10,11]. It is particularly facilitated in the brain, as the brain contains large quantities of oxidizable lipids and metals, and, moreover, has fewer antioxidant mechanisms than other tissues [8].Free radicals are chemical entities characterized by an orbital containing an unpaired electron [12]. This electron confers on these molecules a strong propensity to react with target molecules by giving or withdrawing one electron from the target molecules to complete their own orbital [13]. Superoxide, a free radical, can be generated in the brain by several mechanisms such as The role of oxidative stress in pilocarpine-induced status epilepticus was investigated by measuring lipid peroxidation level, nitrite content, GSH concentration, and superoxide dismutase and catalase activities in the hippocampus of Wistar rats. The control group was subcutaneously injected with 0.9% saline. The experimental group received pilocarpine (400 mgAEkg )1 , subcutaneous). Both groups were killed 24 h after treatment. After the induction of status epilepticus, there were significant increases (77% and 51%, respectively) in lipid peroxidation and nitrite concentration, but a 55% decrease in GSH content. Catalase activity was augmented 88%, but superoxide dismutase activity remained unaltered. These results show evidence of neuronal damage in the hippocampus due to a decrease in GSH concentration and an increase in lipid peroxidation and nitrite content. GSH and catalase activity are involved in mechanisms responsible for eliminating oxygen free radicals during the establishment of status epilepticus in the hippocampus. In contrast, no correlations between superoxide dismutase and catalase activities were observed. Our results suggest that GSH and catalase activity play an antioxidant role in the hippocampus during status epilepticus.Abbreviations ROS, reactive oxygen species; SE, status elipticus.
