Acute Seizure Activity Promotes Lipid Peroxidation, Increased Nitrite Levels and Adaptive Pathways Against Oxidative Stress in the Frontal Cortex and Striatum
Previous experiments have shown that the generation of free radicals in rat brain homogenates is increased following pilocarpine-induced seizures and status epilepticus (SE). This study was aimed at investigating the changes in neurochemical mechanisms such as lipid peroxidation levels, nitrite content, glutathione reduced (GSH) concentration, superoxide dismutase and catalase activities in the frontal cortex and the striatum of Wistar adult rats after seizures and SE induced by pilocarpine. The control group was treated with 0.9% saline and another group of rats received pilocarpine (400 mg/kg, i.p.). Both groups were sacrificed 24 h after the treatments. Lipid peroxidation level, nitrite content, GSH concentration and enzymatic activities were measured by using spectrophotometric methods. Our findings showed that pilocarpine administration and its resulting seizures and SE produced a significant increase of lipid peroxidation level in the striatum (47%) and frontal cortex (59%). Nitrite contents increased 49% and 73% in striatum and frontal cortex in pilocarpine group, respectively. In GSH concentrations were decreases of 54% and 58% in the striatum and frontal cortex in pilocarpine group, respectively. The catalase activity increased 39% and 49% in the striatum and frontal cortex, respectively. The superoxide dismutase activity was not altered in the striatum, but it was present at a 24% increase in frontal cortex. These results suggest that there is a direct relationship between the lipid peroxidation and nitrite contents during epileptic activity that can be responsible for the superoxide dismutase and catalase enzymatic activity changes observed during the establishment of seizures and SE induced by pilocarpine.