engleski

Electroconvulsive schock induced seizures: Changes in GPX and SOD activity

Preserved morphological and functional cell membrane integrity is fundamental for normal functioning of brain cells. Seizure activity, when continued for sufficient time, induces neuronal death (1). Seizures trigger a variety of biochemical processes including an influx of extracellular Ca2+ through voltage-dependent and glutamate-operated channels, activation of membrane phosholipases, liberation of free fatty acids (FFA), diacylglycerols, eicosanoids, lipid peroxides and free radicals (2). These lipid metabolites along with abnormal ion homeostasis may be involved in cell injury and cell death (3). The aim of this study was to determine brain antioxidant enzyme activities in rats with experimentally induced seizures. Electroconvulsive shock (ECS) was applied as a single or in series (every day or every other day). Rats were decapitated 3 min after single ECS and 24 hours after last ECS in models of repeated ECS. Experimentally caused seizures induce the decrease of GPX and SOD activity in all mentioned models. Decreased SOD activity was found in cerebral cortex of all treated animals, in cerebellum of the animals which received repeated ECS, in hippocampus of animals which received single ECS and in pons-medulla region of animals which received daily ECS. Decreased GPX activity was found in cerebral cortex of all treated animals, in hippocampus of the animals which received repeated ECS and in cerebellum and pons-medulla region of animals which received daily ECS. (1) Lees, G.J. (1991) Brain Res., 16, 283 (2) Duggan, L.L., Choi, D.W. (1994) Ann. Neurol., 35, 17 (3) Pellegrini-Giampietro, D.E., Cherci, G., Alesiani, M., Carla, V., Moroni, F. (1988) J Neurochem., 51, 1960

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