Superoxide dismutase, glutathione peroxidase activities and the hydroperoxide concentration are modified in the hippocampus of epileptic rats

被引:120
作者
Bellissimo, MI
Amado, D
Abdalla, DSP
Ferreira, EC
Cavalheiro, EA
Naffah-Mazzacoratti, MD
机构
[1] Univ Fed Sao Paulo, UNIFESP, Escola Paulista Med, Disciplinas Bioquim, BR-04023900 Sao Paulo, SP, Brazil
[2] Univ Fed Sao Paulo, UNIFESP, Escola Paulista Med, Disciplinas Neurol, BR-04023900 Sao Paulo, SP, Brazil
[3] Univ Sao Paulo, Dept Analises Clin & Toxicol, BR-05508900 Sao Paulo, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
pilocarpine; epilepsy; superoxide dismutase; glutathione peroxidase; hydroperoxide;
D O I
10.1016/S0920-1211(01)00269-8
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The relationship between free radical and scavenger enzymes has been found in the epileptic phenomena and reactive oxygen species have been implicated in seizure-induced neurodegeneration. Using the epilepsy model obtained by systemic administration of pilocarpine (PILO) in rats, we investigated the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities as well as the hydroperoxide (HPx) concentration in the hippocampus of rats during status epilepticus (SE). silent and chronic periods. The enzyme activities as well as the HPx concentration were measured using spectrophotometric methods and the results compared to values obtained from saline-treated animals. The SOD activity decreased after long-lasting SE period and during the chronic phase. In addition, FIN levels increased in same periods whereas the GPx activity increased only in the hippocampus of animals submitted to I h of SE. Animals presenting partial seizures, those submitted to 5 h of SE and animals from the silent period (seizure free) showed normal levels of SOD, GPx and HPx. These results show a direct evidence of lipid peroxidation during seizure activity that could be responsible for neuronal damage in the hippocampus of rats, during the establishment of PILO model of epilepsy. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:121 / 128
页数:8
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