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超氧化物歧化酶、谷胱甘肽过氧化物酶活性以及氢过氧化物浓度在癫痫大鼠的海马体中发生改变。

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

作者信息

Bellissimo M I, Amado D, Abdalla D S, Ferreira E C, Cavalheiro E A, Naffah-Mazzacoratti M G

机构信息

Disciplinas de Neurologia Experimental, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), Rua Botucatu 862, 04023-900 Sao Paulo, Brazil.

出版信息

Epilepsy Res. 2001 Aug;46(2):121-8. doi: 10.1016/s0920-1211(01)00269-8.

DOI:10.1016/s0920-1211(01)00269-8
PMID:11463513
Abstract

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, HPx levels increased in same periods whereas the GPx activity increased only in the hippocampus of animals submitted to 1 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.

摘要

在癫痫现象中已发现自由基与清除酶之间的关系,并且活性氧已被认为与癫痫发作诱导的神经退行性变有关。利用通过对大鼠全身给予毛果芸香碱(PILO)获得的癫痫模型,我们研究了癫痫持续状态(SE)、静止期和慢性期大鼠海马中超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)的活性以及氢过氧化物(HPx)的浓度。使用分光光度法测量酶活性以及HPx浓度,并将结果与盐水处理动物获得的值进行比较。在持久的SE期和慢性期后,SOD活性降低。此外,同期HPx水平升高,而GPx活性仅在经历1小时SE的动物海马中升高。出现部分性发作的动物、经历5小时SE的动物以及静止期(无癫痫发作)的动物,其SOD、GPx和HPx水平正常。这些结果直接证明了在癫痫发作活动期间脂质过氧化,这可能是在PILO癫痫模型建立过程中导致大鼠海马神经元损伤的原因。

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