Oxidative stress in the hippocampus after pilocarpine-induced status epilepticus in Wistar rats
Oxidative stress in the hippocampus after pilocarpine-induced status epilepticus in Wistar rats
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DOI：
10.1111/j.1742-4658.2004.04537.x
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发表时间：
2005-03-01
期刊：
影响因子：
5.4
通讯作者：
Fonteles, MMF
中科院分区：
文献类型：
--
作者：
Freitas, RM;Vasconcelos, SMM;Fonteles, MMF
通过测定大鼠海马区脂质过氧化水平、亚硝酸盐含量、谷胱甘肽含量、超氧化物歧化酶和过氧化氢酶活性，探讨氧化应激在匹罗卡品诱发癫痫持续状态中的作用。对照组皮下注射0.9%生理盐水。试验组皮下注射匹罗卡品400 mg·kg~(-1)。两组均于治疗后24小时处死。癫痫持续状态诱导后，脂质过氧化水平和亚硝酸盐浓度显著升高(分别为77%和51%)，而谷胱甘肽含量下降55%。过氧化氢酶活性增加了88%，但超氧化物歧化酶活性保持不变。这些结果表明，由于GSH浓度下降，脂质过氧化和亚硝酸盐含量增加，海马神经元损伤。谷胱甘肽和过氧化氢酶活性参与了在海马区癫痫持续状态建立过程中清除氧自由基的机制。相反，没有观察到超氧化物歧化酶和过氧化氢酶活性之间的相关性。我们的结果表明，在癫痫持续状态期间，GSH和过氧化氢酶活性在海马区起着抗氧化作用。
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 mg.kg(-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.