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氧化应激损伤线粒体参与癫痫病理过程 被引量：20

Oxidative stress damage to mitochondria mediated the pathological processes in epilepsy
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摘要 Recent studies show that epileptic seizures result in mass free radical production and induce oxidative damage because of relative deficiency in anti-oxygen system.Mitochondrium is crucial to sustaining energy metabolism,regulating cell death,synthesising neurotransmitter and oxidating fatty acid.Mitochondrium is not only the place for free radical production,but also the target of oxidative damage.Mitochondrial oxidative stress and resultant dysfunction enhance epileptic susceptibility.Seizure-induced free radical can influence energy metabolism,destroy DNA construction and induce apoptosis in neurontoxic consequences in epilepsy. Recent studies show that epileptic seizures result in mass free radical production and induce oxidative damage because of relative deficiency in anti- oxygen system. Mitochondrium is crucial to sustaining energy metabolism, regulating cell death, synthesising neurotransmitter and oxidating fatty acid. Mitochondrium is not only the place for free radical production, but also the target of oxidative damage. Mitochondrial oxidative stress and resultant dysfunction enhance epileptic susceptibility. Seizure - induced free radical can influence energy metabolism, destroy DNA construction and induce apoptosis in neurontoxic consequences in epilepsy.
作者 刘朝巍 张涛 杨卓
机构地区 生物活性材料教育部重点实验室 生物活性材料教育部重点实验室
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2008年第1期198-200,共3页 Chinese Journal of Pathophysiology
基金 国家自然科学基金资助项目(No.30370386 No.30470453)
关键词 癫痫 氧化性应激 线粒体 自由基 Epilepsy Oxidative stress Mitochondria Free radicals
分类号 R363 [医药卫生—病理学]
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共引文献34

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中国病理生理杂志
2008年 第1期

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