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氧化应激损伤线粒体参与癫痫病理过程

Oxidative stress damage to mitochondria mediated the pathological processes in epilepsy

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【作者】 刘朝巍张涛杨卓

【Author】 LIU Zhao-wei1,ZHANG Tao1,YANG Zhuo2(Key Laboratory for Biological Active Material of Ministry of Education,1College of Life Science,2College of Medicine,Nankai University,Tianjin 300071,China.)

【机构】 生物活性材料教育部重点实验室 南开大学生命科学院生物活性材料教育部重点实验室南开大学生命科学院南开大学医学院天津300071

【Abstract】 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.

【关键词】 癫痫氧化性应激线粒体自由基
【Key words】 EpilepsyOxidative stressMitochondriaFree radicals
【基金】 国家自然科学基金资助项目(No.30370386;No.30470453)
  • 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,2008年01期
  • 【分类号】R742.1
  • 【被引频次】31
  • 【下载频次】516
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