氧化应激损伤线粒体参与癫痫病理过程3.pdf

1·98 · 中国病理生理杂志 　Ch ine se Jou rnal of Pathop hysiology　2008, 24 ( 1) : 198 - 200 [文章编号 ] 　1000 - 47 18 (2008) 0 1 - 0 198 - 03 氧化应激损伤线粒体参与癫痫病理过程 1 1 2 △ 刘朝巍 , 　张 　涛 , 　杨 　卓 ( 1 2 ) 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 O x ida tive stress dam age to m itochondr ia m ed ia ted the pa tholog ica l processes in ep ilep sy 1 1 2 L IU Zhao - wei , ZHAN G Tao , YAN G Zhuo 1 2 ( Key L abora tory f or B iolog ica l A ctive M a teria l of M in is try of E duca tion, Colleg e of L if e S cience, Colleg e of M ed icine, N anka i Un ivers ity, T ianj in 30007 1, Ch ina. E - m a il: zhuoy ang @ nanka i. edu. cn) 　　【A Rev iew 】　R ecent studies show that ep ilep tic seizu res resu lt in m ass free radical p roduction and induce oxidative dam age becau se of relative deficiency in an ti - oxygen system. M itochondrium is crucial to su stain ing energy m etabolism , regu lating cell death, syn thesising neurotran sm itter and oxidating fatty acid. M itochondrium is not on ly the p lace for free radical p roduction, but also the target of oxidative dam age. M itochondrial oxidative stre ss and re su ltan t dysfunction enhance ep ilep tic su scep tib ility. Seizure - induced free radical