锰对大鼠脑线粒体能量代谢及氧化损伤影响  

Effect of manganese exposure on energy metabolism and oxidative damage of mitochondria in rat brain

作　　者：张芳林[1] 徐兆发[1] 高键[1] 徐斌[1] 邓宇[1] 贾克[1] 

机构地区：[1]中国医科大学公共卫生学院环境卫生学教研室,沈阳110001

出　　处：《中国公共卫生》2008年第8期954-955,共2页Chinese Journal of Public Health

基　　金：辽宁省教育厅科学研究项目(2004C025)

摘　　要：目的通过N-乙酰半胱氨酸(NAC)干预研究锰对大鼠脑纹状体和皮质线粒体能量代谢和氧化损伤的影响。方法Wistar大鼠24只,按体重随机分成3组:对照组、MnCl2组、NAC预处理组,连续染毒21 d。取大鼠脑纹状体和皮质,梯度离心获得线粒体,测量顺乌头酸酶、线粒体复合体I活性,丙二醛(MDA)、还原型谷胱甘肽(GSH)含量和线粒体膜电位。结果与对照组比较,MnCl2组顺乌头酸酶〔(18.64 nmol/(min.mg pro)〕线粒体复合体I〔(48.92nmol/(min.mg pro)〕的活性显著降低;MDA含量〔37.98nmol/(g pro)〕显著升高,GSH含量〔3.99μmol/(g pro)〕显著降低;线粒体膜电位(荧光强度为25.54)显著降低(P<0.05)。与MnCl2组比较,NAC预处理组顺乌头酸酶〔(22.95nmol/(min.mg pro)〕、线粒体复合体I〔(66.89nmol/(min.mg pro)〕的活性显著升高;MDA含量〔(31.44 nmol/(g pro)〕显著降低,GSH含量〔5.56μmol(g pro)〕显著升高;线粒体膜电位(荧光强度为37.71)显著升高(P<0.05)。结论锰可导致大鼠脑线粒体能量代谢障碍和氧化损伤;NAC预处理能有效预防锰所致大鼠脑线粒体能量代谢障碍和氧化损伤。Objective To explore the effect of MnCl2 exposure on energy metabolism and oxidative damage of mitochondria in rat brain and the preventive effect of NAC. Methods 24 Wistar rats were randomly divided into control group （NaCI）, MnCl2 group, NAC pretreatment group by body weight. The rats were given injection for 21d. The animals in all groups were decapitated and the samples of striatum and cortex were collected. Mitochondria were prepared using differential centrifugation. The activities of aconitase, mitochondrial complex I, the level of MDA, GSH and mitochondrion membrane potential were investigated. Results Compared with the control group, the activities of aconitase （ 18.64nmol/min. mg pro）, mitochondrial complex Ⅰ（48.92 nmol/（min·mg pro））in MnC12 group were significantly decreased.The level of MDA[37.98 （nmol/g· pro） ） in MnC12 group was significantly increased. The level of GSH [3.99 mol/（g·pro） ） in MnCl2 group was significantly decreased. The mitochondrion membrane potential（Light density was 25.54） in MnCl2 group was significantly decreased （ P 〈 0.05）. Compared with MnCl2 group, the activities of aconitase （22.95 nmol/（min·mg· pro） ）, mitochondrial complex Ⅰ （66.89 nmol/（min, mgopro））in NAC pretreated group were significantly increased. The level of MDA （31.44 nmol/（g· pro））in NAC pretreated group was significamly decreased. The level of GSH [5.56 umol/（g· pro））in NAC pretreated group was significantly increased. The mitochondrion membrane potential （Light density was 37.71） in NAC pretreated group was significantly increased （ P 〈 0.05 ）. Conclusion Manganese could induce the decline of energy metabolism and cause oxidative damage of mitochondria in rat brain. And the change could be prevented by pretreating with NAC.

关 键 词：锰 N-乙酰半胱氨酸 能量代谢 氧化损伤 线粒体损伤 

分 类 号：O614.71[理学—无机化学]