钙稳态失衡在镉致鸡脑神经元线粒体损伤中的作用  

The Effect of Calcium Homeostasis Disequilibrium on the Impairment of the Neuron Mitochondria in the Chicken Brain Induced by Cadmium

作　　者：李文军[1] 赵兰[1] 徐世文[1] 

机构地区：[1]东北农业大学动物医学学院,哈尔滨150030

出　　处：《畜牧兽医学报》2008年第8期1122-1126,共5页ACTA VETERINARIA ET ZOOTECHNICA SINICA

基　　金：黑龙江省教育厅资助(10551038)

摘　　要：为了探讨镉对鸡脑神经元线粒体损伤的机制,本试验以体外培养的鸡脑神经元为研究对象,在含终浓度为0、5、10、15μmol/L CdCl2的DMEM培养液中培养24 h后,应用MTT法测定神经元的抑制率,透射电镜观察神经元线粒体形态学变化,流式细胞仪检测神经元线粒体膜电位(ΔΨm)的变化,以Fura-2/AM为探针检测神经元内游离钙子浓度([Ca2+]i)。结果显示:随着CdCl2浓度升高,细胞抑制率增加,细胞内[Ca2+]i上升,ΔΨm呈降低趋势,透射电镜结果显示,线粒体出现嵴模糊、断裂、消失,基质肿胀和空泡化。表明CdCl2通过升高细胞内[Ca2+]i,诱导通透性转变孔道开放,降低ΔΨm,从而造成神经元线粒体损伤。To explore the mechanism of Cadmium Chloride on chondriosome damage of chicken neurons, neurons cultured in vitro were chose as the research object. Neurons were cultivated in the DMEM for 24 h with the final concentration of CdCl2 was 0,5,10,15 μmol/L, respectively. The inhibition ratio of neurons was evaluated with MTT colorimetric assay. The mitochondrial membrane potential （△ψm） was assessed by flow cytometry, and the calcium ion concentration within neurons（[Ca^2＋ ]i） was detected using the Fura-2/AM as the probe. The results showed that the cells inhibition ratio was increased, [Ca^2＋ ]i was increased,△ψm tended to degrade and the chondriosome cristae appeared ambiguity, fragmentation, disappearance, mitochondrial matrix was intumesced and vacuolized. The results indicated that CdCl2 could cause the impairment of the mitochondrial membrane of neurons by increasing the [Ca^2＋ ]i , inducing the PT pore to open, degrading △ψm.

关 键 词：氯化镉 神经元 线粒体 钙稳态 

分 类 号：X503.22[环境科学与工程—环境工程] Q24[生物学—细胞生物学]