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Oxidative Stress and Apoptotic Changes of Rat Cerebral Cortical Neurons Exposed to Cadmium in Vitro

查看全文 作  者:YUAN [1]Yan;BIAN Jian [1]Chun;LIU Xue [1]Zhong;ZHANG [1]Ying;SUN [1]Ya;LIU Zong [1]Ping 高影响力作者 机构地区:[1]College of Veterinary Medicine,Yangzhou University,Yangzhou 225009,Jiangsu,China高影响力机构 出  处:《Biomedical and Environmental Sciences》索引2012年第25卷第2期,共10页高影响力期刊 基  金:supported by the National Nature Science Foundation of China (no.30972229 and 31101866);a project Funded by Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD) 摘  要:Objective To investigate the cytotoxic mechanism of cadmium(Cd) on cerebral cortical neurons.Methods The primary cultures of rat cerebral cortical neurons were treated with different concentrations of cadmium acetate(0,5,10,and 20 μmol/L),and then the cell viability,apoptosis,ultrastructure,intracellular [Ca2+]i and reactive oxygen species(ROS) levels,mitochondrial membrane potential(ΔΨ),activities of catalase(CAT) and superoxide dismutase(SOD) were measured.Results A progressive loss in cell viability and an increased number of apoptotic cells were observed.In addition,Cd-induced apoptotic morphological changes in cerebral cortical neurons were also demonstrated by Hoechst 33258 staining.Meanwhile,ultrastructural changes were distortion of mitochondrial cristae and an unusual arrangement.Simultaneously,elevation of intracellular [Ca2+]i and ROS levels,depletion of ΔΨ were revealed in a dose-dependent manner during the exposure.Moreover,CAT and SOD activities in the living cells increased significantly.Conclusion Exposure of cortical neurons to different doses of Cd led to cellular death,mediated by an apoptotic mechanism,and the apoptotic death induced by oxidative stress may be a potential reason.And the disorder of intracellular homeostasis caused by oxidative stress and mitochondrial dysfunction may be a trigger for apoptosis in cortical neurons. 关 键 词:皮层神经元 细胞凋亡 氧化应激 镉暴露 大鼠脑 超氧化物歧化酶 线粒体膜电位 超微结构变化
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