中文摘要：

目的将在服的外皮的神经原上调查镉(Cd ) 的细胞毒素的机制。方法老鼠的主要文化服的外皮的神经原与镉的不同集中被对待醋酸盐( 0 ， 5 ， 10 ，和 20 mol/L )，然后房间生存能力， apoptosis ，超微结构，细胞内部[Ca2+] i 和反应的氧种类( ROS )铺平， mitochondrial 膜潜力()，过氧化氢酶(猫)的活动和 superoxide dismutase (草皮)被测量。结果 A 在房间生存能力和 apoptotic 房间的一个增加的数字的进步损失被观察。另外，在服的外皮的神经原的词法变化也是的导致 Cd 的 apoptotic 由染色的 Hoechst 33258 示威了。同时， ultrastructural 变化是 mitochondrial cristae 和不平常的安排的失真。同时，举起细胞内部[Ca2+] i 和 ROS 层次，弄空在暴露期间以一种剂量依赖者方式被揭示。而且，在生活房间的猫和草皮活动显著地增加了。到 Cd 的不同剂量的外皮的神经原的结论暴露导致了细胞的死亡，由 apoptotic 机制调停了，并且 apoptotic 死亡由氧化应力导致了可以是一个潜在的原因。并且氧化应力和 mitochondrial 机能障碍引起的细胞内部的动态平衡的混乱可以是为在外皮的神经原的 apoptosis 的一个扳机。

英文摘要：

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.