论文部分内容阅读
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.
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 activity 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 i ncreased 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.