【摘要】 目的研究染锰不同浓度对SH-SY5Y细胞总超氧化物歧化酶(T-SOD)、锰超氧化物歧化酶(Mn-SOD)活性及丙二醛(MDA)含量的影响,并观察维生素C对染锰多巴胺能神经细胞的保护作用,探讨锰的神经毒性作用机制及防治措施。方法人神经母细胞瘤SH-SY5Y细胞在分别含0,25,50,100,200,300μmol/L浓度氯化锰(MnCl2)及10 mmol/L维生素C+300μmol/LMnCl2的培养基中培养72 h后,试剂盒检测MnCl2对细胞T-SOD、Mn-SOD活性和MDA含量的影响及维生素C的保护作用。结果MnCl2能显著降低SH-SY5Y细胞T-SOD、Mn-SOD活性;而随着MnCl2浓度的增加,细胞MDA含量显著升高,且呈剂量-效应关系。维生素C预处理可显著降低染锰细胞的氧化应激水平。结论MnCl2可显著降低SH-SY5Y细胞T-SOD、Mn-SOD的活性,并使细胞内MDA生成量增多,提示氧化应激可能是锰产生多巴胺能神经毒性的重要机制之一,而维生素C对锰诱导的氧化应激具有明显的抑制作用。更多还原

【Abstract】 Objective To study the toxicity of MnCl2 and the protective effect of vitamin C in human neuroblastoma cells in vitro.Methods SH-SY5Y cell cultures were pretreated individually with 0,25,50,100,200,300 μmol/L MnCl2 and 10 mmol/L vitamin C+300 μmol/L Mn-Cl2 for 72 hours.The activities of T-SOD and Mn-SOD,and the levels of MDA in SH-SY5Y cells were detected respectively.Results Mn-Cl2 could decrease the activities of T-SOD and Mn-SOD,and increase the levels of MDA in a dose-dependent manner.However,vitamin C could significantly inhibit the oxidative stress in MnCl2-induced SH-SY5Y cells.Conclusion Oxidative stress is responsible for manganese-induced neurotoxicity and vitamin C may be protective for manganism.更多还原