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应用未分化型PC12细胞为体外模型,研究甲基汞对多巴胺能神经元的毒性作用机制.利用MTT法检测甲基汞的细胞毒性,Hoechst33258荧光染色观察细胞形态变化,流式细胞术定量分析细胞周期分布和凋亡比率,并进一步通过比色法评价各项氧化应激指标.结果显示,甲基汞以剂量依赖性方式降低了细胞存活率,干扰细胞周期,造成S期细胞阻滞,细胞出现典型的凋亡性死亡特征.另外,甲基汞暴露导致PC12细胞内O2.-、H2O2和.OH等活性氧含量急剧增加,脂质过氧化程度升高,且SOD、CAT和GSH-Px等抗氧化酶活性降低.因此,甲基汞对多巴胺能神经元具有强烈的毒性,毒性作用机制涉及到干扰细胞周期、诱导细胞凋亡和引发严重的氧化损伤.
Undifferentiated PC12 cells were used as an in vitro model to study the mechanism of methylmercury toxicity on dopaminergic neurons.MTT assay was used to detect the cytotoxicity of methylmercury.Hoechst33258 staining was used to observe the morphological changes of cells and flow cytometry Cycle distribution and apoptosis ratio, and further evaluate the indicators of oxidative stress by colorimetric method.The results showed that methylmercury in a dose-dependent manner to reduce the cell survival rate, interfere with the cell cycle, resulting in S phase cell arrest, cells Typical apoptotic death characteristics were observed.MHC exposure resulted in a dramatic increase of reactive oxygen species (O2 .-, H2O2 and .OH) and increased lipid peroxidation in PC12 cells, and SOD, CAT and GSH-Px Methylmercury has a strong toxicity on dopaminergic neurons, the mechanism of toxicity involves interfering with the cell cycle, inducing apoptosis and triggering serious oxidative damage.