• 关键词：甲基汞  细胞凋亡  氧化应激  未分化型PC12细胞

• 基金项目：国家自然科学基金面上项目(No.30371053)

• 张鹏
• 大连理工大学环境与生命学院生物工程系, 大连 116024

• 徐永平
• 大连理工大学环境与生命学院生物工程系, 大连 116024

• 李晓宇
• 大连理工大学环境与生命学院生物工程系, 大连 116024

• 金礼吉
• 大连理工大学环境与生命学院生物工程系, 大连 116024

• 摘要：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.

• Abstract：Undifferentiated PC12 cells were used as an in vitro model to study the toxicity of methylmercury toward dopaminergic neurons.Methylmercury-induced cytotoxicity was detected by MTT assay.The morphological changes were observed by Hoechst33258 staining.The number of cells in different parts of the cell cycle and the rate of apoptosis were analysed quantitatively by flow cytometry.Further,various oxidative stress indicators were assessed by means of colorimetry.The results showed that methylmercury decreased the cell viability in a dose-dependent manner,induced S-phase arrest by disturbing the cell cycle,and resulted in the appearance of typical apoptotic features.Moreover,exposure to methylmercury led to extreme overproduction of O₂^-·,H₂O₂ and ·OH,elevation of lipid peroxidation,and decreased the activities of SOD,CAT and GSH-Px in PC12 cells.Therefore,methylmercury is highly toxic to dopaminergic neurons.The underlying mechanism may be involved in disturbing the cell cycle,inducing apoptotic cell death,and triggering serious oxidative damage.

• Key words：methylmercury  apoptosis  oxidative stress  undifferentiated PC12 cells

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