【摘要】 [目的 ]探讨农药鱼藤酮对神经细胞线粒体的毒性作用机制。 [方法 ]采用 0 5、0 75、1 0 0 μmol/L三种浓度的鱼藤酮对神经瘤细胞 (SH SY5Y)染毒 2 4h ,通过线粒体特异性染料罗丹明 1 2 3进行荧光标记 ,利用激光扫描共聚焦显微镜观察染毒细胞线粒体的膜电位变化 ,并与未染毒的细胞对照组进行比较。 [结果 ]经图象扫描每个细胞得到 1 6个荧光强度变化数值 ,并对其荧光变化值进行分析。表明鱼藤酮可引起线粒体膜电位的改变 ,高、中剂量组荧光强度变化值(1 2 4 84±0 2 4 0 5、1 2 4 86± 0 30 5 7)与低剂量组、溶剂对照组、空白对照组荧光强度变化值 (1 52 3 0± 0 442 0、1 770 1±0 391 9、1 72 5 4±0 2 70 5)差异均存在显著性 (P <0 0 5) ,且随剂量增高 ,有降低趋势。 [结论 ]提示线粒体膜电位的改变是鱼藤酮神经细胞毒性作用的重要环节之一。更多还原

【Abstract】 To study of Rotenone cytotoxicity to human dopamimergic SH SY5Y cells. Human dopaminergic SH SY5Y cells were exposed to rotenone at the concentrations of 0 5, 0 75 or 1 00 μmol/L for 24 h, respectively. The mitochondrial potential was determined by incubating the cells with rhodamine 123, a mitochondrial specific dye, followed by laser scanning confocal microtechnique (LCSM) analyses of fluorescence signal. Every cell was obtained sixteenth fluorescence signal by scan and these signal were analyzed. Therefore, Rotenone treatment significantly decreased fluorescence signal as compared to controls, The fluorescence signal of high dose was 1.248 4±0.240 5, including middle dose(1 248 6±0 305 7), low dose(1 523 0±0 442 0), solvent group(1 770 1±0 391 9), control group(1 725 4±0 270 5). These data indicated a diminished mitochondrial membrane potential after rotenone treatment( P <0 05). The effects were rotenone concentration dependent.[Conclusion] These data confirmed that mitochondria may serve as one of the primary target for Rotenone cytotoxicity by altering the membrane potential.更多还原