六价铬诱导L-02肝细胞凋亡与线粒体功能损伤的关系研究

Study of L-02 hepatocyte apoptosis induced by hexavalent chromium associated with mitochondria function damage

目的 研究六价铬[Cr（Ⅵ）]对L-02肝细胞凋亡率和线粒体功能的影响。初步探讨二者之间的关系。方法 选取0、2、4、8、16、32和64μmol／L Cr（Ⅵ）溶液处理L-02肝细胞6h，采用流式细胞分析检测细胞凋亡率；荧光分光光度法检测线粒体膜通透性转运孔（PTP）的开放程度和线粒体膜电位（△ψm）的变化。结果 2～64μmol／LCr（Ⅵ）对L-02肝细胞具有细胞毒性，随着Cr（Ⅵ）浓度的增加L-02肝细胞凋亡率升高；线粒体PTP开放程度增加；线粒体膜电位（△ψm）降低，且与对照组比较差异均有显著性（P〈0．05）。结论 Cr（Ⅵ）诱导L-02肝细胞凋亡与线粒体功能损伤有关。

Objective To explore the effect of hexavalent chromium on apoptosis of L-02 hepatocytes and the functions of mitochondria. Methods L-02 hepatocytes in all tests were incubated with 0,2,4,8,16,32和64μmol/L of Cr（Ⅵ） for 6h. Apoptosis of L-02 hepatocytes in the presence of Cr（Ⅵ） was quantified by flow cytometry（FCM）. The permeability transition pore （PTP）of mitochondria and mitochondrial membrane potential as indicators of mitochondrial damage were measured by fluorescent spectrometer. Results Concentration-dependent decrease in cell apoptosis rate of Cr（Ⅵ）-treated L-02 hepatocytes were observed. The results of permeability transition pore（PTP） of mitochondria, mitochondrial membrane potential in all concentrations of Cr（Ⅵ） had significant difference when compared to the control cells （P 〈 0.05）. Conclusion The results demonstrated that L-02 hepatocytes apoptosis induced by Cr（Ⅵ） associated with mitochondrial damages.