[Study of L-02 hepatocyte apoptosis induced by hexavalent chromium associated with mitochondria function damage].
[Study of L-02 hepatocyte apoptosis induced by hexavalent chromium associated with mitochondria function damage].
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发表时间：
2006-07
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通讯作者：
Jing-wei Xiao;Cai-gao Zhong;Bin Li
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作者：
Jing-wei Xiao;Cai-gao Zhong;Bin Li
目的探讨六价铬对L-02肝细胞凋亡及线粒体功能的影响。方法将L-02肝细胞分别与0、2、4、8、16、32 [见正文] 64 μ mol/L的Cr（VI）孵育6 h。流式细胞术（FCM）定量测定Cr（VI）存在下L-02肝细胞的凋亡。用荧光分光光度计测定线粒体通透性转换孔（FTP）和线粒体膜电位作为线粒体损伤的指标。结果Cr（VI）处理的L-02肝细胞凋亡率呈浓度依赖性降低。各浓度Cr（VI）组线粒体膜电位、线粒体通透性转换孔（PTP）与对照组比较差异均有统计学意义（P < 0.05）。结论Cr（VI）诱导L-02肝细胞凋亡与线粒体损伤有关。
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 [see text] 64 micromol/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 (FTP) 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.