[六价铬诱导L-02肝细胞凋亡与线粒体功能损伤的研究]

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

作者信息

Xiao Jing-wei, Zhong Cai-gao, Li Bin

机构信息

Institute for Occupational Health and Poison Control, China CDC, Beijing 100050, China.

出版信息

Wei Sheng Yan Jiu. 2006 Jul;35(4):416-8.

PMID:16986512

Abstract

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.

摘要

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：在所有实验中，将L-02肝细胞与0、2、4、8、16、32[见正文]64微摩尔/升的六价铬孵育6小时。通过流式细胞术（FCM）对存在六价铬时L-02肝细胞的凋亡进行定量。用荧光光谱仪测量线粒体的通透性转换孔（FTP）和线粒体膜电位作为线粒体损伤的指标。