摘要
目的:探讨氯化镉(CdCl2)对肝癌细胞的杀伤作用及其机制。方法:四甲基偶氮唑盐(MTT)法观察氯化镉对SMMC-7721、HepG-2和MCF-7细胞生长的抑制作用;应用镉-血红蛋白饱和法检测细胞株MT蛋白含量;应用DNA梯形条带和DNA片段分析观察细胞凋亡。结果:氯化镉诱导的细胞毒效应是时间、剂量依赖性的,凋亡是细胞死亡的主要原因,无论细胞中的MT是基础表达的还是被诱导表达的,其含量越低,对镉剂诱导的凋亡的敏感性越高,它们之间呈负相关。结论:氯化镉能特异性杀伤肝癌细胞,促进细胞凋亡是其作用机制。
Objective: To explore the effect of Cadmium Chloride on killing of Hepatoma cells and its mechanism. Methods: The MTT technique was used to observe the inhibitive effect s of Cadmium Chloride against SMMC-7721 ,HepG2 and MCF-7 cell proliferation. MT concentrations were estimated by the Cd-hemoglobin radioassay method. Apoptosis was confirmed by DNA ladder and analysis of DNA fragments. Results: Cd-induced cytotoxicity in SMMC-7721, HepG-2 and MCF-7 cells was both dose-and time-dependent, apoptosis was the primary form of cell elimination after Cd exposure. The less metallothionein present the less a cell or tissue is resistant to cadmium induced cell apoptosis regardless of whether basal or induced MT was considered. The relationship between cellular MT content including basal and Zn-indueed MT and Cd-induced apoptotic rates was negtive. Conclusion:Cadmium Chloride can specially kill Hepatoma cells by promoting cell apoptosis.
出处
《中国肿瘤临床》
CAS
CSCD
北大核心
2006年第9期503-505,共3页
Chinese Journal of Clinical Oncology
基金
吉林省科技发展项目资助(课题编号:20040402-2)
关键词
氯化镉
肝癌
细胞调亡
Cadmium Chloride apoptosis Hepatoma