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氯化镉致癌机理的研究
引用本文:王晓丽,李永安,冯彪,凌翎,李志超,郭丽,范洪学. 氯化镉致癌机理的研究[J]. 中国公共卫生学报, 1999, 0(2)
作者姓名:王晓丽  李永安  冯彪  凌翎  李志超  郭丽  范洪学
作者单位:白求恩医科大学预防医学院毒理教研室
摘    要:应用氯化镉致人胚肺成纤维细胞恶性转化实验、染色体分析、流式细胞术对氯化镉的致癌机理进行研究。结果表明,氯化镉诱导的染色体畸变可能是其致癌机理之一;用流式细胞仪检测转化细胞突变型P53蛋白和细胞周期素D1的表达,发现转化细胞中突变型P53蛋白和细胞周期素D1的表达量均明显高于阴性对照组(P<001),初步证实了突变型P53蛋白的表达及细胞周期素D1的过表达在镉致癌机理中起协同作用

关 键 词:氯化镉  人胚肺成纤维细胞  恶性转化  致癌机理

Mechanism of Carcinogenesis Induced by CdCl 2 Department of Toxicology
Wang Xiaoli,et al.. Mechanism of Carcinogenesis Induced by CdCl 2 Department of Toxicology[J]. , 1999, 0(2)
Authors:Wang Xiaoli  et al.
Affiliation:Changchu 130021
Abstract:The mechanism of carcinogenesis induced by CdCl 2 was studied through experiments of the malignant transformation of human embryo lung fibroblast in vitro,chromosome analysis and flow cytometry.on one hand,we think that it may be one of the carcinogenic mechanisms that CdCl 2 induces chromosomal aberration.On the other hand,the p 53 and cyclin D 1 expression quatities were determined by frow cytometry and the expressions of p 53 and cyclin D 1 in transformation cells were remarkably higher than control group(P<0 01),which preliminarily shows that p 53 protein cooperates with cyclin D 1 overexpression in playing a role during CdCl 2 induced carcinogenesis.this study will lay a foundation on further studying molecular mechanism of carcinogenesis induced by CdCl 2.
Keywords:CdCl 2 Human Embryo Lung Fibroblast Malignant Transformation Carcinogenic Mechanism  
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