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镉诱导致突变性的分子机制。

Molecular mechanisms of cadmium induced mutagenicity.

作者信息

Filipic M, Fatur T, Vudrag M

机构信息

Department of Genetic Toxicology and Cancer Biology, National Institute of Biology, Vecna pot 111, 1000 Ljubljana, Slovenia.

出版信息

Hum Exp Toxicol. 2006 Feb;25(2):67-77. doi: 10.1191/0960327106ht590oa.

Abstract

Cadmium is a human carcinogen of worldwide concern because it accumulates in the environment due to its extremely long half-life. Its compounds are classified as human carcinogens by several regulatory agencies. Cadmium affects cell proliferation, differentiation, apoptosis and other cellular activities and can cause numerous molecular lesions that would be relevant to carcinogenesis. For a long time cadmium has been considered as a non-genotoxic carcinogen, as it is only weakly mutagenic in bacterial and mammalian cell test systems. Recently, we presented evidence that when assayed in a test system, in which both intragenic and multilocus mutations can be detected, cadmium acts as a strong mutagen which induces predominantly multilocus deletions. In this review, we discuss two mechanisms that play an important role in cadmium mutagenicity: (i) induction of reactive oxygen species (ROS); and (ii) inhibition of DNA repair. Experimental evidence suggests that cadmium at low, for environmental exposure relevant concentrations, induces mutations by inducing oxidative DNA damage and that it decreases genetic stability by inhibiting the repair of endogenous and exogenous DNA lesions, which in turn increase the probability of mutations and consequently cancer initiation by this metal.

摘要

镉是一种全球关注的人类致癌物,因其极长的半衰期而在环境中累积。其化合物被多个监管机构列为人类致癌物。镉会影响细胞增殖、分化、凋亡及其他细胞活动,并能导致许多与致癌作用相关的分子损伤。长期以来,镉一直被视为非遗传毒性致癌物,因为它在细菌和哺乳动物细胞测试系统中仅有微弱的致突变性。最近,我们提供了证据表明,在一个能够检测基因内和多位点突变的测试系统中进行检测时,镉是一种强诱变剂,主要诱导多位点缺失。在这篇综述中,我们讨论在镉致突变性中起重要作用的两种机制:(i)活性氧(ROS)的诱导;以及(ii)DNA修复的抑制。实验证据表明,在与环境暴露相关的低浓度下,镉通过诱导氧化性DNA损伤而诱发突变,并且它通过抑制内源性和外源性DNA损伤的修复来降低遗传稳定性,进而增加突变的概率以及由此种金属引发癌症的可能性。

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