Molecular mechanisms of arsenic carcinogenesis
Molecular mechanisms of arsenic carcinogenesis
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DOI：
10.1023/b:mcbi.0000007261.04684.78
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发表时间：
2004-01-01
影响因子：
4.3
通讯作者：
Shi, XL
中科院分区：
文献类型：
--
作者：
Huang, CS;Ke, QD;Shi, XL
砷是一种广泛分布于环境中的类金属化合物。人类接触这种化合物与癌症发病率的增加有关。虽然确切的机制仍有待研究，但已有许多致癌途径被提出。砷的潜在致癌作用包括氧化应激、基因毒性损伤、DNA修复抑制、表观遗传事件和某些导致基因异常表达的信号转导通路的激活。本文综述了有关砷致癌分子机制的研究现状，重点介绍了ROS和信号转导途径。
Arsenic is a metalloid compound that is widely distributed in the environment. Human exposure of this compound has been associated with increased cancer incidence. Although the exact mechanisms remain to be investigated, numerous carcinogenic pathways have been proposed. Potential carcinogenic actions for arsenic include oxidative stress, genotoxic damage, DNA repair inhibition, epigenetic events, and activation of certain signal transduction pathways leading to abberrant gene expression. In this article, we summarize current knowledge on the molecular mechanisms of arsenic carcinogenesis with an emphasis on ROS and signal transduction pathways.