Signaling by carcinogenic metals and metal-induced reactive oxygen species

被引：124

作者：

Harris, Gabriel Keith ^{[1
]}

Shi, Xianglin ^{[1
]}

机构：

[1] NIOSH, Natl Res Council Associate, Pathol & Physiol Res Branch, Morgantown, WV 26505 USA

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2003年 / 533卷 / 1-2期

关键词：

Metals; Signal transduction; Reactive oxygen species;

D O I：

10.1016/j.mrfmmm.2003.08.025

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Epidemiological data indicate that exposure to metal and metalloid species, including arsenic(III), chromium(VI), and nickel(II), increases the risk of cancer, particularly of the lung and skin. Alterations in normal signal transduction as a result of exposure to carcinogenic metals, and to metal-catalyzed reactive oxygen species (ROS) formation, appear to play an important role in the etiology of metal-induced carcinogenesis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases, and nuclear transcription factors. This article reviews current literature on the effects of carcinogenic metals and metal-induced ROS on cancer-related signaling pathways. In addition, the mechanisms by which those changes occur, and the role of those changes in carcinogenesis are discussed. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：183 / 200

页数：18

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