期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 255, 期 1-2, 页码 67-78出版社
KLUWER ACADEMIC PUBL
DOI: 10.1023/B:MCBI.0000007262.26044.e8
关键词
arsenic; free radicals; oxidative stress; signal transduction; carcinogenesis
类别
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015636] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES012072, P20ES009871] Funding Source: NIH RePORTER
- NCRR NIH HHS [P20 RR15636] Funding Source: Medline
- NIEHS NIH HHS [P20 ES09871, P30 ES-012072] Funding Source: Medline
Arsenic is a known toxin and carcinogen that is present in industrial settings and in the environment. The mechanisms of disease initiation and progression are not fully understood. In the last a few years, there has been increasing evidence of the correlation between the generation of reactive oxygen species ( ROS), DNA damage, tumor promotion, and arsenic exposure. This article summarizes the current literature on the arsenic mediated generation of ROS and reactive nitrogen species ( RNS) in various biological systems. This article also discusses the role of ROS and RNS in arsenic- induced DNA damage and activation of oxidative sensitive gene expression.
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