4.6 Article Proceedings Paper

Oxidative mechanism of arsenic toxicity and carcinogenesis

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

资金

  1. NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015636] Funding Source: NIH RePORTER
  2. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES012072, P20ES009871] Funding Source: NIH RePORTER
  3. NCRR NIH HHS [P20 RR15636] Funding Source: Medline
  4. NIEHS NIH HHS [P20 ES09871, P30 ES-012072] Funding Source: Medline

向作者/读者索取更多资源

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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