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Arsenic Methylation, Oxidative Stress and Cancer - Is there a Link?
Citation:
HUGHES, M. F. Arsenic Methylation, Oxidative Stress and Cancer - Is there a Link? JOURNAL OF THE NATIONAL CANCER INSTITUTE. Oxford University Press, Cary, NC, 101(24):1-2, (2009).
Impact/Purpose:
This paper is a perspective on a manuscript soon to be published by JNCI. This paper focuses on the role of metabolism of arsenic in its toxic effects.
Description:
Arsenic is a multiorgan human carcinogen. The best-known example of this effect occurred in subgroups of the Taiwanese population who were chronically exposed to high levels of naturally occurring arsenic in drinking water and developed cancers of the skin, lung, urinary bladder, and potentially the kidney (I). Nonneoplastic effects that are attributed to arsenic exposure under similar conditions include vascular disease, hypertension, diabetes, and dermal lesions (2,3). Many countries today still have arseniccontaminated drinking water and are facing a potential public health crisis (4). Although the carcinogenicity of arsenic in humans has been known for more than 100 years, there is no definitive understanding of the mechanism of action for this effect This gap in knowledge has been partly because of the lack of positive animal carcinogenicity studies for a number of years, because arsenic is not a point mutagen, and because the mechanism for the biotransformation of arsenic was not completely known. In the 1990s, attention became focused on the potential tumor-promoting and carcinogenic effects of the methylated metabolites of arsenic. Investigations found that dimethylarsinic acid [DMAs(V)], a pentavalent metabolite of inorganic arsenic, was a multiorgan tumor promoter in rodents (5) and was carcinogenic in rat urinary bladder following chronic dietary or drinking water exposure (6,7). Arsenic was also found to be carcinogenic in more recent studies using transgenic animals (5) or transplacental exposure in mice (8).
