摘要：Arsenic is a naturally occurring metalloid that has been associated with increased incidence of human cancer in certain highly exposed populations. Arsenic is released to the environment by natural means such as solubilization from geologic formations into water supplies. It is also released to occupational and community environments by such activities as nonferrous ore smelting and combustion of fuels containing arsenic. Several lines of evidence indicate that arsenic acts indirectly with other agents to ultimately enhance specific genotoxic effects that may lead to carcinogenesis. Work described here indicates that arsenite specifically potentiates chromosomal aberrations induced by a DNA crosslinking agent, 1,3-butadiene diepoxide, but does not effect the induction of sister chromatid exchanges under the same treatment conditions. It is proposed that the specific co-clastogenic effects of arsenite seen here may be mediated by its interference with DNA repair activities. Further understanding of the mechanism by which arsenic interacts with other environmental agents will result in more accurate estimates of risk from exposure to arsenic. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (841K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 79 80 81 82
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