Record Display for the EPA National Library Catalog

RECORD NUMBER: 463 OF 892

OLS Field Name OLS Field Data
Main Title Metabolism and Disposition of Inorganic Arsenic in Laboratory Animals and Humans.
Author McKinney, J. D. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1992
Year Published 1992
Report Number EPA/600/J-92/373;
Stock Number PB93-107183
Additional Subjects Metabolism ; Arsenic inorganic compounds ; Toxicity ; Carcinogens ; Glutathione ; Methylation ; Thiols ; Oxidation ; Reduction(Chemistry) ; Reprints ;
Holdings
Library Call Number Additional Info Location Last
Modified
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Status
NTIS  PB93-107183 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 06/08/1993
Collation 8p
Abstract
The carcinogenicity of inorganic arsenic in humans, particularly in the lung and skin, has been reasonably well established through epidemiological investigations. Studies of metabolism and disposition of inorganic arsenic in various animal species are particularly relevant to determining the factors that might account for the lack of an animal model. Numerous studies of this type have been reported, but there do not appear to be clear qualitative or quantitative differences in the overall fate and disposition of inorganic arsenic in most animals versus humans, although little is known at the cellular and subcellular level. Sulphur chemistry, especially thiol status, is emerging as an important regulating factor in the overall fate and distribution of inorganic arsenic in the body, playing a role in the initial reduction of arsenate to arsenite and subsequent methylation, and possibly in determining tissue affinity and distribution properties. The metabolism of inorganic arsenic can be viewed as a redox cycle in which thiol compounds such as glutathione (GSH) possibly function as reducing agents and methyl donors as oxidizing agents. One explanation for the possible sensitivity of certain malnourished human populations to the carcinogenic effects of inorganic arsenic may be related to the reduced availability of nonprotein sulphhydryl compounds such as GSH needed to drive the redox cycle and facilitate arsenic detoxification. Future carcinogenicity studies of inorganic arsenic in animals could be designed to address directly the aspect of the problem.