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THE IMPACT OF SELENIUM STATUS ON THE METABLISM AND DISPOSITION OF ARSENIC AND ITS IMPLICATIONS FOR EPIDEMIOLOGIC INVESTIGATIONS
Citation:
Kenyon, E M., M F. Hughes, L. M. Del Razo, AND O. A. Levander. THE IMPACT OF SELENIUM STATUS ON THE METABLISM AND DISPOSITION OF ARSENIC AND ITS IMPLICATIONS FOR EPIDEMIOLOGIC INVESTIGATIONS. SEGH Meeting, San Diego, CA, June 18 - 22, 2000.
Description:
The Impact of Selenium Status on the Metabolism and Disposition of Arsenic and Its Implications for Epidemiologic Investigations
E. M. Kenyon1*, M.F. Hughes1, L.M. Del Razo2, and O.A. Levander3
1Office of Research and Development, Experimental Toxicology Division, NHEERL, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
2Toxicology Section, CINVESTAV - IPN, Mexico City, Mexico
3U.S. Department of Agriculture, Human Nutrition Research Center, Nutrient Requirements and Functions Laboratory, Beltsville, MD 20705
Abstract
Metabolic and toxicologic interactions between arsenic (As) and selenium (Se) are multifaceted and complex. These interactions are of practical significance because many populations are simultaneously exposed to inorganic As in drinking water and varying levels of Se in the diet. The goal of our studies has been to investigate whether dietary Se status alters As metabolism and disposition after exposure to arsenate [As(V)] or arsenite [As(III)]. Weanling female B6C3F1 mice were maintained for 28 days on Torula yeast based diets deficient (0.02 ppm Se), sufficient (0.2 ppm Se) or excessive (2.0 ppm Se) in Se; mice then received by oral gavage either 0.5 or 5 mg (As)/kg as [73As]sodium arsenate or 0.5 mg (As)/kg as [73As]sodium arsenite. Se deficient mice dosed with 5 mg (As)/kg As(V) exhibited slower whole body clearance from 8 hours onward. Total (urine + feces) cumulative excretion of As-derived radioactivity was significantly lower in Se deficient As(V)-exposed mice at both dose levels compared to Se sufficient mice. Significantly less As-derived radioactivity was also excreted in the feces of Se deficient mice exposed to 5 mg (As)/kg As(V) compared to Se sufficient mice. There was also a trend towards lower cumulative excretion of dimethylarsinic acid in urine of Se deficient compared to Se sufficient mice which was significant for mice exposed to As(III). Both thioredoxin reductase (TR) activity and total hepatic Se were significantly increased in Se deficient mice treated with As(III) compared to untreated Se deficient mice. Overall, these studies indicate that Se deficiency is associated with altered As metabolism and disposition. Further studies to evaluate the potential toxicological consequences of As exposure in Se deficiency are warranted, as is consideration of population Se status in the design and interpretation of epidemiologic studies.