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TISSUE DISTRIBUTION OF ARSENIC SPECIES IN MICE CHRONICALLY EXPOSED TO METHYLARSONOUS ACID
Citation:
PAUL, D., A. H. ZAVALA, V. DEVESA I PEREZ, D. J. THOMAS, AND M. STYBLO. TISSUE DISTRIBUTION OF ARSENIC SPECIES IN MICE CHRONICALLY EXPOSED TO METHYLARSONOUS ACID. Presented at Society of Toxicology Annual Meeting, Seattle, WA, March 16 - 20, 2008.
Impact/Purpose:
Here, we examined the concentrations of As species in urinary bladder, brain, heart, kidney, liver, lung, pancreas, adipose tissue, skeletal muscle, and spleen of male C57BL/6 mice exposed for 8 weeks to MAsIII (0.1, 1.0, 2.5 5.0 ppm As) in drinking water and in control mice drinking tap water.
Description:
The metabolism of inorganic arsenic (iAs) in humans yields toxic and carcinogenic methyl-As (MAs) and dimethyl-As (DMAs) intermediates. Methylarsonous acid (MAsIII) is the most acutely toxic species of characterized iAs metabolites. Here, we examined the concentrations of As species in urinary bladder, brain, heart, kidney, liver, lung, pancreas, adipose tissue, skeletal muscle, and spleen of male C57BL/6 mice exposed for 8 weeks to MAsIII (0.1, 1.0, 2.5 5.0 ppm As) in drinking water and in control mice drinking tap water. Mice were fed a Purina Rodent Diet (5058) with the total As content of 24 to 66 ng/g. As speciation analysis was carried out in digested tissue homogenates by hydride generation-atomic absorption spectrometry, with cryotrapping for separation of arsines. Exposure to MAs did not affect water consumption or body weights and did not produce any overt signs of toxicity. DMAs was the major metabolite of MAs in all tissues except for the kidney, which retained mostly MAs. Highest concentrations of DMAs were found in urinary bladder. The presence of iAs in tissues of mice varied according to the lot of diet consumed. iAs derived from diet was retained mainly in kidney, heart, lung, and brain. Concentrations of iAs in some tissues decreased with exposure to MAsIII. Regardless of exposure level he lowest concentrations of all As species were found in adipose tissue. These data suggest that exposures to MAsIII result in accumulation of MAs in the kidney and DMAs in urinary bladder. Thus, interactions of MAs and DMAs with specific molecular targets in these two tissues may represent common mechanisms for adverse effects associated with chronic exposures to both iAs and MAsIII. (This abstract does not reflect U.S. EPA policy.)