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Comparison of speciated arsenic levels in the liver and brain of mice between arsenate and arsenite exposure at the early life.

Environmental toxicology

Animals, Animals, Newborn, Arsenates, toxicity, Arsenic, metabolism, Arsenites, Brain, growth & development, Cacodylic Acid, Female, Lactation, Liver, Male, Maternal Exposure, adverse effects, Maternal-Fetal Exchange, Methylation, Mice, Pregnancy, Tissue Distribution, Water Pollutants, Chemical

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      Abstract

      The aim of this study was to compare the risk from exposure to arsenate (iAs(V) ) or arsenite (iAs(III) ) at the early life. Mother mice were exposed to equimolar dose of iAs(V) and iAs(III) via drinking water during gestation and lactation. Their offspring continually drank the same water after weaning. Levels of speciated arsenic in both liver and brain were analyzed by hydride generation of volatile arsines and atomic absorption spectrophotometry (HG-AAS). In the liver, inorganic arsenic (iAs) levels significantly increased from postnatal day (PND) 15, and those on PND 35 were significantly higher than on PND 15 and 21 in iAs(III) exposed mice, but iAs levels did not significantly differ until PND 35 in iAs(V) exposed mice; Furthermore, all speciated arsenic levels on PND 35 and dimethylarsinic acid (DMA) levels on PND 1 were significantly higher in iAs(III) exposed mice than those in iAs(V) exposed mice. In the brain, iAs levels increased significantly on PND 21, but those declined sharply on PND 35 in either iAs(III) or iAs(V) exposed mice, however the mean difference between the two exposure groups was not significant; whereas DMA levels in iAs(III) exposed mice were significantly higher than those in iAs(V) exposed mice on both PND 1 and 35. In conclusion, findings from this study suggested that iAs(III) was preferentially accumulated into liver, and expected to result in more efficient methylation capacity than iAs(V) ; either iAs(V) or iAs(III) might be accumulated in the brain readily, when immature blood brain barrier can not limit it into brain. Hence, exposure to either iAs(V) or iAs(III) at the early life may increase the risk of iAs exposure in the brain. Copyright © 2012 Wiley Periodicals, Inc., a Wiley company.

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      Journal
      22907888
      10.1002/tox.21808

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