ToxSci Advance Access originally published online on December 12, 2008
Toxicological Sciences 2009 107(2):309-311; doi:10.1093/toxsci/kfn257
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Published by Oxford University Press 2008.
Unraveling Arsenic—Glutathione Connections
Pharmacokinetics Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, MD B143-1, U.S. Environmental Protection Agency, 109 Alexander Drive, Research Triangle Park, North Carolina 27711
1 For correspondence via fax: 919-541-1937. E-mail: thomas.david@epa.gov.
Received December 3, 2008; accepted December 5, 2008
| The first 150 words of the full text of this article appear below. |
The paper by Muniz Ortiz et al. (2009)
in this issue of Toxicological Sciences extends a long line of research on the role of glutathione (GSH) in the metabolism and toxicity of arsenic (As). These investigators used Drosophila as their model organism and the tools of classical and molecular genetics to investigate the genetic basis of variation in sensitivity to the toxic effects of inorganic As. By measuring eclosion (egg hatching) rates for different Drosophila strains cultured on arsenite-containing medium, they identified strains that differed manyfold in sensitivity to As. Using As-sensitive or -resistant strains, they showed an As-resistant phenotype to be related to the genotype for glutathione synthetase (GS). The GS gene encodes the enzyme that catalyzes the second and final step in a pathway that produces GSH from its constituent amino acids. Armed with this information, they used RNA interference to show that altered expression of the GS
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