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Mutagenesis Advance Access originally published online on December 8, 2006
Mutagenesis 2007 22(1):63-67; doi:10.1093/mutage/gel051
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© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Mutagenesis induced by the nitric oxide donor sodium nitroprusside in mouse cells

Dong-Hyun Lee and Gerd P. Pfeifer*

Division of Biology, Beckman Research Institute of the City of Hope 1500 East Duarte Road, Duarte, CA 91010, USA

Nitric oxide (NO) is an important bioactive molecule derived from endogenous or exogenous sources. NO can exhibit genotoxicity through the formation of reactive nitrogen species. Nitric oxide releasing compounds, such as sodium nitroprusside, are widely used for the therapy of hypertension and other disorders. Here we have characterized the mutagenicity of sodium nitroprusside in mouse embryo fibroblasts carrying the cII mutation reporter gene. Sodium nitroprusside dose-dependently increased the cII mutant frequency to levels ~5-fold above background. The mutational spectrum induced by sodium nitroprusside was characterized by an increase in the fraction of G->T transversion mutations (P < 0.003) but the proportion of transition mutations was not increased. We discuss the potential origin of the G->T mutations induced by this compound in mammalian cells.

*To whom correspondence should be addressed. Tel: +1 626 301 8853; Fax: +1 626 358 7703; Email: gpfeifer{at}coh.org


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