Skip Navigation



Mutagenesis Advance Access published online on December 8, 2006
Mutagenesis, doi:10.1093/mutage/gel051
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/1/63    most recent
gel051v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Lee, D.-H.
Right arrow Articles by Pfeifer, G. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, D.-H.
Right arrow Articles by Pfeifer, G. P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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
Received August 23, 2006
Revised September 22, 2006
Accepted October 3, 2006

Original article

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

Dong-Hyun Lee 1 and Gerd P. Pfeifer 1 *

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

* To whom correspondence should be addressed.
Gerd P. Pfeifer, E-mail: gpfeifer{at}coh.org


  Abstract

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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.