Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by González-Beltrán, F.
Right arrow Articles by Morales-Ramírez, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by González-Beltrán, F.
Right arrow Articles by Morales-Ramírez, P.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Mutagenesis, Vol. 18, No. 1, 13-17, January 2003
© 2003 UK Environmental Mutagen Society/Oxford University Press

Repairability during G1 of lesions eliciting sister chromatid exchanges induced by methylmethanesulfonate or ethylmethanesulfonate in bromodeoxyuridine-substituted and unsubstituted DNA strands

F. González-Beltrán and P. Morales-Ramírez1

1 Departamento de Biología, Instituto Nacional de Investigaciones Nucleares, Apartado Postal 18-1027, D.F. Mexico, México

The repairability during G1 of DNA lesions eliciting sister chromatid exchanges (SCE) induced by methylmethanesulfonate (MMS) and ethylmethanesulfonate (EMS) in BrdU-substituted and unsubstituted DNA strands was determined in murine salivary gland cells in vivo. The SCE frequency was determined after exposure to MMS or EMS during early and late G1 in the first or second cell division. The inducibility and repairability of SCE-eliciting lesions during G1 in BrdU-substituted and unsubstituted strands were estimated considering that in the first division induction occurs on the unsubstituted strand and during the second division in one unsubstituted and one BrdU- substituted DNA strand. The results indicate that DNA lesions induced by MMS are 50% repaired in both the BrdU-substituted and unsubstituted strands and those induced by EMS are 60% repaired in the unsubstituted strand but only 20% in the BrdU-substituted strand. The increase in sensitivity of the BrdU-substituted strand to SCE induction with respect to the unsubstituted strand was 155 and 45% for MMS and EMS, respectively. These results imply that SCE-inducing lesions produced by MMS and EMS are only partially repaired and that BrdU incorporation could sensitize DNA not only to the induction of lesions eliciting SCE, but also to the induction of non-repairable lesions.

1 To whom correspondence should be addressed. Tel: +52 5 3297200; Fax: +52 5 3297332; Email: pmr{at}nuclear.inin.mx


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


This article has been cited by other articles:


Home page
MutagenesisHome page
P Morales-Ramirez, R Rodriguez-Reyes, E Toribio-Escobedo, C Olvera-Nestor, and B Garcia-Firo
Mechanism of in vivo sister-chromatid exchange induction by 5-azacytidine
Mutagenesis, May 1, 2007; 22(3): 177 - 181.
[Abstract] [Full Text] [PDF]


Home page
MutagenesisHome page
N. Wyatt, C Falque-Gonzalez, D Farrar, D Tuffnell, D Whitelaw, L. Knudsen, and D Anderson
In vitro susceptibilities in lymphocytes from mothers and cord blood to the monofunctional alkylating agent EMS
Mutagenesis, March 1, 2007; 22(2): 123 - 127.
[Abstract] [Full Text] [PDF]



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.