Skip Navigation

This Article
Right arrow Full Text (PDF)
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 arrow Search for citing articles in:
ISI Web of Science (70)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Pflaum, M.
Right arrow Articles by Epe, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pflaum, M.
Right arrow Articles by Epe, B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1994 Oxford University Press

research-article

Visible light generates oxidative DNA base modifications in high excess of strand breaks in mammalian cells

Michael Pflaum, Serge Boiteux 1 and Bernd Epe 2

Institute of Pharmacology and Toxicology, University of Würzburg Versbacherstrasse 9, D-97078 Würzburg, Germany
1Groupe Réparation des Lésions Radio- et Chirnioinduites URA 147 CNRS, U 140 INSERM, Institut Gustave Roussy, 94805 Villejuif, France

2To whom correspondence should be addressed

The DNA damage induced by visible light in L1210 mouse leukaemia cells was analysed by an alkaline elution assay with specific repair endonucleases. DNA single-strand breaks and DNA modifications sensitive to FPG protein (formamido-pyrimidine-DNA glycosylase), endonuclease III and exo-nuclease III were quantified in parallel. The light-induced cellular DNA damage was found to consist of many base modifications sensitive to FPG protein, which most probably are predominantly 7,8-dihydro-8-oxoguanine (8-hydroxy-guanine) residues. Base modifications sensitive to endonuclease III are virtually absent. The yield of the FPG-sensitive base modifications is 10-fold higher than that of single-strand breaks plus AP sites (sites of base loss). The described ratios of the various modifications indicate that the damage most probably results from a reaction of DNA with singlet oxygen (type II reaction) or directly with an excited endogenous photosensitizer (type I reaction) and is not mediated by hydroxyl radicals. Experiments with cut-off filters indicate that wavelengths between 400 and 500 nm are responsible for most of the modifications. The FPG-sensitive base modifications are repaired efficiently (t1/2 approximately 1 h at 37°C). This is perhaps why the light-induced DNA damage is apparently associated with only low mutagenicity.


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
 FASEB J.Home page
A. Besaratinia, S.-i. Kim, and G. P. Pfeifer
Rapid repair of UVA-induced oxidized purines and persistence of UVB-induced dipyrimidine lesions determine the mutagenicity of sunlight in mouse cells
FASEB J, July 1, 2008; 22(7): 2379 - 2392.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
R. A. Sharma and P. B. Farmer
Biological Relevance of Adduct Detection to the Chemoprevention of Cancer
Clin. Cancer Res., August 1, 2004; 10(15): 4901 - 4912.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
P. Duez, M. Hanocq, and J. Dubois
Photodynamic DNA damage mediated by {{delta}}-aminolevulinic acid-induced porphyrins
Carcinogenesis, May 1, 2001; 22(5): 771 - 778.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
O. Will, H.-C. Mahler, A.-P. Arrigo, and B. Epe
Influence of glutathione levels and heat-shock on the steady-state levels of oxidative DNA base modifications in mammalian cells
Carcinogenesis, February 1, 1999; 20(2): 333 - 337.
[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.