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 (10)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zhao, C.
Right arrow Articles by Hemminki, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhao, C.
Right arrow Articles by Hemminki, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol. 23, No. 2, 307-310, February 2002
© 2002 Oxford University Press

MOLECULAR EPIDEMIOLOGY

The in vivo levels of DNA alkylation products in human lymphocytes are not age dependent: an assay of 7-methyl- and 7-(2-hydroxyethyl)-guanine DNA adducts

Chunyan Zhao,1 and Kari Hemminki

Department of Biosciences at Novum, Karolinska Institute, 14157 Huddinge, Sweden

Abstract

Endogenous DNA damage is assumed to be a major contributor to aging and cancer. This study compares the steady-state levels of 7-methyl- and 7-(2-hydroxyethyl)-guanine DNA adducts in lymphocytes isolated from the younger (mean age 39.8 years) and the older (mean age 82.8 years) healthy subjects. Using a 32P-post-labelling method, these adducts were measured in lymphocyte DNA from a total of 34 subjects. The results show that the amount of both 7-methyl- and 7-(2-hydroxyethyl)-guanine adducts in the younger age group was similar to that in the older age group. Our findings show that at steady-state the levels of DNA alkylation products are independent of age, suggesting that endogenous DNA damage, through methylation or lipid peroxidation, and the repair of such damage may not be deficient in lymphocytes of older individuals.


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
 Hum Exp ToxicolHome page
V. Niot-Mansart, A. Muhamedi, and J.-P. Arnould
A competitive ELISA detecting 7-methylguanosine adduct induced by N-nitrosodimethylamine exposure
Human and Experimental Toxicology, February 1, 2005; 24(2): 89 - 94.
[Abstract] [PDF]

Home page
 MutagenesisHome page
R. De Bont and N. van Larebeke
Endogenous DNA damage in humans: a review of quantitative data
Mutagenesis, May 1, 2004; 19(3): 169 - 185.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
J. J. Hu, M. C. Hall, L. Grossman, M. Hedayati, D. L. McCullough, K. Lohman, and L. D. Case
Deficient Nucleotide Excision Repair Capacity Enhances Human Prostate Cancer Risk
Cancer Res., February 1, 2004; 64(3): 1197 - 1201.
[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.