| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Health Foundation, Division of Carcinogenesis and Molecular Epidemiology, Valhalla, New York 10595 [R. G. N., J. E. O., F-L. C.], and Division of Basic Science, New York University, College of Dentistry and Department of Environmental Medicine, New York University Medical School, New York, New York 10010 [J. B. G.]
Highly DNA-reactive
,ß-unsaturated aldehydes such as acrolein and crotonaldehyde are common environmental pollutants present in cigarette smoke and automobile exhaust and are also released endogenously by lipid peroxidation. Acrolein- and crotonaldehyde-derived 1,N2-propanodeoxyguanosine (AdG and CdG, respectively) have been detected in the tissues of carcinogen-treated rodents and as background lesions in DNA from humans and untreated rodents. To determine whether cigarette smoking increases the levels of AdG and CdG, gingival tissue DNA from 11 smokers (4 males and 7 females; 3058 years old) and 12 nonsmokers (8 males and 4 females; 2166 years old) was analyzed using a previously described 32P-postlabeling high-performance liquid chromatography method. The results showed that the mean AdG levels in smokers were significantly higher than those in nonsmokers (1.36 ± 0.90 µmol/mol guanine in smokers versus 0.46 ± 0.26 µmol/mol guanine in nonsmokers; P = 0.003). The mean CdG 1 levels in smokers and nonsmokers were 0.53 ± 0.44 and 0.06 ± 0.07 µmol/mol guanine, respectively, corresponding to an 8.8-fold increase for smokers (P = 0.0015). Similar to CdG 1, levels of CdG 2 were increased 5.5-fold in smokers as compared to nonsmokers, from 0.31 ± 0.40 to 1.72 ± 1.26 µmol/mol guanine (P = 0.0014). Furthermore, the total levels of cyclic adduct (AdG and CdG) in smokers were 4.4-fold greater than those in nonsmokers (P = 0.0003). This study shows the detection of the potentially promutagenic 1,N2-propanoguanine adducts in human oral tissues and demonstrates for the first time an increase of structurally identified adducts in oral tissue DNA by cigarette smoking.
1 Supported by National Cancer Institute Grant CA 43159 and National Institute of Dental Research Grant DE 10549.
2 To whom correspondence should be addressed, at American Health Foundation, Division of Carcinogenesis and Molecular Epidemiology, 1 Dana Road, Valhalla, NY 10595. Phone: (914) 789-7161; Fax: (914) 592-6317; E-mail: ChungAHF.aol.com.
Received 12/ 1/97. Accepted 1/ 2/98.
This article has been cited by other articles:
![]() |
S.-i. Kim, G. P. Pfeifer, and A. Besaratinia Lack of Mutagenicity of Acrolein-Induced DNA Adducts in Mouse and Human Cells Cancer Res., December 15, 2007; 67(24): 11640 - 11647. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. S. Hecht Smoking and lung cancer--a new role for an old toxicant? PNAS, October 24, 2006; 103(43): 15725 - 15726. [Full Text] [PDF] |
||||
![]() |
Z. Feng, W. Hu, Y. Hu, and M.-s. Tang From the Cover: Acrolein is a major cigarette-related lung cancer agent: Preferential binding at p53 mutational hotspots and inhibition of DNA repair PNAS, October 17, 2006; 103(42): 15404 - 15409. [Abstract] [Full Text] [PDF] |
||||
![]() |
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] |
||||
![]() |
A. J. Kurtz and R. S. Lloyd 1,N2-Deoxyguanosine Adducts of Acrolein, Crotonaldehyde, and trans-4-Hydroxynonenal Cross-link to Peptides via Schiff Base Linkage J. Biol. Chem., February 14, 2003; 278(8): 5970 - 5976. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. H. Phillips Smoking-related DNA and protein adducts in human tissues Carcinogenesis, December 1, 2002; 23(12): 1979 - 2004. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Bartsch, U. Nair, A. Risch, M. Rojas, H. Wikman, and K. Alexandrov Genetic Polymorphism of CYP Genes, Alone or in Combination, as a Risk Modifier of Tobacco-related Cancers Cancer Epidemiol. Biomarkers Prev., January 1, 2000; 9(1): 3 - 28. [Abstract] [Full Text] |
||||
![]() |
Q. Yang, M. Hergenhahn, A. Weninger, and H. Bartsch Cigarette smoke induces direct DNA damage in the human B-lymphoid cell line Raji Carcinogenesis, September 1, 1999; 20(9): 1769 - 1775. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |