COMPARATIVE P-32 ANALYSIS OF CIGARETTE SMOKE-INDUCED DNA DAMAGE IN HUMAN-TISSUES AND MOUSE SKIN
- 1 November 1986
- journal article
- research article
- Vol. 46 (11) , 5869-5877
Abstract
Previous studies using a highly sensitive 32P-postlabeling assay for the analysis of carcinogen/mutagen-induced DNA damage have shown the presence of tobacco smoking-related DNA adducts in human placenta (Everson, R.B., Randerath, E., Santella, R.M., Cefalo, R.C., Avitts, T. A., and Randerath, K., Science (Wash. DC), 231: 54-57, 1986). The occurrence of such adducts in smokers'' bronchus and larynx is reported here. Since the chemical nature of these adducts could not be characterized by direct methods due to the extremely low levels of individual adducts (< 0.03 fmol per .mu.g DNA), we have sought an experimental animal model for studying the formation of tobacco-related DNA adducts. Because cigarette smoke condensate is known to initiate tumors in mouse skin, ICR mice were treated topically with cigarette tar equivalent to 1.5, 3, 6, and 9 cigarettes for 0.4, 3, 5, and 7 days, respectively, and skin DNA was isolated 1 day after the last treatment. When DNA from exposed mice was analyzed by the 32P-postlabeling assay, 12 distinct 32P-labeled DNA adduct spots, as well as a diagonal radioactive zone, which presumably reflected the presence of incompletely resolved adducts, were noted on polyethyleneimine-cellulose TLC fingerprints. One derivative in particular (adduct 1) was seen to increase rapidly during the early treatment phase and also to persist to 8 days after treatment. The prominent adduct 1 was observed in the same location on the fingerprints of DNA samples from smokers. Cochromatography experiments suggested identity of human and mouse DNA adduct 1. Similarly, several other human and mouse adducts (adducts 3, 5, 6, and 9) appeared identical, and the diagonal radioactive zone was also present on DNA adducts maps from smokers. While absolute levels of individual human adducts were too low to be accurately quantitated, semiquantitative estimation of total tobacco-related aromatic DNA adducts in the human specimens gave values of 1 adduct in (1.7-2.9) .times. 107 nucleotides (0.10-0.18 fmol per .mu.g DNA), with adduct 1 constituting 8.5-14% of the total. On the basis of these results, it appears now feasible to determine the chemical origin of smoking-induced DNA adducts in human tissues by preparation of authentic 32P-labeled reference adducts from animals treated with characterized subfractions of cigarette tar, 32P-postlabeling, and cochromatography of 32P-labeled human and animal adducts.This publication has 17 references indexed in Scilit:
- Isolation of a cigarette smoke fraction responsible for the inhibition of benzo[a]pyrene metabolism in the isolated perfused rabbit lungChemico-Biological Interactions, 1984
- 32P-Postlabeling test for covalent DNA binding of chemicals in vivo: application to a variety of aromatic carcinogens and methylating agentsCarcinogenesis: Integrative Cancer Research, 1984
- Highly persistent polycyclic aromatic hydrocarbon-DNA adducts in mouse skin: Detection by 32P-postlabeling analysisCancer Letters, 1983
- 32P-postlabeling analysis of non-radioactive aromatic carcinogen — DNA adductsCarcinogenesis: Integrative Cancer Research, 1982
- 32P-labeling test for DNA damage.Proceedings of the National Academy of Sciences, 1981
- 32P-base analysis of DNAAnalytical Biochemistry, 1981
- INHIBITION INVIVO OF THE FORMATION OF ADDUCTS BETWEEN METABOLITES OF BENZO(A)PYRENE AND DNA BY ARYL-HYDROCARBON HYDROXYLASE INDUCERS1981
- Benzo[ a ]pyrene Diol Epoxides as Intermediates in Nucleic Acid Binding in Vitro and in VivoScience, 1976
- Ion-exchange thin-layer chromatographyJournal of Chromatography A, 1966
- A procedure for the isolation of deoxyribonucleic acid from micro-organismsJournal of Molecular Biology, 1961