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© 1991 Oxford University Press

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Comparison of pulmonary DNA adduct levels, measured by 32P-postlabelling and aryl hydrocarbon hydroxylase activity in lung parenchyma of smokers and ex-smokers

O. Geneste, A.-M. Camus, M. Castegnaro, S. Petruzzelli 1, P. Macchiarini 1, C.A. Angeletti 2, C. Giuntini 1 and H. Bartsch 3

International Agency for Research on Cancer 150 cours Albert-Thomas, 69372 Lyon Cedex 08, France
1CNR Institute of Clinical Physiology Italy
2Surgical Clinic, Section of Thoracid Surgery, University of Pisa Italy

3To whom reprint requests should be sent

In order to compare pulmonary DNA adducts and aryl hydrocarbon hydroxylase (AHH) activity, we have measured these two parameters in non-neoplastlc surgical lung parenchymal samples from four ex-smokers and 19 smokers, out of 20 patients operated for lung cancer, and three for non-malignant lung diseases. DNA adducts were determined by scintillation counting after 32P-postlabelling analysis. The microsomal fractions of the same lung specimen were assayed for AHH activity by a fluorometric method. Autoradiograms of DNA adducts found in lungs of smokers revealed two distinct diagonal radioactive zones that were absent in ex-smokers. The smokers had significantly higher levels (1.68–13.4 DNA adducts/108 nucleotides; mean ± SD 5.38 ± 3.19) than ex-smokers (0.23–2.21; 1.09 ± 0.84). AHH activity in smokers ranged from 0.01 to 0.69 pmol/min/mg. This activity was significantly (P < 0.05) higher in smokers (0.26 ± 0.26) who had smoked until 1 week before surgery than in those who had stopped smoking for <7 days (0.11 ± 0.11). A positive linear correlation between DNA adduct levels and AHH activity (r = 0.69; P < 0.001; n = 19) was found in smokers. This relationship could explain why AHH inducibility appears to be a crude marker for lung cancer risk in smokers.


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