Szyfter K, Szmeja Z, Szyfter W
Kliniki Otolaryngologicznej AM im. K. Marcinkowskiego w Poznaniu.
Otolaryngol Pol. 1993;47(6):496-501.
There is known a strong association between induction of cancer of respiratory tracts and tobacco smoking. Exposure to polycyclic aromatic hydrocarbons (PAH) present in tobacco smoke can induce DNA lesions including bulky DNA adducts. The studied group consisted of 6 men, aged 46-71 years, all intensive cigarette smokers, without reported occupational exposition to PAH. Treatment did not include radio- and chemotherapy. DNA isolated from surgically removed tumors, surrounding tissue histologically characterized as non-malignant and peripheral blood white cells was analyzed by 32P-postlabelling assay with P1 nuclease enhancement. Both, P1 nuclease digestion and the chromatographic systems used for separation of DNA adducts were established for PAH: DNA analysis. The main adduct was identified as diol-epoxide metabolite of B (a) P. The mean number of adducts in tumor samples, surrounding tissue and white blood cells was calculated, respectively, to 82.3, 59.9 and 41.7 PAH: DNA adducts per 10(8) nucleotides. The only accessible reference was for DNA from white blood cells. The amount of PAH: DNA adducts in white blood cells of larynx cancer patients exceeded that found in healthy blood donors (both: smokers and non-smokers) as well as in workers exposed occupationally to high concentration of PAHs in the ambient air. Hence, it is concluded that carcinogen: DNA adducts as pre-mutagenic lesions can provide a diagnostic information. It concerns the target cells as well as a surrogate tissue. In any case the study has only a preliminary character because of limited number of subjects studied.