Expression of pulmonary cytochrome P4501 A1 and carcinogen DNA adduct formation in high risk subjects for tobacco-related lung cancer

Bartsch, H., Castegnaro, M., Rojas, M., Camus, A.-M., Alexandrov, K. and Lang, M. (1992). Expression of pulmonary cytochrome P4501 A1 and carcinogen DNA adduct formation in high risk subjects for tobacco-related lung cancer. In: Sixth International Congress of Toxicology: Toxicology from Discovery and Experimentation to the Human Perspective, Rome, Italy, (477-483). 28 June-3 July 1992. doi:10.1016/0378-4274(92)90222-6


Author Bartsch, H.
Castegnaro, M.
Rojas, M.
Camus, A.-M.
Alexandrov, K.
Lang, M.
Title of paper Expression of pulmonary cytochrome P4501 A1 and carcinogen DNA adduct formation in high risk subjects for tobacco-related lung cancer
Conference name Sixth International Congress of Toxicology: Toxicology from Discovery and Experimentation to the Human Perspective
Conference location Rome, Italy
Conference dates 28 June-3 July 1992
Journal name Toxicology Letters   Check publisher's open access policy
Place of Publication Shannon, Co. Clare, Ireland
Publisher Elsevier
Publication Year 1992
Sub-type Fully published paper
DOI 10.1016/0378-4274(92)90222-6
ISSN 0378-4274
1879-3169
Volume 64-5
Start page 477
End page 483
Total pages 6
Language eng
Formatted Abstract/Summary
Cigarette smoking is the strongest risk factor for lung cancer (LC), but genetically determined variations in pulmonary metabolism of tobacco-derived carcinogens may affect individual risk. Results from a case-control study on LC patients demonstrated the pronounced effect of tobacco smoke on pulmonary xenobiotic metabolism and prooxidant state, and suggested the existence of a metabolic phenotype at higher risk for tobacco-associated LC: LC patients who were recent smokers had significantly induced BP-3-hydroxylase (AHH) and ethoxycoumarin O-deethylase (ECDE) activities in lung parenchyma, when compared with smoking non-cancer patients. In recent smokers, lung AHH activity was positively correlated with the level of tobacco smoke-derived DNA adducts as determined by 32P-postlabelling. Pulmonary AHH activity also showed a good correlation with the intensity of immunohistochemical staining for cyt. P4501A by a monoclonal Ab in lung tissue sections: smoking and peripheral type of lung cancers were positively related to high levels of this cyt. P450 species, probably reflecting high rates of induction. These results suggest that high pulmonary CYP1A1 expression (controlling in part carcinogen DNA-adduct formation) in tobacco smokers, appears to be associated with LC risk. High risk subjects may thus be identifiable through genotyping assays for CYP1A1 polymorphism.
Keyword Lung cancer
CYP1A-related enzymes
Carcinogen DNA adducts
Metabolic phenotypes
Cigarette smoking
Q-Index Code E1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Conference Paper
Collection: National Research Centre for Environmental Toxicology Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 42 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 42 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Mon, 30 Nov 2009, 15:00:52 EST