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Effects of Cigarette Smoking on Aryl Hydrocarbon Hydroxylase Activity in Lungs and Tissues of Inbred Mice¹

Department of Medicine, University of Kentucky School of Medicine, Lexington 40506, and Veterans Administration Hospital, Lexington, Kentucky 40507

Inbred strains of mice have been classified as aromatic hydrocarbon responsive or nonresponsive depending upon whether the parenteral administration of these substances increases hepatic aryl hydrocarbon hydroxylase (AHH) activity. Aromatic hydrocarbon responsiveness is controlled by genes at a small number of loci. Using 3-methylcholanthrene as inducing agent, strains A/J, C3H/HeJ, and C57BL/6J have been classified as responsive, whereas strains AKR/J, DBA/2J, and SWR/J are nonresponsive. Inhalation of cigarette smoke by both hepatic responsive and nonresponsive mice induces AHH activity in lung, but not in liver, stomach, small intestine, or kidney. The responsive strains have significantly higher levels of basal and induced AHH in the lung than do the hepatic nonresponsive strains. However, because of the especially low basal activity of AHH in lungs of hepatic nonresponsive strains, the ratio of AHH activity in animals treated with cigarette smoke to that in untreated animals is higher in nonresponsive than in responsive strains. AHH activity in lung is fully induced within 6 to 12 hr after smoke inhalation and remains at the same level whether animals are treated 1 day or daily for 4 weeks. AHH in lung returns to basal levels within 5 days after cessation of smoking.

¹ This investigation was supported by University of Kentucky Tobacco and Health Research Institute Projects KTRB 043 and 064 and by Research Grant AM 16013 from the NIH.

² To whom reprint requests should be addressed.

Received 7/ 5/74. Accepted 9/16/74.