Responses of rodent hepatic, renal and pulmonary aryl hydrocarbon hydroxylase following exposure to cigarette smoke

Abstract

Using the British-American Tobacco Co. (B.-A.T.)-Mason inhalation system which releases a precisely-calibrated dilution of tobacco smoke into a chamber, male and female rats, guinea pigs, hamsters and gerbils were exposed to the optimum smoke concentration found to induce rat renal aryl hydrocarbon hydroxylase (AHH) (40 puffs of a 1 : 5 dilution of smoke from cigarettes prepared from a blend of Canadian flue-cured tobaccos). The tissue activity was measured in 9000 g supernatants of homogenates of lung, liver and kidney 6 h following exposure. Cigarette smoke was found to be a potent inducer of AHH, dilutions as high as 1 : 40 inducing this enzyme in rat kidney. Marked tissue, sex and species differences in basal AHH were observed. Induction up to 6-fold, was observed only in lung and kidney of male and female rats. In hamsters and gerbils, lung AHH was induced in both sexes but only renal AHH in female hamsters. In male and female guinea pigs, only the renal AHH was induced some 5-fold. Hepatic AHH was not inducible in any of the species studied. The analysis of changes in AHH activity in a responsive species and tissue(s) could be a valuable technique for the quantitative evaluation of biological effects of low concentrations of cigarette smoke.