Pulmonary aryl hydrocarbon hydroxylase: Tobacco smoke-exposed guinea pigs

Abstract

Exposure of various species of laboratory animals (rats, hamsters, and mice) to tobacco smoke or tobacco smoke condensate usually results in increased activity of aryl hydrocarbon hydroxylase (AHH) in the lung. In an ongoing study on tobacco smoke toxicity, guinea pigs were exposed to smoke from five regular Canadian flue-cured tobacco cigarettes. The activity of AHH was measured 1, 3, 6, 12, and 24 hr after smoke exposure. Contrary to what has been observed in other species, cigarette smoke did not enhance AHH activity in the guinea pig lung, but rather depressed it. Exposure to the vapor phase of cigarette smoke did not depress AHH activity in the lung, while exposure to whole smoke from nicotine-free cigarettes resulted in a depression of AHH activity similar to that obtained with regular flue-cured tobacco cigarettes. 3-Methylcholanthrene injected ip at 50 mg/kg also failed to induce benzo(a)pyrene hydroxylase in the lung of guinea pigs 18 hr later, and Arochlor 1254 (500 mg/kg, ip) produced even a marked depression of AHH activity. In contrast, benzo(a)pyrene injected ip at 50 mg/kg did induce pulmonary AHH 18 hr later. All three chemicals were inducers of hepatic AHH. Treatment of Sprague-Dawley rats with the same chemicals produced a marked induction of this enzyme in both the lung and the liver. The present study suggests that this species difference in the inducibility of pulmonary AHH will have to be taken into account in future studies on acute and chronic toxicity of tobacco smoke.