Effects of cigarette smoke on rat lung and liver ornithine decarboxylase and aryl hydrocarbon hydroxylase activities and lung benzo(a)pyrene metabolism.

Abstract

The response of rat lung and liver ornithine decarboxylase (ODC) and aryl hydrocarbon hydroxylase (AHH) activities and lung benzo(a)pyrene (BP) metabolism was studied after exposing the rats to cigarette smoke. A close analysis of the time curves for ODC and AHH activities in rat lung and liver after a single exposure to cigarette smoke resulted in no clear correlation between the two parameters. Prolonged treatment (10 days) produced an increase in pulmonary ODC activity; hepatic ODC activity was unaffected. 10-day treatment was ineffective in raising AHH activity above values observed after a single treatment. BP metabolism, as determined in isolated perfused lungs by the appearance of organic- and water-soluble metabolites in the perfusion medium, the amount of covalently bound metabolites in lung tissue and the disappearance of unchanged 3-H BP from the perfusate, was markedly increased in response to cigarette smoke treatment. The data presented indicate that induction of AHH activity and increased metabolism of BP do not necessarily require a pre-existing increase in ODC activity.