SummaryCaffeine through drinking water, at low (100 p g/ml), moderate (200 and 400 1u g/ml) and high (800 p g/ml) doses, as well as by intragastric administration at 40 and 160 mg/kg doses, increased the hepatic and pulmonary cytochrome P-450 (Cyt. P-450) levels in mice. The extent of elevation in the enzyme levels was dependent on the dose of caffeine. Maximum inducibility of hepatic arylhydrocarbon hydroxylase (AHH) was observed at the highest doses of caffeine by the two modes of treatment. However, the activities of AHH at the highest doses were not statistically different from the enzyme activities at the lowest doses. Caffeine treatment of animals through drinking water did not change the pulmonary AHH activity, whereas the intragastric administration of caffeine increased the enzyme activity in the lungs. Moreover, intragastric administration was more effective in inducing the hepatic AHH activity. Maximum increases in hepatic and pulmonary glutathione-S-transferase (GST), and in hepatic reduced glutathione (GSH), by the two modes of caffeine treatment of the animals was similar. The enhancement in AHH, Cyt. P-450, GST, and GSH may account for the anticarcinogenic activity of caffeine.Key Words: caffeine, arylhydrocarbon hydroxylase, cytochrome P-450, glutathione-S-transferase, reduced glutathione Environmental pollutants, several drugs, and nutritional factors are likely to have impact on the process of carcinogenesis. Caffeine, which is the most widely consumed drug throughout the world, is a natural ingredient of coffee, tea, cocoa and an additive to many medications and beverages, such as soft drinks and diet aids [1]. The pharmacological and pathological activities of caffeine have received
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