Alloxan, when given intravenously at a dose of 60 mg/kg body weight 2 hours prior to subcutaneous injection of the potent pancreatic carcinogen N-nitrosobis (2-oxopropyl) amine (BOP), inhibited the induction of hyperplastic and neoplastic pancreatic lesions in a statistically significant fashion (P less than 0.01). The number of lesions per animal affected was markedly less in these animals, compared with BOP-treated control animals. BOP administration 2 weeks after alloxan treatment, at which time pancreatic islet cell regeneration is considered completed, did not alter either the incidence or number of lesions. The results support our view that the pancreatic islet cells are the primary source of BOP metabolism. The concomitant inhibition of gallbladder tumors, but not of common duct neoplasms, in hamsters receiving BOP 2 hours after alloxan could indicate that alloxan's inhibitory effects on BOP carcinogenesis are not restricted to the pancreas.