MODIFICATION OF PANCREATIC CARCINOGENESIS IN THE HAMSTER MODEL .3. INHIBITORY EFFECT OF ALLOXAN

  • 1 January 1983
    • journal article
    • research article
    • Vol. 110  (3) , 310-314
Abstract
Alloxan, when given i.v. at a dose of 60 mg/kg body wt 2 h prior to s.c. 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 < 0.01). The number of lesions per animal affected was markedly less in these animals, compared with BOP-treated control animals. BOP administration 2 wk after alloxan treatment, at which time pancreatic islet cell regeneration is considered completed, did not alter either the incidence or number of lesions. The pancreatic islet cells may be the primary source of BOP metabolism. The concomitant inhibition of gallbladder tumors, but not of common duct neoplasms, in hamsters receiving BOP 2 h after alloxan could indicate that alloxan''s inhibitory effects on BOP carcinogenesis are not restricted to the pancreas.