Differences in experimental pancreatic carcinogenesis induced by oral or subcutaneous administration of 2,2'-dihydroxydi-n-propylnitrosamine in duct-ligated hamsters.
After ligation of the main pancreatic duct in the splenic lobe, Syrian golden hamsters were treated, either p.o. or s.c., for 15 weeks with dihydroxydi-n-propylnitrosamine for induction of pancreatic duct carcinomas. The incidence, location, and type of proliferative lesions distal and proximal to the ligature were recorded and compared to those of dihydroxydi-n-propylnitrosamine-treated hamsters without duct ligation. Proliferative duct lesions, including carcinomas, developed on either side of the ligation. While after s.c. administration the incidence was similar to that in nonligated animals, a markedly decreased incidence was found in p.o.-treated animals with duct ligation. The data suggest that the blood stream might be one major access route of the carcinogen to the pancreatic duct cell. Furthermore, it is assumed that an umimpaired release of pancreatic juice in the duodenum is necessary for the enteral resorption of dihydroxydi-n-propylnitrosamine.
D000230:Adenocarcinoma / Q000139:chemically induced / Q000473:pathology; D000284:Administration, Oral; D000818:Animals; D006224:Cricetinae; D005260:Female; D007279:Injections, Subcutaneous; D008647:Mesocricetus; D009374:Neoplasms, Experimental / Q000139:chemically induced; D009602:Nitrosamines / Q000008:administration & dosage*; D010183:Pancreatic Ducts / Q000187:drug effects* / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000139:chemically induced*; D011230:Precancerous Conditions / Q000139:chemically induced* / Q000473:pathology
D009602:Nitrosamines; C012457:diisopropanolnitrosamine