BLOCKING EFFECTS OF SYNTHETIC TRYPSIN-INHIBITOR (CAMOSTAT) ON PANCREATIC CARCINOGENESIS IN HAMSTERS INITIATED WITH N-NITROSOBIS(2-OXOPROPYL)AMINE

Citation
F. Furukawa et al., BLOCKING EFFECTS OF SYNTHETIC TRYPSIN-INHIBITOR (CAMOSTAT) ON PANCREATIC CARCINOGENESIS IN HAMSTERS INITIATED WITH N-NITROSOBIS(2-OXOPROPYL)AMINE, Pancreas, 9(1), 1994, pp. 78-82
Citations number
22
Categorie Soggetti
Endocrynology & Metabolism",Physiology
Journal title
ISSN journal
08853177
Volume
9
Issue
1
Year of publication
1994
Pages
78 - 82
Database
ISI
SICI code
0885-3177(1994)9:1<78:BEOST(>2.0.ZU;2-E
Abstract
The effects of concomitant administration of a synthetic trypsin inhib itor (camostat) on pancreatic carcinogenesis in hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP) were investigated. Thirty-two fem ale Syrian golden hamsters were given weekly 10 mg/kg s.c. injections of BOP for 5 weeks while simultaneously receiving a 500 ppm camostat d iet (BOP + camostat group). Additional groups of 30 animals received e ither the s.c. injections of BOP (BOP group), or the 500 ppm camostat diet (camostat group) during the same 5-week period. Thirty weeks afte r the first BOP administration, the incidence of pancreatic adenocarci nomas in the BOP + camostat group was significantly lower than in the group administered BOP only (p < 0.05). Similarly, the total numbers o f pancreatic adenocarcinomas or dysplastic lesions were significantly decreased in the BOP + camostat group as compared with the BOP group ( p < 0.01). None of the animals receiving camostat alone developed any adenocarcinomas or dysplastic lesions of the pancreas. The results of the present experiments clearly show that camostat can inhibit inducti on of hamster pancreatic ductal neoplasms when administered simultaneo usly with BOP.