sincalide and nitrosobis(2-oxopropyl)amine

sincalide has been researched along with nitrosobis(2-oxopropyl)amine* in 2 studies

Other Studies

2 other study(ies) available for sincalide and nitrosobis(2-oxopropyl)amine

ArticleYear
Cholecystokinin inhibits DNA alkylation induced by N-nitrosobis (2-oxopropyl)amine (BOP) in hamster pancreas.
    Cancer letters, 1992, Mar-15, Volume: 62, Issue:3

    Cholecystokinin (CCK) inhibits pancreatic cancer but not hepatic tumor induction by N-nitrosobis (2-oxopropyl) amine (BOP) in hamsters when administered with or shortly before BOP. In this study, we evaluated the capability of sulfated CCK-8 to inhibit DNA alkylation in the hamster pancreas. We examined the pattern of O6-methylguanine (G6-Me) and N7-methylguanine (G7-Me) in pancreatic ductal, acinar and liver tissues from Syrian hamsters treated with a single dose of BOP (20 mg/kg s.c.) and with five s.c. injections of CCK-8 (200 pM/kg, 30 min apart). The first CCK injection was given either 90 min before, or together, or 3 h after POP administration. The amount of G6-Me in liver DNA did not differ significantly. We observed a decrease of G7-Me in the liver of the group treated with CCK together with POP as compared to POP alone (P less than 0.005). Lower amounts of G6-Me were found in ductal preparations (P less than 0.01) of the animals treated with CCK before POP as compared to POP alone. CCK also modified the pattern of alkylation in the acinar tissue, but without a clear relationship with the timing of administration. The results suggest that the inhibitory effect of CCK-8 on pancreatic carcinogenicity of BOP could be related to its capability to modify DNA alkylation by yet unknown mechanisms.

    Topics: Alkylation; Animals; Cholecystokinin; Cricetinae; DNA; Guanine; Liver Neoplasms; Nitrosamines; Pancreas; Sincalide

1992
Alteration of pancreatic endocrine cell patterns and their secretion during pancreatic carcinogenesis in the hamster model.
    Cancer research, 1989, Nov-15, Volume: 49, Issue:22

    Proliferation of endocrine cells was found to occur during early, i.e., first 12 weeks, exocrine pancreatic carcinogenesis after 6 weekly treatments of Syrian hamsters with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). Cells containing insulin (Ins), glucagon (Glu), and somatostatin (Som) were noted in all stages of tumor development and were present in adenocarcinomas and in metastases to the liver. Some of the cancer cells were of amphicrine (hybrid) type, i.e., produced both mucin and endocrine substances. Measurement of these hormones revealed a significant decrease in plasma Ins during early stages of carcinogenesis with concomitant increase of Ins level in pancreatic juice at 12 weeks after 6 weekly BOP treatments. Plasma Glu and Som were not changed. The changes noted, particularly in relation to Ins, suggest that proliferation of endocrine cells in pancreatic carcinogenesis may be associated with alterations in hormone secretion.

    Topics: Animals; Carcinogens; Cricetinae; Glucagon; Insulin; Insulin Secretion; Islets of Langerhans; Male; Mesocricetus; Nitrosamines; Pancreas; Pancreatic Juice; Pancreatic Neoplasms; Reference Values; Secretin; Sincalide; Somatostatin

1989
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