N-nitroso-bis(2-acetoxypropyl)amine as a further pancreatic carcinogen in Syrian golden hamsters.

Paper

N-nitroso-bis(2-acetoxypropyl)amine as a further pancreatic carcinogen in Syrian golden hamsters.

Published Aug 1, 1976 · P. Pour, J. Althoff, R. Gingell

Cancer research

Q1 SJR score

29

Citations

0

Influential Citations

Semantic Scholar

Abstract

N-Nitroso-bis(2-acetoxypropyl)amine, a possible beta metabolite of N-nitroso-di-n-propylamine, was shown to be a potent carcinogen in the Syrian golden hamster. After a single s.c. treatment, the pancreas was the most affected organ, followed by the liver, respiratory tract, and kidneys. However, repeated application resulted in a higher incidence of neoplasms of the respiratory tract than of the pancreas and kidneys. The effect of N-nitroso-bis(2-acetoxypropyl)amine on toxicity, target tissues, and carcinogenicity was similar to that of N-nitroso-bis(2-hydroxypropyl)amine. The assumption that these two compounds may have similar metabolic pathways was confirmed; N-nitroso-bis(2-acetoxypropyl)amine was readily deesterified to N-nitroso-bis(2-hydroxypropyl)amine in vivo and in vitro.

Non-RCT

Animal Study

Study Snapshot

N-nitroso-bis(2-acetoxypropyl)amine is a potent pancreatic carcinogen in Syrian golden hamsters, with similar toxicity, target tissues, and carcinogenicity to N-nitroso-bis(2-hydroxypropyl)amine.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

N-nitroso-bis(2-acetoxypropyl)amine as a further pancreatic carcinogen in Syrian golden hamsters.

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References

Pancreatic neoplasms in an animal model: Morphological, biological, and comparative studies

Induced pancreatic neoplasms in Syrian golden hamsters resemble human pancreatic tumors in both biological and morphological aspects.

Cancer of the pancreas induced in the Syrian golden hamster.

Syrian golden hamsters can develop pancreatic cancer with a short tumor latency and closely resemble human tumors after receiving subcutaneous DIPN applications for life.

A further pancreatic carcinogen in Syrian golden hamsters: N-nitroso-bis(2-acetoxypropyl)amine.

N-nitroso-bis(2-acetoxypropyl)amine (BAP) is a potent pancreatic carcinogen in Syrian golden hamsters, with similar carcinogenic potency and organotropic spectrum to BHP, and is readily converted to BHP in vivo.

Induction of pancreatic neoplasms by 2,2'-dioxopropyl-N-propylnitrosamine.

Chronic administration of 2,2'-dioxopropyl-N-propylnitrosamine (DOPN) in Syrian golden hamsters leads to a high incidence of pancreatic duct adenomas and carcinomas, with no tumors in the upper respiratory tract or kidneys.

Effect of beta-oxidized nitrosamines on syrian hamsters. III. 2,2'-Dihydroxydi-n-propylnitrosamine.

DHPN, an injected metabolite of di-n-propylnitrosamine, is carcinogenic in Syrian hamsters, causing neoplasms in the respiratory tract, pancreas, liver, and kidneys.

Citations

Animal Models: Challenges and Opportunities to Determine Optimal Experimental Models of Pancreatitis and Pancreatic Cancer.

This review highlights the advantages and limitations of various animal models for studying pancreatitis and pancreatic cancer, providing guidance for selecting the appropriate model and conducting and presenting research results.

Animal models of exocrine pancreatic carcinogenesis

Experimental models in rodent species can effectively evaluate risk factors and biological behavior of exocrine pancreatic carcinomas.

Genotoxicity of carcinogenic N-nitrosopropylamine derivatives in the hepatocyte primary culture/DNA-repair test.

The hepatocyte primary culture/DNA repair test effectively detects genotoxic effects of carcinogenic N-nitrosopropylamine derivatives, with comparable capacity to the bacterial mutagenesis test.

Histogenesis of pancreatic carcinomas: A study based on 248 cases

Ductal origin of pancreatic carcinomas is supported by the presence of both papillary and atypical hyperplasia, suggesting precancerous lesions.

Studies of pancreatic carcinogenesis in different animal models.

Carcinogen exposure in pancreatic acinar cells leads to metaplastic transformation and cell proliferation, with acinar cells showing sensitivity to continued exposure and a surprising degree of plasticity.