Bioactivation of <i>N</i>-nitrosomethylbenzylamine and <i>N</i>-nitrosomethyl-amylamine in oesophageal papillomas

Dirsch, Olaf; Koenigsmann, Monika; Lüdeke, Barbara; Scherer, E.; Kleihues, Paul

doi:10.1093/carcin/11.9.1583

Cited by 5 publications

(2 citation statements)

References 15 publications

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“…In previous studies with NMBA, oesophageal papillomas have been induced whether the carcinogen was administered i.p., s.c., in drinking water or in the diet [Fong et al, 1978;Barch et al, 1991;Siglin et al, 1995;Dirsch et al, 1990;Craddock et al, 1986] so that the use of an i.p., route of exposure in the current experiment would not be a limitation. The dose of 2.5 mg/kg NMBA which we employed is known to induce a high level of DNA damage in the oesophagus.…”

Section: Discussionmentioning

confidence: 99%

Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat

et al. 1998

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Fumonisins and N-nitrosamines (NNO) are suggested risk factors in the development of human oesophageal cancer; exposure to both occurs in high risk populations in Africa and People's Republic of China. The hypothesis that the two would interact in oesophageal carcinogenesis was therefore tested by treating male rats with the known oesophageal carcinogen N-methylbenzylnitrosamine (NMBA), and fumonisin B 1 (FB 1 ). The treatment groups were: Group 1, NMBA (2.5 mg/kg) intraperitoneally twice per week from week 2 to 4 inclusive; Group 2, as for group 1 but in addition FB 1 (5 mg/kg) daily from weeks 1 to 5 inclusive by gavage; Group 3, FB 1 (5 mg/kg) alone daily from weeks 1 to 5 inclusive by gavage, and Group 4, vehicle treatment from week 1 to 5 inclusive. Two of 12 animals in group 1 developed oesophageal papillomas and a further two had oesophageal dysplasia. Data were similar in group 2, animals receiving both NMBA and FB 1 , with one of 12 animals having papillomas and three of 12 with dysplasia. Sphingolipid biosynthesis was affected in the kidney and slightly in the liver after fumonisin treatment but not in the oesophagus or lung as determined by sphinganine:sphingosine ratios in urine and tissues. These data show that there is no synergistic interaction between NMBA and FB 1 in the rat oesophagus when the two compounds are administered together. It is nevertheless important to examine other experimental models and treatment protocols which may be more relevant to the human situation and also to pursue epidemiological investigations of the role of fumonisins in oesophageal cancer. Nat.

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Section: Discussionmentioning

confidence: 99%

Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat

et al. 1998

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“…Although the final transformation of NMBA may occur in esophageal mucosal cells, it is first metabolized in the liver by cytochrome P-4502E1. This P-450 isozyme catalyzes the oxidation of a number of xenobiotics, including alcohol [78]. Human and rat esophageal cells or microsomes metabolically activate NMBA and several other esophageal nitrosamine carcinogens, including the tobacco smoke constituent N-nitrosonornicotine (NNN) and N-nitrosomethyl-n-amylamine (NMNA) [79] [80].…”

Section: Animal Models Of Esophageal Squamous Cell Carcinomamentioning

confidence: 99%

Esophageal Carcinogenesis

Watanabe¹,

Shimizu²,

Kochi³

et al. 2014

OJPathology

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Esophageal cancer is the sixth leading cause of cancer death and remains one of the least survivable cancers. Esophageal cancers show wide variations in incidence in different population, suggesting that environmental or lifestyle risk factors could be controlled to reduce risk of these diseases. There are two major histopathologic types (squamous cell carcinoma and adenocarcinoma) of esophageal epithelial malignancy. Recently, the rate of adenocarcinoma is increasing in developed countries: in the United States, 50% or more is adenocarcinoma and, in about 70%, the increase especially in a white male serves as adenocarcinoma. Esophageal adenocarcinoma develops in the lower esophagus. In contrast, in Japan, the increase in adenocarcinoma is not clear and most (90%) of esophageal cancers are squamous cell carcinoma. Such squamous cell carcinoma occurs onto the middle part esophagus mostly, and 60% or more of the whole esophagus cancer also develops in the middle and upper parts. These differences also influence the treatment results. The scope of this article is to discuss carcinogenesis in the esophagus by giving an overview about its histopathological characteristics and molecular mechanisms.

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Esophageal carcinogenesis in the rat: A model for aerodigestive tract cancer

Wargovich¹,

Imada²

1993

J. Cell. Biochem.

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A number of chemical carcinogens have been used to study the process of esophageal carcinogenesis. Among the most prominent of these models is the induction of cancer of the esophagus in the rat by the nitrosamine N-nitrosomethylbenzylamine (NMBA). In the rat, tumors can occur within 15 weeks of carcinogen administration. The rat model has been used to investigate the mechanism of action of several chemopreventive agents. Among these, the garlic-derived agent diallyl sulfide has been shown to be a specific inhibitor of NMBA metabolism. Other investigators have used the model to seek out the relationship of dietary factors and alcohol in esophageal tumorigenesis. With striking histologic parallels to human esophageal carcinoma, the NMBA model provides useful information to study this cancer.0 1993 Wiley-Liss, Inc.

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Bioactivation of N-nitrosomethylbenzylamine and N-nitrosomethyl-amylamine in oesophageal papillomas

Cited by 5 publications

References 15 publications

Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat

Absence of a synergistic effect between fumonisin B1 and N-nitrosomethylbenzylamine in the induction of oesophageal papillomas in the rat

Esophageal Carcinogenesis

Esophageal carcinogenesis in the rat: A model for aerodigestive tract cancer

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