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- W2138651567 abstract "Publisher Summary This chapter focuses on the 4-(methylnitrosamino)-1- (3-pyridyl)-1-butanone (NNK), whichis derived from nicotine. Significant levels of NNK are found in tobacco products and tobacco smoke. NNK is rapidly and extensively metabolized in rodents, primates, and humans. NNK is a strong lung specific carcinogen, independent of species and route of administration. NNK is carcinogenic in laboratory animals, generating tumors at sites similar to those observed in smokers. It also causes liver, nasal, and pancreatic tumors. This compound induces lung adenocarcinomas in rodents at doses that are comparable to those experienced by smokers. This type of cancer is now the most common type of lung cancer observed in humans, having surpassed squamous cell carcinoma. NNK requires metabolic activation to elicit its carcinogenic properties. Both DNA alkylation pathways are important to the carcinogenic properties of this potent lung carcinogen. The DNA methylation pathway is well-characterized and is a critical pathway for the elicitation of NNK-induced pulmonary tumors in A/J mice. Therefore, genetic susceptibility is likely to be critical in the determination of lung cancer risk in humans. The major metabolic pathways consist of carbonyl reduction, N-oxidation and a-carbon hydroxylation. Glucuronidation is an important pathway of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) metabolism. Each of these four pathways is described in the chapter." @default.
- W2138651567 created "2016-06-24" @default.
- W2138651567 creator A5061577144 @default.
- W2138651567 date "2009-01-01" @default.
- W2138651567 modified "2023-09-25" @default.
- W2138651567 title "Chapter 5 Molecular Mechanisms of 4‐(Methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone‐Induced Lung Carcinogenesis" @default.
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