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Chemical Carcinogenesis and Mutagenesis
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Of the various environmental hazardous compounds, cigarette smoke enjoys the highest causal relationship with cancer risk in humans. Tobacco smoking plays a major role in the etiology of lung, oral cavity, and esophageal cancers as well as a variety of chronic degenerative diseases. Although cigarette smoke is a mixture of about 4000 chemicals, including more than 60 known human carcinogens, 4-methylnitrosamino-1-(3-pyridyl)-1-butanone (nicotine-derived nitrosamino ketone [NNK]) is the most carcinogenic tobacco-specific nitrosamine. NNK induces lung tumors in mice, rats, and hamsters, and the International Agency for Research on Cancer has designated NNK and NNN (N-nitrosonornicotine) as known human carcinogens. NNK is metabolically activated by CYP P-450 enzymes in the lung and generates O6-methylguanine in DNA. The reaction generates G:C to A:T mutations, with the subsequent activation of K-Ras proto-oncogene and the development of tumor initiation.
Experimental Nasal Cavity Tumors Induced by Tobacco-Specific Nitrosamines (TSNA)*
Published in D. V. M. Gerd Reznik, Sherman F. Stinson, Nasal Tumors in Animals and Man, 2017
A. Rivenson, K. Furuya, S. S. Hecht, D. Hoffmann
The above-mentioned bioassays in rats, mice, and hamsters demonstrate the carcinogenic activities of the tobacco-specific nitrosamines NNN and NNK. NNK is a powerful carcinogen; NNN is a moderately active carcinogen. NAB appears to have only weak activity. The carcinogenicity of NATB is currently being assayed in Fischer-344 rats in a dose response study which also includes NNN and NNK. The emergence of NNK as a highly active carcinogen points to the role of the nitrosamines in the tobacco-induced cancers in man.
B
Published in Filomena Pereira-Maxwell, Medical Statistics, 2018
A graphical display of the distribution of an ordinal or quantitative variable, which is especially useful when the latter displays a skewed distribution. Box-and-whisker plots are also termed boxplots. Figure B.6 compares the distribution of NNAL, a major metabolite of the tobacco-specific nitrosamine carcinogen NNK, among male cigarette smokers, male waterpipe smokers and their non-smoking wives, in rural Eg ypt. On average, NNAL levels were higher for cigarette smokers, followed by waterpipe smokers, and they also displayed greater variability in these two groups. The distribution among non-smoking wives was positively skewed in both instances, and possibly reverse J-shaped among those exposed to waterpipe smoke. The ‘box’ represents the central 50% of the data, and is further divided in two halves by the median. The upper and lower boundaries of the box represent the upper and lower quartiles (see interquartile range or IQR). The ‘whiskers’ usually represent the minimum and maximum values of the variable in question, except when these are outlying observations, in which case the whiskers are made to represent the ‘inner fences’, i.e. values no further than 1.5 x IQR from the lower and upper quartiles. Outliers are marked individually outside of the range defined by the whiskers; those outside the ‘outer fences’ (further than 3.0 x IQR from the lower and upper quartiles) are usually identified using a different symbol. HAMILTON (1990) gives details on the construction of boxplots. See also dot plot, stem-and-leaf plot.
Comparison of the content of tobacco alkaloids and tobacco-specific nitrosamines in ‘heat-not-burn’ tobacco products before and after aerosol generation
Published in Inhalation Toxicology, 2018
Won Tae Jeong, Hyun Ki Cho, Hyung Ryeol Lee, Ki Hoon Song, Heung Bin Lim
TSNAs in tobacco leaves are generally produced by nitrosation of TAs and the curing process, and they may exhibit differences in terms of the content depending on the tobacco variety and cultivation environment (e.g., the nitrate concentration) (Fisher et al., 2012). Recently, the selection of tobacco cultivars with low nornicotine and nicotine contents, which are precursors of NNN and NNK in tobacco leaves, and a change in the curing process have resulted in a lowering of the level of TSNAs (Hecht & Hoffmann, 1988; Appleton et al., 2013). Like nicotine, they can also be released by heat during smoking (Jaccard et al., 2018). Unlike our expectations, NNK and NAB were significantly increased after aerosol generation, but NNN and NAT showed no significant pattern or dependence on smoking conditions. Although estimation of the inhaled amount according to the content of these components was unclear, the understanding of the reduction and increase of TSNAs after aerosol generation has been obtained, in part, from various literature, including those published by tobacco companies.
Formulation of smokeless tobacco products with a wide range of pH to study nicotine pharmacokinetics and pharmacodynamics
Published in Pharmaceutical Development and Technology, 2022
Stephen W. Hoag, Elena V. Mishina, Lauren Viray, Fang Wang, Gary Hollenbeck, Bartosz Koszowski, Wallace B. Pickworth
Nitrosamines were extracted from products using an aqueous solution of ammonium acetate and shaken mechanically. Tobacco extracts were filtered, and an aliquot was assayed by liquid chromatography with tandem mass spectrometry (LC/MS/MS) utilizing electrospray ionization in the positive mode to determine 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and N-Nitrosonornicotine (NNN). The content of NNK and NNN in a tobacco sample was quantified using internal standards (d4-NNK and d4-NNN). NNK and NNN concentrations in aliquots were measured in ng/mL and then reported as ng/g ( Lawler et al. 2013; US Food and Drug Administration 2017; CORESTA Method #72 2016 ).
Korean male active smokers: quantifying their smoking habits and the transformation factor among biomarkers in urine and blood
Published in Biomarkers, 2020
Jiyeon Yang, Shervin Hashemi, Wonseok Han, Chaelin Lee, Younseok Kang, Youngwook Lim
The tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is a metabolite of the tobacco-specific nitrosamine (TSNA) 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). NNK is probably the most common systemic lung carcinogen, causing lung cancer, which is only found in tobacco and tobacco products (Xia et al.2011). NNAL is primarily defaecated through urination (Xia et al.2005). Therefore, urinary NNAL is an important biomarker for determining a subject’s exposure to NNK.