• Asian Pacific Journal of Cancer Prevention
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• v.16 no.13
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• pp.5311-5317
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• 2015

Cigarette smoke derivatives like NNK (4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone) and NNAL (4-(methylnitrosamino)-1-(3-pyridyl)-1-butan-1-ol) are well-known carcinogens. We analyzed the interaction of enzymes involved in the NER (nucleotide excision repair) pathway with ligands (NNK and NNAL). Binding was characterized for the enzymes sharing equivalent or better interaction as compared to +Ve control. The highest obtained docking energy between NNK and enzymes RAD23A, CCNH, CDK7, and CETN2 were -7.13 kcal/mol, -7.27 kcal/mol, -8.05 kcal/mol and -7.58 kcal/mol respectively. Similarly the highest obtained docking energy between NNAL and enzymes RAD23A, CCNH, CDK7, and CETN2 were -7.46 kcal/mol, -7.94 kcal/mol, -7.83 kcal/mol and -7.67 kcal/mol respectively. In order to find out the effect of NNK and NNAL on enzymes involved in the NER pathway applying protein-protein interaction and protein-complex (i.e. enzymes docked with NNK/NNAL) interaction analysis. It was found that carcinogens are well capable to reduce the normal functioning of genes like RAD23A (HR23A), CCNH, CDK7 and CETN2. In silico analysis indicated loss of functions of these genes and their corresponding enzymes, which possibly might be a cause for alteration of DNA repair pathways leading to damage buildup and finally contributing to cancer formation.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.169-176
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• 2004

ETS (environmental tobacco smoke) is composed of exhaled mainstream smoke (MS) from the smoker, sidestream smoke (SS) emitted from the smoldering tobacco between puffs and contaminants that diffuse through the cigarette paper and mouth between puffs. These emissions contain both vapor phase and particulate contaminants. ETS is a complex mix of over 4,000 compounds. This mix contains many known or suspected human carcinogens and other toxic agents. More of these toxic compounds are found in SS than in MS. Workplace exposure to ETS can result in significant smoke intake, and passive smoke exposure may be related to impair respiratory function and an increase risk of lung cancer in nonsmokers. For nonsmokers sharing a work environment with cigarette smokers, the workplace must be considered hazardous independently of any specific industrial toxic exposure. The risk is particularly important when a high percentage of the workers smoke or where smokers and nonsmokers work in poorly ventilated areas. Nicotine is converted in the body to cotinine; cotinine therefore can be used as an indirect measure of a person's recent exposure to tobacco smoke. Levels of nicotine in hair and levels of cotinine in body fluids (saliva and urine) have been shown to increase with increasing environmental nicotine levels and with self-reported ETS exposure. The measurement of nicotine or cotinine in hair may be more appropriate for longer-term exposure to tobacco. The purpose of this study is to comparing airborne nicotine levels and hair cotinine level in restaurant workers. Concentration of airborne nicotine and hair nicotine (and cotinine) is closely related to exposed frequency of sidestream smoke in the workplace. Nicotine in hair is a better predictor of airborne nicotine than hair cotinine. Hair nicotine can be a useful tool to assess ETS exposure interventions. It may have limiting levels of ETS exposure by placing regulatory restrictions on smoking in workplaces and in public spaces.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.9
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• pp.4057-4060
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• 2015

Cigarette smoke contains oxidants and free radicals which are carcinogens that can induce mutations in humans. Single nucleotide polymorphisms (SNPs) are the most frequent genetic alterations found in the human genome. In the present study, we have examined the ability of the murine double minute 2 (Mdm2) (rs769412) A>G polymorphism in cigarette smokers to predict risk of cancers. Our results showed that of smokers, 87% were found with AA genotype, 10% with heterozygous AG genotype, and 3% with GG genotype. The heterozygous AG genotype was observed in a lower percentage of smokers (10%) as compared to non-smokers (18%), whereas, homozygous AA genotype was observed in lower percentage of non-smokers (81%) as compared to the smokers (87%). The results from present study support the association with an allele and AG genotype in non-smokers. However, further studies are required to establish the role of Mdm2 (rs769412) C>T in cigarettes smokers and diseases.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.176-176
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• 2003

Cigarette smoke is a complex mixture of thousands of compounds, many of which are known or suspected human carcinogens. A preventive effect of the consumption of vegetables or fruits on various types of cancer has been confirmed from numerous studies.(omitted)

• Korean Journal of Environmental Agriculture
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• v.19 no.2
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• pp.147-153
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• 2000

Cigarette smoking deals a harmful effect directly to smokers and even to non-smokers through environmental tobacco smoke. The major damaging component in cigarette smoke is nicotine which converts to various carcinogens. Among the carcinogenic metabolites, nitrosamine-4-(methylnitrosamino)-1- (3-pyridyl)-1- butanone (NNK) is responsible for many types of lung cancers. Recent studies report that activation of NNK is markedly inhibited in the presence of cotinine, a safer metabolite from nicotine. It is well known that tea extract have potentials to prevent cancers. This study aims to correlate green tea's potential for cancer prevention with an accelerated formation of cotinine. In the presence of tea extract, a nicotine to cotinine conversion was studied in established cell lines and xenopus oocytes. Among three lines of cell used, PLC/PRF5 and 293 cells showed a fast turnover from nicotine to cotinine while HepG2 cell line showed a marginal difference between groups treated and non-treated with tea extract. A microinjection procedure using Xenopus oocyte was utilized to probe for the effect of tea extract in accelerating nicotine conversion to cotinine. According to this procedure, tea extract's unusual potential for converting nicotine to cotinine is also substantiated. Overall, this present study indicated that tea extract have an unusual effect on conversion of nicotine to cotinine in cells.

• Analytical Science and Technology
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• v.17 no.5
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• pp.410-415
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• 2004

In order to learn the emission characteristics of hazardous pollutants associated with environmental tobacco smoking (ETS), we measured the concentrations of major aromatic VOC and carbonyl compounds released from ETS. By acquiring the different smoke types of ETS, we were able to determine that the concentrations of those species range from ppb (normal exhaled air of smoker prior to smoking) to ppm levels (direct release of ETS without filter). Using these measurement data, we also evaluated the body-retaining rate of these compounds as the result of ETS. The results of our analysis indicated that predominant portion of them (e.g., > 99%) are retained as the result of cigarette smoking. To learn more about the potential impact of ETS, more extensive study may be required to assess the gross picture of pollutant deposition inside respiratory intake and their health-effects.

• Biomolecules & Therapeutics
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• v.11 no.4
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• pp.238-244
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• 2003

Nicotine is one of the major hazardous components in cigarettc smoke. Nicotine deals a harmful effect to smokers and passive smokers due to its rapid conversion to various carcinogenic metabolites. Nitrosamine-4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is believed to cause lung cancers among the nicotine-derived carcinogens. Recent studies report that NNK synthesis can be inhibited by the metabolism pathway to produce a stable metabolite cotinine from nicotine. Tea polyphenols have been known to contain factors to prevent cancers and to retard progression of cancers. This study aims to correlate tea polyphenol's potential for cancer prevention with an accelerated formation of cotinine. The conversion from nicotine to cotinine in the presence of tea extracts or three polyphenols (Catechin, epicatechin gallate, epigallocatechin gallate) was measured in established cell lines and in Xenopus oocytes. Among three lines of cell used, PLC/PRF5 and HEK293 cells showed a fast turnover from nicotine to cotinine while HepG2 cell line showed a marginal difference between groups treated and non-treated with tea polyphenols. When Xenopus oocytes were microinjected with nicotine, tea polyphenols appear to accelerate the conversion of nicotine to cotinine. Among the polyphenols tested in this study, (＋)－catechin showed the best efficiency overall in accelerating conversion from nicotine to cotinine both in the cell lines and in the oocytes. In summary, the present study indicated that tea polyphenols have a positive effect on conversion of nicotine to cotinine.

• Tuberculosis and Respiratory Diseases
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• v.49 no.5
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• pp.576-584
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• 2000

Background : With the increase of cigarette consumption by women and the young, the incidence of lung cancer is expected to increase during the next three or four decades in Korea. The purpose of this study was to analyze the smoking habits in patients with lung cancer and to identify the gender differences in terms of their susceptibility to cigarette related carcinogens. Method : This investigation was a hospital-based case control study, which included the data of 178 case subjects (72 females, 106 males) with lung cancer and 218 control subjects (97 females, 121 males) with diseases unrelated to smoking. The information was obtained through a direct personal interview and a questionnaire related to personal smoking history. Results : The relative frequency of the squamous cell carcinoma was substantially higher in males than in females (61.3% in males, and 29.2% in females), while adenocarcinoma including bronchoalveolar cell carcinoma was higher in females(31.9% in females, 18.9% in males). Kreyberg I lung cancer was of relatively higher frequencies in males and smokers, while Kreyberg II lung cancer was higher in females and never smokers. The odds ratios (ORs) at each exposure level were consistently higher in females than males. For all cell types, the risk of lung cancer was increased with the quantity of smoked cigarettes, duration of smoking, and depth of inhalation. Odds ratio was distinctly higher in Kreyberg I lung cancer than in total lung cancer and a steeper gradient of risk with increased smoking was observed in females. Conclusion : The relative risk for lung cancer was consistently higher in females than in males at every level of exposure to cigarette smoke. This is believed to be due to the higher susceptibility of females to tobacco carcinogens, such as gender associated differences of carcinogen activation and/or the elimination of smoking related metabolites.