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Littérature scientifique sur le sujet « Tobacco-related nitrosamines »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Tobacco-related nitrosamines"

Cogliano, Vincent, Kurt Straif, Robert Baan, Yann Grosse, Béatrice Secretan, and Fatiha El Ghissassi. "Smokeless tobacco and tobacco-related nitrosamines." Lancet Oncology 5, no. 12 (2004): 708. http://dx.doi.org/10.1016/s1470-2045(04)01633-x.

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Myers, Steven R., and M. Yeakub Ali. "Haemoglobin adducts as biomarkers of exposure to tobacco-related nitrosamines." Biomarkers 13, no. 2 (2008): 145–59. http://dx.doi.org/10.1080/13547500701470561.

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Bošković, Maria, Blanka Roje, Felicia Fei-Lei Chung, et al. "DNA Methylome Changes of Muscle- and Neuronal-Related Processes Precede Bladder Cancer Invasiveness." Cancers 14, no. 3 (2022): 487. http://dx.doi.org/10.3390/cancers14030487.

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Bladder cancer (BC) is the ninth leading cause of cancer death with one of the highest recurrence rates among all cancers. One of the main risks for BC development is exposure to nitrosamines present in tobacco smoke or in other products. Aberrant epigenetic (DNA methylation) changes accompanied by deregulated gene expression are an important element of cancer pathogenesis. Therefore, we aimed to determine DNA methylation signatures and their impacts on gene expression in mice treated with N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), a carcinogen similar to compounds found in tobacco smoke. Following BBN administration mice developed non-invasive or invasive bladder cancers. Surprisingly, muscle- and neuronal-related pathways emerged as the most affected in those tumors. Hypo- and hypermethylation changes were present within non-invasive BC, across CpGs mapping to the genes involved in muscle- and neuronal-related pathways, however, methylation differences were not sufficient to affect the expression of the majority of associated genes. Conversely, invasive tumors displayed hypermethylation changes that were linked with alterations in gene expression profiles. Together, these findings indicate that bladder cancer progression could be revealed through methylation profiling at the pre-invasive cancer stage that could assist monitoring of cancer patients and guide novel therapeutic approaches.

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Amin, Shantu, Dhimant Desai, Stephen S. Hecht, and Dietrich Hoffmann. "Synthesis of Tobacco-SpecificN-Nitrosamines and Their Metabolites and Results of Related Bioassays." Critical Reviews in Toxicology 26, no. 2 (1996): 139–47. http://dx.doi.org/10.3109/10408449609017927.

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Doukas, Sotirios G., Dimitra P. Vageli, Panagiotis G. Doukas, Dragana Nikitovic, Aristidis Tsatsakis, and Benjamin L. Judson. "The Effect of Tobacco Smoke N-Nitrosamines, NNK and NDEA, and Nicotine, on DNA Mismatch Repair Mechanism and miRNA Markers, in Hypopharyngeal Squamous Cell Carcinoma: An In Vivo Model and Clinical Evidence." Current Oncology 29, no. 8 (2022): 5531–49. http://dx.doi.org/10.3390/curroncol29080437.

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Deregulation of the DNA mismatch repair (MMR) mechanism has been linked to poor prognosis of upper aerodigestive tract cancers. Our recent in vitro data have provided evidence of crosstalk between deregulated miRNAs and MMR genes, caused by tobacco smoke (TS) N-Nitrosamines, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), in hypopharyngeal cells. Here, we explored whether chronic exposure to TS components can affect MMR mechanism and miRNA profiles in hypopharyngeal mucosa. Using a mouse model (C57Bl/6J wild type) of in vivo 14-week exposure to NNK (0.2 mmol/L) and N-Nitrosodiethylamine (NDEA; 0.004 mmol/L), with or without nicotine (0.02 μmol/L), we provide direct evidence that TS components can promote dysplasia, significant downregulation of Msh2 and Mlh1 genes and deregulation of miR-21, miR-155, miR-34a, and miR-451a. By analyzing eight human specimens from tobacco smokers and eight controls, we provide clinical evidence of a significant reduction in hMSH2 and hMLH1 mRNAs in hypopharyngeal squamous cell carcinoma (HSCC). In summary, deregulation of the MMR mechanism and miRNAs is caused by chronic exposure to TS-related N-Nitrosamines, with or without nicotine, in the early stages of upper aerodigestive tract carcinogenesis, and can also be detected in human HSCC. Thus, we encourage future studies to further elucidate a possible in vivo dose-dependent effect of individual or combined N-Nitrosamines, NNK and/or NDEA, and nicotine, on the MMR mechanism and their clinical testing to elaborate prognosis and risk assessment.

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Ahijevych, Karen. "Biological Models for Studying and Assessing Tobacco Use." Annual Review of Nursing Research 27, no. 1 (2009): 145–68. http://dx.doi.org/10.1891/0739-6686.27.145.

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The purpose of this chapter on biological models for studying and assessing tobacco use is to provide an introduction to some of the common concepts and biomarkers in this arena to ultimately inform intervention research by nurse scientists. An overview of selected biomarkers of tobacco exposure in individuals includes exhaled carbon monoxide, cotinine (the proximate metabolite of nicotine), and measurement of an individual’s puffing pattern termed smoking topography. Common tobacco contents discussed include tobacco specific nitrosamines (TSNA) and polycyclic aromatic hydrocarbons (PAH) some of which increase disease risk including cancer. Exemplars of additives to cigarettes by the tobacco industry will be described including menthol, one additive marketed by the industry. Genetics and tobacco addiction has emerged as a rapidly expanding field. Illustrative of this area are twin studies, nicotinic receptors, CYP2A6 polymorphisms, and genes that impact dopamine receptors. The cadre of nurse scientists conducting research in this much needed area is small. The opportunity for nurse scientists educated in biological inquiry in tobacco-related research is great. Nurse scientists actively involved in multidisciplinary translational teams to address nicotine addition are needed.

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Kankanamage, Rumasha N. T., Abhisek Brata Ghosh, Di Jiang, et al. "Metabolites of Tobacco- and E-Cigarette-Related Nitrosamines Can Drive Cu2+-Mediated DNA Oxidation." Chemical Research in Toxicology 33, no. 8 (2020): 2072–86. http://dx.doi.org/10.1021/acs.chemrestox.0c00027.

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Rodgman, A. "Studies of Polycyclic Aromatic Hydrocarbons in Cigarette Mainstream Smoke: Identification, Tobacco Precursors, Control of Levels: A Review." Beiträge zur Tabakforschung International/Contributions to Tobacco Research 19, no. 7 (2001): 361–79. http://dx.doi.org/10.2478/cttr-2013-0724.

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AbstractDuring the period of tobacco smoke research from the early 1950s to the mid-1960s it was repeatedly asserted that a) tobacco and many tobacco components were involved in the pyrogenesis of polycyclic aromatic hydrocarbons (PAHs), several of which were reported to initiate tumors on the skin of laboratory animals and b) tobacco additives (flavorants, casing materials, humectants) were highly likely to be similarly involved in PAH pyrogenesis. Extensive knowledge on PAHs was deemed highly necessary because of their claimed importance in the smoking-health issue. The numerous assertions about the generation of PAHs in cigarette mainstream smoke (MSS) triggered extensive and intensive research both within and outside the Tobacco Industry to define the nature of the PAHs, their per cigarette MSS delivery amounts, their precursors, etc. It was not until 1960 that VAN DUUREN et al. (1) reported three specific aza-arenes in cigarette MSS that were asserted to be involved in smokers’ respiratory tract cancer. As noted in a recent Letter to the Editors (2), the presence of these three aza-arenes in tobacco smoke has never been confirmed. Between 1960 and 1965, other MSS components (phenols as promoters, polonium-210, N-nitrosamines, ciliastatic compounds) were asserted to be responsible for smoking related diseases. However, no major assertions were made that phenols, polonium-210, or the N-nitrosamines were derived from flavorants, casing materials, or humectants. Some investigators did report that several ciliastats were derived from added sugars and glycerol. The ciliastat proposal was drastically diminished in importance by the findings in the 1960s that only a relatively small proportion of the ciliastats reached the smoker's cilia. During that time, pertinent skills and competencies in research on tobacco smoke composition, particularly the PAH fraction, have been developed. Such skills permitted the isolation in crystalline form of 14 PAHs and the quantitation of these and many other PAHs. They were also used to put in perspective the pyrogenesis of PAHs from a) specific tobacco components, b) additives, and c) processed tobaccos (reconstituted tobacco sheet [RTS], expanded tobacco). R.J. Reynolds Tobacco Company (RJRT) pioneered the use of RTS (1953) and expanded tobaccos (1969) in cigarette blends and generated much previously unpublished data on the effect of such processed tobaccos on MSS composition.

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Brown, Buddy G., August J. Borschke, and David J. Doolittle. "An Analysis of the Role of Tobacco-Specific Nitrosamines in the Carcinogenicity of Tobacco Smoke." Nonlinearity in Biology, Toxicology, Medicine 1, no. 2 (2003): 154014203914343. http://dx.doi.org/10.1080/15401420391434324.

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Cigarette smoke is a complex mixture consisting of more than 4500 chemicals, including several tobacco-specific nitrosamines (TSNA). TSNA typically form in tobacco during the post-harvest period, with some fraction being transferred into mainstream smoke when a cigarette is burned during use. The most studied of the TSNA is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). NNK has been shown to be carcinogenic in laboratory animals. Studies examining the carcinogenicity of NNK frequently are conducted by injecting rodents with a single dose of 2.5 to 10 μmol of pure NNK; the amount of NNK contained in all of the mainstream smoke from about 3700 to 14,800 typical U.S. cigarettes. Extrapolated to a 70-kg smoker, the carcinogenic dose of pure NNK administered to rodents would be equivalent to the amount of NNK in all of the mainstream smoke of 22 to 87 million typical U.S. cigarettes. Furthermore, extrapolating results from rodent studies based on a single injection of pure NNK to establish a causative role for NNK in the carcinogenicity of chronic tobacco smoke exposure in humans is not consistent with basic pharmacological and toxicological principles. For example, such an approach fails to consider the effect of other smoke constituents upon the toxicity of NNK. In vitro studies demonstrate that nicotine, cotinine, and aqueous cigarette “tar” extract (ACTE) all inhibit the mutagenic activity of NNK. In vivo studies reveal that the formation of pulmonary DNA adducts in mice injected with NNK is inhibited by the administration of cotinine and mainstream cigarette smoke. Cigarette smoke has been shown to modulate the metabolism of NNK, providing a mechanism for the inhibitory effects of cigarette smoke and cigarette smoke constituents on NNK-induced tumorigenesis. NNK-related pulmonary DNA adducts have not been detected in rodents exposed to cigarette smoke, nor has the toxicity of tobacco smoke or tobacco smoke condensate containing marked reductions in TSNA concentrations been shown to be reduced in any biological assay. In summary, there is no experimental evidence to suggest that reduction of TSNA will reduce the mutagenic, cytotoxic, or carcinogenic potential of tobacco smoke.

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Smith, Danielle M., Richard J. O’connor, Binnian Wei, Mark Travers, Andrew Hyland, and Maciej L. Goniewicz. "Nicotine and Toxicant Exposure Among Concurrent Users (Co-Users) of Tobacco and Cannabis." Nicotine & Tobacco Research 22, no. 8 (2019): 1354–63. http://dx.doi.org/10.1093/ntr/ntz122.

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Abstract Background Smoking cannabis may potentially increase exposure to numerous toxic chemicals that are commonly associated with tobacco use. There is a paucity of data related to toxicant exposures among concurrent users of tobacco and cannabis (co-users). Methods Data are from the Population Assessment of Tobacco and Health Study Wave 1 Biomarker Restricted-Use Files. Analyses focused on adults who provided urine samples (N = 5859). Urine samples were analyzed for biomarkers of exposure to nicotine, tobacco-specific nitrosamines, polycyclic aromatic hydrocarbons, and volatile organic compounds. Using weighted linear regression, we compared adjusted geometric mean concentrations of 15 biomarkers between user groups of various tobacco product types according to their self-reported past 30-day cannabis use. Results Past 30-day cannabis use was similar across various types of tobacco product use subgroups (range: 13%–23%) and significantly more common compared to non-tobacco users (1.0%; p &lt; .001). Across all groups of tobacco users, those who co-used cannabis exhibited significantly higher concentrations of the biomarker of exposure to acrylonitrile (CYMA) compared to non-cannabis users (by 39%–464%). Tobacco–cannabis co-users also showed significantly elevated levels of the biomarker of exposure to acrylamide (AAMA) compared to exclusive tobacco users, and significantly higher exposure to many polycyclic aromatic hydrocarbons (including fluorene and pyrene). Conclusions Co-users exhibited higher concentrations for biomarkers of exposure to many combustion byproducts, compared to exclusive tobacco users. More robust measurements of cannabis use can address potential confounding in assessments of exposures to tobacco-related constituents, and potential health effects resulting from co-use. Implications With disproportionately greater rates of cannabis use occurring among tobacco users, it is critical to consider how concurrent cannabis use may influence health-related outcomes among smokers. Our findings suggest potential additive toxicant exposures among co-users of tobacco and cannabis. Lack of consideration and measurement of cannabis use in assessing tobacco-related exposures may confound estimates thought to be attributable to tobacco, particularly for non-specific biomarkers. Assessing tobacco and cannabis use in tandem will allow for more precise measurement of outcomes related to one or both substances, and can provide additional information on potential health effects related to co-use.

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