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Bibliographies thématiques / Tobacco-related nitrosamines

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Articles de revues

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"

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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. F

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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

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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

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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 a

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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

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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 com

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