Genotoxicity of environmental tobacco smoke / Kristi Husgafvel-Pursiainen (2004)  

Public Titre : Genotoxicity of environmental tobacco smoke : a review Type de document : document électronique Auteurs : Kristi Husgafvel-Pursiainen, Auteur Editeur : Elsevier Science Direct Année de publication : 2004 Collection : Mutation Research: Reviews in Mutation Research, ISSN 1388-2139 num. 567 Importance : p.427–445 Langues : Anglais (eng) Catégories : [TABAC] tabagisme:risque:facteur associé:génétique [TABAC] tabagisme:tabagisme passif Index. décimale : TA 7.4 Effets du tabagisme passif Résumé : Environmental tobacco smoke (ETS), or second-hand smoke, is a widespread contaminant of indoor air in environments where smoking is not prohibited. It is a significant source of exposure to a large number of substances known to be hazardous to human health. Numerous expert panels have concluded that there is sufficient evidence to classify involuntary smoking (or passive smoking) as carcinogenic to humans. According to the recent evaluation by the International Agency for Research on Cancer, involuntary smoking causes lung cancer in never-smokers with an excess risk in the order of 20% for women and 30% for men. The present paper reviews studies on genotoxicity and related endpoints carried out on ETS since the mid-1980s. The evidence from in vitro studies demonstrates induction of DNA strand breaks, formation of DNA adducts, mutagenicity in bacterial assays and cytogenetic effects. In vivo experiments in rodents have shown that exposure to tobacco smoke, whole-body exposure to mainstream smoke (MS), sidestream smoke (SS), or their mixture, causes DNA single strand breaks, aromatic adducts and oxidative damage to DNA, chromosome aberrations and micronuclei. Genotoxicity of transplacental exposure to ETS has also been reported. Review of human biomarker studies conducted among non-smokers with involuntary exposure to tobacco smoke indicates presence of DNA adducts, urinary metabolites of carcinogens, urinary mutagenicity, SCEs and hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene mutations (in newborns exposed through involuntary smoking of the mother). Studies on human lung cancer from smokers and never-smokers involuntarily exposed to tobacco smoke suggest occurrence of similar kinds of genetic alterations in both groups. In conclusion, these overwhelming data are compatible with the current knowledge on the mechanisms of carcinogenesis of tobacco-related cancers, occurring not only in smokers but with a high biological plausibility also in involuntary smokers. En ligne : https://doi.org/10.1016/j.mrrev.2004.06.004 Format de la ressource électronique : Article en ligne Permalink : https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10025

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Multi-endpoint in vitro toxicological assessment of snus and tobacco-free nicotine pouch extracts / Fan Yu (2024)  

Public Titre : Multi-endpoint in vitro toxicological assessment of snus and tobacco-free nicotine pouch extracts Type de document : document électronique Auteurs : Fan Yu, Auteur ; Emma Bishop, Auteur ; Fabio Miazzi, Auteur Editeur : Elsevier Science Direct Année de publication : 2024 Collection : Mutation Research: Reviews in Mutation Research, ISSN 1388-2139 num. 895 Importance : 10 p. Présentation : ill., graph.; tab. Langues : Anglais (eng) Catégories : [TABAC] chimie du tabac:constituant:alcaloïde:nicotine [TABAC] chimie du tabac:tabac non fumé:tabac à sucer:snus [TABAC] étude [TABAC] tabagisme:effet du tabac [TABAC] tabagisme:tabagisme actif Mots-clés : Pouche de nicotine Index. décimale : TA 1.2 Tabac non fumé Résumé : ‘Modern’ oral tobacco-free nicotine pouches (NPs) are a nicotine containing product similar in appearance and concept to Swedish snus. A three-step approach was taken to analyse the biological effects of NPs and snus extracts in vitro. ToxTracker was used to screen for biomarkers for oxidative stress, cell stress, protein damage and DNA damage. Cytotoxicity, mutagenicity, and genotoxicity were assessed in the following respective assays: Neutral Red Uptake (NRU), Ames and Mouse Lymphoma Assay (MLA). Targeted analysis of phosphorylation signalling and inflammatory markers under non-toxic conditions was used to investigate any potential signalling pathways or inflammatory response. A reference snus (CRP1.1) and four NPs with various flavours and nicotine strengths were assessed. Test article extracts was generated by incubating one pouch in 20 mL of media (specific to each assay) with the inclusion of the pouch material. NP extracts did not induce any cytotoxicity or mutagenic response, genotoxic response was minimal and limited signalling or inflammatory markers were induced. In contrast, CRP1.1 induced a positive response in four toxicological endpoints in the absence of S9: Srxn1 (oxidative stress), Btg2 (cell stress), Ddit3 (protein damage) and Rtkn (DNA damage), and three endpoints in presence of S9: Srxn1, Ddit3 and Rtkn. CRP1.1 was genotoxic when assessed in MLA and activated signalling pathways involved in proliferation and cellular stress and specifically induced phosphorylation of c-JUN, CREB1, p53, p38 MAPK and to a lesser extent AKT1S1, GSK3α/β, ERK1/2 and RSK1 in a dose-dependent manner. CRP 1.1 extracts resulted in the release of several inflammatory mediators including cytokines IL-1α, IL5, IL6, IL8, IL-1RA, MIF and TNF-β, receptor IL-2RA, and growth factors FGF-basic, VEGF and M-CSF. In conclusion these assays contribute to the weight of evidence assessment of the potential comparative health risks of NPs and snus. En ligne : https://doi.org/10.1016/j.mrgentox.2024.503738 Format de la ressource électronique : Article en ligne Permalink : https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10531

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