Titre : | Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2) (2020) |
Auteurs : | M. KUNTIC ; M. OELZE ; S. STEVEN ; S. KROLLER-SCHON ; P. STAMM ; S. KALINOVIC ; K. FRENIS ; K. VUJACIC-MIRSKI ; M. T. BAYO JIMENEZ ; M. KVANDOVA ; K. FILIPPOU ; A. AL ZUABI ; V. BRUCKL ; O. HAHAD ; S. DAUB ; F. VARVERI ; T. GORI ; R. HUESMANN ; T. HOFFMANN ; F. P. SCHMIDT ; J. F., Jr KEANEY ; A. DAIBER ; T. MUNZEL |
Type de document : | Article : Périodique |
Dans : | European Heart Journal (Vol.41, n°26, 7 July 2020) |
Article en page(s) : | 2472-2483 |
Langues: | Anglais |
Discipline : | PRO (Produits, mode d'action, méthode de dépistage / Substances, action mode, screening methods) |
Mots-clés : |
Thésaurus mots-clés E-CIGARETTE ; CERVEAU ; CARDIOLOGIE ; ENZYMES ; MODELE ANIMAL ; FACTEUR DE RISQUE ; POUMON ; MECANISME D'ACTION ; PHARMACOLOGIE ; EFFET SECONDAIRE ; TOXICITE |
Résumé : |
Aims: Electronic (e)-cigarettes have been marketed as a 'healthy' alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms.
Methods and results: Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental effects on endothelial function, markers of oxidative stress, inflammation, and lipid peroxidation than vapour containing nicotine. These effects of e-cigarette vapour were largely absent in mice lacking phagocytic NADPH oxidase (NOX-2) or upon treatment with the endothelin receptor blocker macitentan or the FOXO3 activator bepridil. We also established that the e-cigarette product acrolein, a reactive aldehyde, recapitulated many of the NOX-2-dependent effects of e-cigarette vapour using in vitro blood vessel incubation. Conclusions: E-cigarette vapour exposure increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. Our study identifies the toxic aldehyde acrolein as a key mediator of the observed adverse vascular consequences. Thus, e-cigarettes have the potential to induce marked adverse cardiovascular, pulmonary, and cerebrovascular consequences. Since e-cigarette use is increasing, particularly amongst youth, our data suggest that aggressive steps are warranted to limit their health risks. |
Domaine : | Tabac / Tobacco / e-cigarette |
Refs biblio. : | 41 |
Affiliation : | Center for Cardiology, University Medical Center, Mainz, Germany |
Lien : | https://doi.org/10.1093/eurheartj/ehz772 |
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