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). (13th November 2019)

• Record Type: Journal Article
• Authors: Kuntic, Marin; Oelze, Matthias; Steven, Sebastian; Kröller-Schön, Swenja; Stamm, Paul; Kalinovic, Sanela; Frenis, Katie; Vujacic-Mirski, Ksenija; Bayo Jimenez, Maria Teresa; Kvandova, Miroslava; Filippou, Konstantina; Al Zuabi, Ahmad; Brückl, Vivienne; Hahad, Omar; Daub, Steffen; Varveri, Franco; Gori, Tommaso; Huesmann, Regina; Hoffmann, Thorsten; Schmidt, Frank P; Keaney, John F; Daiber, Andreas; Münzel, Thomas
• Is Part Of: European heart journal. Volume 41:Number 26(2020)
• Page Start: 2472
• Page End: 2483
• Publication Date: 2019-11-13
• Subjects: Behavioural risk factor -- Lifestyle drug -- E-cigarette vapour -- Endothelial dysfunction -- Oxidative stress; Cardiology -- Periodicals; Heart -- Diseases -- Periodicals; 616.12005
• DOI: 10.1093/eurheartj/ehz772
• Languages: English
• ISSNs: 0195-668X

Abstract

Abstract: 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.