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)
| Autor: | Marin Kuntic, Konstantina Filippou, John F. Keaney, Regina Huesmann, Thorsten Hoffmann, Andreas Daiber, Paul Stamm, Katie Frenis, Miroslava Kvandova, Maria Teresa Bayo Jimenez, Vivienne Brückl, Ksenija Vujacic-Mirski, Franco Varveri, Frank P. Schmidt, Matthias Oelze, Swenja Kröller-Schön, Omar Hahad, Steffen Daub, Sebastian Steven, Ahmad Al Zuabi, Tommaso Gori, Sanela Kalinovic, Thomas Münzel |
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| Rok vydání: | 2019 |
| Předmět: |
Behavioural risk factor
Inflammation Electronic Nicotine Delivery Systems 030204 cardiovascular system & hematology Pharmacology medicine.disease_cause Vascular Medicine Lifestyle drug Nicotine Lipid peroxidation Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Basic Science Animals Humans Medicine Endothelial dysfunction 030212 general & internal medicine Macitentan NADPH oxidase biology business.industry Brain NADPH Oxidases medicine.disease E-cigarette vapour Editor's Choice Leukemia Myeloid Acute Oxidative Stress medicine.anatomical_structure chemistry E-Cigarette Vapor NADPH Oxidase 2 Neoplastic Stem Cells biology.protein medicine.symptom Cardiology and Cardiovascular Medicine business Oxidative stress medicine.drug Blood vessel |
| Zdroj: | European Heart Journal |
| ISSN: | 1522-9645 0195-668X |
| DOI: | 10.1093/eurheartj/ehz772 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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