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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)
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 oxid...
Autores principales: | , , , , , , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7340357/ https://www.ncbi.nlm.nih.gov/pubmed/31715629 http://dx.doi.org/10.1093/eurheartj/ehz772 |
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author | 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 |
author_facet | 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 |
author_sort | Kuntic, Marin |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7340357 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-73403572020-07-13 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) 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 Eur Heart J Basic Science 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. Oxford University Press 2020-07-07 2019-11-13 /pmc/articles/PMC7340357/ /pubmed/31715629 http://dx.doi.org/10.1093/eurheartj/ehz772 Text en © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Basic Science 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 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) |
title | 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) |
title_full | 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) |
title_fullStr | 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) |
title_full_unstemmed | 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) |
title_short | 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) |
title_sort | 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) |
topic | Basic Science |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7340357/ https://www.ncbi.nlm.nih.gov/pubmed/31715629 http://dx.doi.org/10.1093/eurheartj/ehz772 |
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