The role of acrolein for E-cigarette vapour condensate mediated activation of NADPH oxidase in cultured endothelial cells and macrophages

Publikationstyp:
Zeitschriftenaufsatz
Metadaten:
Abstract
<jats:title>Abstract</jats:title><jats:p>Electronic cigarettes (E-cigarettes) have recently become a popular alternative to traditional tobacco cigarettes. Despite being marketed as a healthier alternative, increasing evidence shows that E-cigarette vapour could cause adverse health effects. It has been postulated that degradation products of E-cigarette liquid, mainly reactive aldehydes, are responsible for those effects. Previously, we have demonstrated that E-cigarette vapour exposure causes oxidative stress, inflammation, apoptosis, endothelial dysfunction and hypertension by activating NADPH oxidase in a mouse model. To better understand oxidative stress mechanisms, we have exposed cultured endothelial cells and macrophages to condensed E-cigarette vapour (E-cigarette condensate) and acrolein. In both endothelial cells (EA.hy 926) and macrophages (RAW 264.7), we have observed that E-cigarette condensate incubation causes cell death. Since recent studies have shown that among toxic aldehydes found in E-cigarette vapour, acrolein plays a prominent role, we have incubated the same cell lines with increasing concentrations of acrolein. Upon incubation with acrolein, a translocation of Rac1 to the plasma membrane has been observed, accompanied by an increase in oxidative stress. Whereas reactive oxygen species (ROS) formation by acrolein in cultured endothelial cells was mainly intracellular, the release of ROS in cultured macrophages was both intra- and extracellular. Our data also demonstrate that acrolein activates the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway and, in general, could mediate E-cigarette vapour-induced oxidative stress and cell death. More mechanistic insight is needed to clarify the toxicity associated with E-cigarette consumption and the possible adverse effects on human health.</jats:p>
Autoren
  • Ivana Kuntic
  • Marin Kuntic
  • Matthias Oelze
  • Paul Stamm
  • Angelica Karpi
  • Hartmut Kleinert
  • Omar Hahad
  • Thomas Münzel
  • Andreas Daiber
DOI
10.1007/s00424-023-02825-9
eISSN
1432-2013
ISSN
0031-6768
Ausgabe der Veröffentlichung
7
Zeitschrift
Pflügers Archiv - European Journal of Physiology
Sprache
en
Online publication date
2023
Paginierung
807 - 821
Datum der Veröffentlichung
2023
Status
Published
Herausgeber
Springer Science and Business Media LLC
Herausgeber URL
http://dx.doi.org/10.1007/s00424-023-02825-9
Datum der Datenerfassung
2023
Titel
The role of acrolein for E-cigarette vapour condensate mediated activation of NADPH oxidase in cultured endothelial cells and macrophages
Ausgabe der Zeitschrift
475

Datenquelle: Crossref

Andere Metadatenquellen:
Author's licence
CC-BY
Autoren
  • Ivana Kuntic
  • Marin Kuntic
  • Matthias Oelze
  • Paul Stamm
  • Angelica Karpi
  • Hartmut Kleinert
  • Omar Hahad
  • Thomas Münzel
  • Andreas Daiber
Hosting institution
Universitätsbibliothek Mainz
Sammlungen
  • DFG-491381577-H
Resource version
Published version
DOI
10.1007/s00424-023-02825-9
Funding acknowledgements
  • Deutsche Forschungsgemeinschaft (DFG)|491381577|Open-Access-Publikationskosten 2022–2024 Universität Mainz - Universitätsmedizin
File(s) embargoed
false
Open access
true
ISSN
1432-2013
Zeitschrift
Pflügers Archiv : European journal of physiology
Schlüsselwörter
  • 610 Medizin
  • 610 Medical sciences
Sprache
eng
Open access status
Open Access
Paginierung
807 - 821
Datum der Veröffentlichung
2023
Public URL
https://openscience.ub.uni-mainz.de/handle/20.500.12030/9418
Herausgeber
Springer
Datum der Datenerfassung
2023
Datum, an dem der Datensatz öffentlich gemacht wurde
2023
Zugang
Public
Titel
The role of acrolein for E-cigarette vapour condensate mediated activation of NADPH oxidase in cultured endothelial cells and macrophages
Ausgabe der Zeitschrift
475

Files

the_role_of_acrolein_for_ecig-20230815141422014.pdf

Datenquelle: OPENSCIENCE.UB

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