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

Introduction:
This article investigates the effects of acrolein, a component of electronic cigarette (E-cigarette) vapor condensate, on cultured endothelial and immune cells. The study aims to understand the mechanisms of oxidative stress and cell death induced by E-cigarette vapor condensate.

Key Points:

* E-cigarette vapor condensate and acrolein exposure cause concentration and time-dependent cytotoxicity in endothelial cells and macrophages.
* acrolein induces oxidative stress and triggers a compensatory antioxidant response via Nrf2-dependent induction of heme-oxygenase-1.
* NaDPh oxidase-dependent ROS formation is responsible for oxidative stress caused by acrolein.
* Rac1 translocation to the membrane and extracellular ROS formation are observed in endothelial cells and macrophages treated with acrolein.
* The study suggests that an appreciable part of the adverse effects of E-cigarette vapor condensate found in human endothelial cells and macrophages may arise from acrolein formed while heating E-cigarette liquid before inhaling.

Main Message:
The study demonstrates that acrolein, a component of E-cigarette vapor condensate, plays a significant role in inducing oxidative stress and cell death in endothelial cells and macrophages. The findings highlight the need for further research to understand the mechanisms of E-cigarette toxicity fully. The study also underscores the importance of developing strategies to limit acrolein exposure in E-cigarette users.

Kuntic I, Kuntic M, Oelze M, et al. The role of acrolein for E-cigarette vapour condensate mediated activation of NaDPh oxidase in cultured endothelial cells and macrophages. Pflugers archiv : European journal of physiology. 2023;475(7):807-821. doi:10.1007/s00424-023-02825-9