Toxic effect of electronic cigarette extracts in iPS cardiomyocytes
2020
University of Nebraska Medical Center, Omaha, USA
Cigarette smoking is an important risk factor for cardiac diseases. In the current study, the effects of electronic cigarette extract (ECE) and conventional cigarette smoke extract (CSE) were assessed in cardiomyocytes.
iPSCs-derived cardiomyocytes were used to evaluate cellular toxicities. Cells were exposed to either ECE or CSE for two consecutive days as an acute exposure, or every other day for 14 days. Concentration of nicotine and the oxidative stress in both ECE and CSE were measured. Motility and beat frequency of cardiomyocytes were determined and the heart failure target panel genes of exposed cardiomyocytes were compared to control unexposed cells.
Despite nicotine concentration in CSE being six-fold higher than ECE (50 μg in CSE and 8 μg in ECE), ECE had similar toxic effect on cardiomyocytes. Both CSE and ECE generate significant cellular reactive oxygen species. A video analysis showed significant changes in myocyte function with both CSE and ECE slowing beating and increasing cell death. Chronic exposure of both ECE and CSE significantly decreased cardiomyocytes' viability long term at all doses.
Target panel gene expression profiles of both ECE and CSE exposed cardiomyocytes were different from controls with distinct pattern of genes that involved cell proliferation, inflammation, and apoptosis.
ECE and CSE produce similar cardiomyocyte toxicities which include generating oxidative stress, negative chronotropic effects, adverse changes in myocardial gene expression and ultimately cell death.
Electronic cigarette extract induced toxic effect in iPS-derived cardiomyocytes
Hesham Basma
Added on: 09-12-2023
[1] https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-020-01629-4
