E-Cigarette Aerosol Exposure Induces Reactive Oxygen Species, DNA Damage, and Cell Death in Vascular Endothelial Cells.
Cigarette smoking remains one of the leading causes of preventable death worldwide. Vascular cell death and dysfunction is a central or exacerbating component in the majority of cigarette smoking related pathologies. The recent development of the electronic nicotine delivery systems known as e-cigarettes provides an alternative to conventional cigarette smoking; however, the potential vascular health risks of e-cigarette use remain unclear. This study evaluates the effects of e-cigarette aerosol extract (EAE) and conventional cigarette smoke extract (CSE) on human umbilical vein endothelial cells (HUVECs). A laboratory apparatus was designed to produce extracts from e-cigarettes and conventional cigarettes according to established protocols for cigarette smoking. EAE or conventional CSE was applied to human vascular endothelial cells for 4-72 h, dependent on the assay. Treated cells were assayed for reactive oxygen species, DNA damage, cell viability, and markers of programmed cell death pathways. Additionally, the anti-oxidants α-tocopherol and n-acetyl-l-cysteine were used to attempt to rescue e-cigarette induced cell death. Our results indicate that e-cigarette aerosol is capable of inducing reactive oxygen species, causing DNA damage, and significantly reducing cell viability in a concentration dependent fashion. Immunofluorescent and flow cytometry analysis indicate that both the apoptosis and programmed necrosis pathways are triggered by e-cigarette aerosol treatment. Additionally, anti-oxidant treatment provides a partial rescue of the induced cell death, indicating that reactive oxygen species play a causal role in e-cigarette induced cytotoxicity.
Department of Cell and Molecular Biology.
Chastain
C
Anderson
Department of Cell and Molecular Biology.
Andrew
A
Majeste
Department of Cell and Molecular Biology.
Jakub
J
Hanus
Department of Cell and Molecular Biology; swang1@tulane.edu.|Department of Ophthalmology, Tulane University, 2000 Percival Stern Hall, 6400 Freret Street, Louisiana 70118.
Shusheng
S
Wang
D000336:Aerosols; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured; D004249:DNA Damage; D004305:Dose-Response Relationship, Drug; D066300:Electronic Nicotine Delivery Systems; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D019570:Inhalation Exposure; D009336:Necrosis; D009538:Nicotine / Q000633:toxicity*; D018722:Nicotinic Agonists / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018570:Risk Assessment; D012906:Smoke / Q000009:adverse effects*; D013997:Time Factors; D062789:Tobacco Products / Q000633:toxicity*
D000336:Aerosols; D000975:Antioxidants; D018722:Nicotinic Agonists; D017382:Reactive Oxygen Species; D012906:Smoke; D009538:Nicotine
anti-oxidants; cardiovascular system; cytotoxicity; e-cigarettes; endothelial cells; oxidative stress.