Summary
Electronic cigarette (e-cigarette) use has risen as individuals look for healthier nicotine delivery systems than conventional
cigarettes, but recent studies have demonstrated variable physiological responses to e-cigarette vapor. The safety of ecigarette
vapor remains an open question. We investigated the molecular cellular response of adenocarcinoma human
alveolar basal epithelial (A549) cells to flavored e-cigarette vapor. E-cigarette and cigarette vapor were extracted via a
vacuum-percolating system into PBS. The effects of a flavored e-liquid containing nicotine (eCSE) and nicotine free e-liquid
(NFeCSE) were compared to cigarette smoke extract (CSE), pure nicotine, glycerol, and PBS. Cells exposed to eCSE and
NFeCSE had decreased cell viability and proliferation. An increase in active caspase-3 was observed in cells exposed to
NFeCSE, while cells exposed to eCSE and CSE displayed no change, suggesting nicotine-mediated protection from
apoptosis. However, phosphorylated Akt, which regulates cellular proliferation, was elevated in response to eCSE, NFeCSE,
CSE, and glycerol. As the glutathione-oxidative stress response was known to integrate cellular factors including
carcinogenesis, inflammation, and cell proliferation, GSH/GSSG levels were measured in cells exposed to e-cigarette
smoke. An increase in oxidative stress was observed in cells treated with CSE, but not eCSE, suggesting components in
CSE independent of nicotine may be contributing to an imbalance in the stress response. These results indicate e-cigarette
vapor affects A549 cell viability dependent on nicotine, and is distinct from CSE-induced mechanisms of oxidative-stress.
Citation
Rigg S, Gielda LM. E-cigarette vapor decreases cellular proliferation through nicotine-dependent mechanisms. J Biosci Med. 2019;7:121-134. doi:10.4236/jbm.2019.77010
