Journal
TOXICOLOGY LETTERS
Volume 333, Issue -, Pages 303-311Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2020.08.003
Keywords
Mitochondrial Bioenergetics; E-cigarettes; Pod-based; Menthol; Tobacco
Categories
Funding
- NIH [1R01HL135613]
- WNY Center for Research on Flavored Tobacco Products (CRoFT) [U54CA228110]
Ask authors/readers for more resources
Current FDA regulations have resulted in a ban of flavored e-cigarette pods, with only menthol and tobacco flavored pods being exempted. Previous work using menthol and tobacco-flavored e-cigarettes have been shown to induce mitochondrial reactive oxygen species. We hypothesized that exposure to pod-based JUUL Menthol and Virginia Tobacco aerosols will alter mitochondrial respiration and electron transport chain protein levels. We determined mitochondrial respiration by using a Seahorse technique and electron transport chain complexes by total OXPHOS antibodies after exposing lung epithelial cells, Beas-2b, to pod-based Menthol and Virginia Tobacco flavored aerosols. Menthol pod exposure resulted in an immediate increase in proton leak and decrease in coupling efficiency, as well as a decrease in complex I, II, and IV. Menthol pod exposure twenty-four hour post-exposure resulted in a decrease in basal respiration, maximal respiration, and spare capacity, as well as a decrease in complex I. Tobacco pod exposure resulted in no significant alterations to mitochondrial respiration, but immediately post final exposure resulted in a significant increase in complex I, IV, and V. Our results indicate that exposure to Menthol flavored e-cigarette pods cause mitochondrial dysfunction in lung epithelial cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available