BS-454195-4 MITOCHONDRIAL REMODELING MEDIATES CARDIAC ELECTROPHYSIOLOGICAL INJURY IN INHALATION EXPOSURE TO FLAVORED ELECTRONIC NICOTINE DELIVERY SYSTEMS.

Electronic nicotine delivery systems (ENDS) utilize “e-liquids” in order to generate “e-vapor”, an inhalable aerosolized mixture containing and flavors. Flavored ENDS are very popular among teens who vape, however, the possible cardiac electrophysiological harm of inhalation exposure flavored not fully understood. To test if flavoring carbonyls e-liquids compromises mitochondrial integrity, increases oxidative stress, leads toxicity. Gas chromatography mass spectrometry (GC/MS), flow cytometry, in-vivo programmed electrical stimulation (PES), confocal microscopy, transmission electron microscopy (TEM) were used atrial like HL-1 myocytes mice overexpressing antioxidant catalase (MCAT) exposed e-vapor. We compared toxicity e-vapor from 30 differently (70% vegetable glycerin, 30% propylene glycol, with 6 mg/ml nicotine) cells using apoptotic annexinV cytometry. Toxicity most was significantly higher than air control. subsequently determined composition quantified concentrations major (cinnamaldehyde, vanillin, ethyl maltol, maltol) GC/MS. Linear regression analysis showed that correlated concentration. then assessed stress (OS) via CellROX cytometry vanilla OS increased but this prevented by N-acetylcycteine pretreatment. Moreover, Mitotracker quantification network indicated decreased footprint likely due network’s disintegration. In-vivo (four weeks, 1 hour/day) duration PES induced ventricular tachycardia WT MCAT mice, controls. Finally, we investigated TEM ultrastructure. While perimeter unaffected, cristae thickness WT, hearts Inhalation negatively affects electrophysiology, part adverse remodeling, stress.