Fig. 1

ECIG-aerosol expposure ndued oxidative stress in presence or absence of nicotine. Reactive oxygen species prodution was induced in response to ECIG exposure (A). Anti-oxidant (GPx) and lipid peroxidanation specific antioxidant (GPx4) was upregulated by ECIG with or without nicotine but GPx was increased promiarily in prsesence of nictoine (B) and (C). HMOX1 in gene level was increaed in response ECIG exposure (D). HSP60 expression was upregulated in response to ECIG expopsure both with nicotine and without nicotine but primarily with nicotine (E). Statistical significance (p ≤ 0.05) between Sham and exposure (nicotine or without nicotine) condition was indicated as *. Statistical significance between nicotine and without nicotine was indicated as #