Fig. 1

P2X7r inhibition prevented mitochondrial dysfunction, induced by ETH, ALD, or e-Cig (1.8% nicotine). After overnight exposure to insults, mito-stress levels in hPAEpiC were measured using a Seahorse analyser, and the SRC were calculated. In figure, A line graph depicts the oxygen consumption rate (OCR), whereas Fig (B), (C), and (D) presents a 30%, 35%, and 42% reduction in spare respiration capacity (SRC) against 100 mM ETH, 100 µM ALD, and 1.75 µg/mL e-Cig (1.8% nicotine) stimulation, respectively. E e-Cig extract with 0% nicotine had no impact on mitochondrial spare respiration. In this figure, OCR represents the electron flow through the electron transport system linked to celluar ATP production and SRC was measured by subtracting the basal OCR from the maximal OCR. Pre-treatment with A80 (10 µM) restored OXPHOS levels in the insult-exposed hPAEpiC. Data were normalized to untreated control cells, and one-way ANOVA was used for statistical analyses, *P ≤ 0.05, ****P ≤ 0.0001, and ns (not significant) where level of significance set at 0.05 (n = 4)