Figure 5.

PG e-cig aerosols increase levels of methylglyoxal (MGO) to inhibit BK channel function in HBECs in vitro. A: 7-day exposure of HBECs to propylene glycol (PG) e-cig aerosols does not significantly change CFTR conductance compared with air-exposed controls. n = 11 lungs. B: PG e-cig aerosols cause a significant reduction in BK activity after 7 days compared with air-exposed controls. n = 9 lungs. C: schematic depicting metabolism of propylene glycol (PG) into methylglyoxal (MGO), which is then converted into d-lactate. ADH = alcohol dehydrogenase. D: mRNA expressions of ADH isoforms ADH4, ADH5, and ADH7 in fully differentiated HBECs from nonsmoker donors. n ≥ 8 lungs. E and F: levels of methylglyoxal (E) and d-lactate (F) are significantly increased in the basolateral media of HBECs after 7 days of PG aerosol exposure compared with air-exposed controls. n ≥ 9 lungs. Data are presented as means ± SE. *P < 0.05. Data were analyzed by two-tailed t test (A, E, and F) or two-tailed Wilcoxon test (B) after assessing normality by Shapiro-Wilk. BK, large conductance, Ca²⁺-activated, and voltage-dependent K⁺; HBECs, human bronchial epithelial cells; ns, not significant.