Acetaldehyde-stimulated PKC activity in airway epithelial cells treated with smoke extract from normal and smokeless cigarettes

Previously, we have found that acetaldehyde, a volatile component of cigare tte smoke, stimulates the protein kinase C (PKC) pathway and inhibits cilia ry motility. A "smokeless" cigarette (Eclipse) now exists in which most of the tobacco is not burned, reducing the pyrolyzed components in the extract . We hypothesized that acetaldehyde is a component of cigarette smoke that activates PKC in the airway epithelial cell, and therefore the Eclipse ciga rette would not activate epithelial cell PKC, In this study, bovine bronchi al epithelial cells (BBEC) were incubated with cigarette smoke extract (CSE ) or Eclipse smoke extract (ESE). We found that PKC activity was significan tly higher In cells exposed to 5% CSE than cells exposed to 5% ESE or media . When acetaldehyde levels of both extracts were measured by gas chromatogr aphy, CSE was found to have 15-20 times greater concentration (mu M) of ace taldehyde than ESE. When BBEC were treated with 5% CSE, ciliary beating was further decreased from baseline levels. This decrease in ciliary beating w as not observed in cells treated with ESE, suggesting that acetaldehyde con tained in CSE slows cilia. These results suggest that volatile components s uch as acetaldehyde in cigarette smoke may inhibit ciliary motility via a P KC-dependent mechanism.