The role of DPPG in lung surfactant exposed to benzo[a]pyrene.

Abstract

Lung surfactant (LS) occurs at the air-water interface in the alveoli. Its main function is to reduce the work needed to expand the alveoli during inhalation and prevent the alveolar collapse during exhalation. Disturbance of this complex interfacial system by the uptake of pollutant molecules can lead to changes in fluidity, permeability, phase separation and domain formation, which in turn can lead to serious impairment in lung function. Knowledge of the LS-pollutant interaction is essential for understanding the mechanism of this process. In this study, we investigate the interaction of LS models with benzo[a]pyrene (BaP). Dipalmitoylphosphatidylcholine (DPPC), dipalmitoylphosphatidylglycerol (DPPG) sodium salt, and their 4 : 1 mixture are used as LS models. Surface pressure-area isotherms and molecular dynamics simulations are employed to study the properties of LS monolayers. It was found that the addition of BaP has a destabilizing effect on the mixed DPPC/DPPG monolayer, manifested by the decrease in surface pressure. Compression of a monolayer during a respiratory cycle may expel BaP to the bulk solution. It was demonstrated that DPPG is an active component that prevents the BaP molecule from entering the water subphase; as a minor component of LS it can effectively reduce this process. In addition, the presence of BaP in LS models induces the reduction of monolayer hydration in the hydrophilic region and the increase in chain ordering in the hydrophobic region. The observed changes in monolayer fluidity and phase behavior can be a source of various lung function disorders.