Oxidant-induced alterations of lung surfactant system.

Lung surfactant is subject to oxidant injury from inhaled pollutants and free radicals generated by activated leukocytes in various disease states. Both lipid and protein components of surfactant can be altered by oxygen radicals. Changes were investigated in the lung surfactant system using a rat model with ozone injury to simulate adult respiratory distress syndrome, in which surfactant activity is thought to be inadequate. A significant decrease in dynamic lung compliance was correlated with the accumulation of protein in the alveolar lavage fluid. The amount of dipalmitoylphosphatidylcholine, the most abundant phospholipid in surfactant, increased two-fold indicating that the acute changes in lung function were related to the inactivation of surfactant by edema fluid and not to a quantitative lack of surfactant phospholipids. The amount of surfactant stored in lamellar bodies of the alveolar type II cells also increased and was abnormal in composition. The amount of cholesterol and albumin increased following ozone stress, suggesting that an altered uptake and incorporation of alveolar components into the lamellar bodies may be an important process in oxidant-induced lung injury. In contrast, lysozyme, an abundant protein in the alveolar fluid and lamellar bodies, rapidly decreased in concentration in the intracellular surfactant. Using an in vitro system we found that lysozyme is very sensitive to ozone injury and may function as a "sacrificial" antioxidant in the alveolar lining fluid.(ABSTRACT TRUNCATED AT 250 WORDS)