Experimental and clinical data have provided evidence for the involvem
ent of oxygen free radicals in the development of acute and chronic lu
ng diseases. Alveolar surfactant is the prime target of oxidative air
pollutants. Lung surfactant consists to 90% of lipids and contains vit
amin E as most important lipophilic antioxidant. Recently, we showed t
hat alveolar surfactant is supplemented with vitamin E during its synt
hesis in type II pneumocytes. Hyperoxia is very often a necessary ther
apeutic intervention which seems to impose oxidative stress on lung ti
ssue. Hyperoxia caused an increase in vitamin E turnover, measured in
type II pneumocytes, lamellar bodies and lung lavages. In contrast, th
e turnover of surfactant cholesterol and surfactant lipids does not ch
ange. Hyperoxia caused an increase in vitamin E uptake by type II pneu
mocytes and an enrichment of vitamin E in lamellar bodies.