Effect of Lung Surfactant Liposomes on the Rabbit Fetal Lung Type II Cell Antioxidant Enzymes Following Prenatal Dexamethasone Treatment

Prematurely born infants are at a high risk of developing neonatal respiratory distress syndrome (RDS), and it is believed that besides an insufficient surfactant (SF) system the initial breathing of O2-enriched air may in some way be responsible for this syndrome. Hyperventilation is a dominant stimulator for SF secretion but it may lead to oxidant-mediated cellular injury to type II cells. Since type II cells are the sole source of SF synthesis, the effect of ventilation support on these cells becomes important. In the present study, the changes in the antioxidant enzymes (AOEs) such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) in the type II cells of fetal rabbit lungs resulting from exogenous SF liposomes and steroid intervention have been investigated. The specific activities of the AOEs were found to be higher in the presence of SF liposomes in prematurely born pups whose mothers were not steroid treated (control), while such an increase was more pronounced in dexamethasone-treated groups. The results indicate that the exogenous surfactant and steroid intervention may favourably alter the AOE defences in the type II cells of fetal rabbits.