BETTER SURVIVAL OF FETAL VS ADULT TYPE II PNEUMOCYTES IN HYPEROXIA IS NOT DUE TO INCREASES IN ANTI-OXIDANT ENZYME ACTIVITY. † 1939

Exposure to hyperoxia results in lung damage and is a factor in development of chronic lung disease. Previous studies of fetal lung in vivo and in organ culture have shown that the activities of antioxidant enzymes (AOE) increase from late gestation to postnatal life. We have recently shown increased activities of AOE in adult type II pneumocytes (T_IIP) exposed to hyperoxia. We hypothesized that fetal T_IIP would show a decreased response. The goal of the present study was to measure the effect of hyperoxia on the activities of catalase, glutathione reductase (GR) glutathione peroxidase (GPX) and cytosolic superoxide dismutase (SOD) in cultures of 19-day fetal rat T_IIP. Control cells were kept in 95%RA /5%CO₂ while the hyperoxia group was exposed to 95%O₂ /5%CO₂ for 24 hours. Viability was determined by exclusion of trypan blue. Results indicate mean ± SEM values of 3 experiments. (AOE in nmol/min/mg protein. adjusted for cell viability.) Fetal T_IIP tolerate hyperoxia better(smaller reduction in viability and no increase in LDH release) than adult T_IIP. Hyperoxia resulted in increased AOE activity for all enzymes measured in adult T_IIP. In fetal T_IIP only GPX and SOD showed a significant increase. Other protective anti-oxidant factors might account for the better survival of fetal T_IIP in hyperoxia.Table

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