Hyperoxia causes an increase in antioxidant enzyme activity in adult and fetal rat type II pneumocytes.

Abstract

It is well known that exposure to hyperoxia results in lung inflammation and damage, which leads to the development of chronic lung disease. Previous studies have shown increased activities of antioxidant enzymes (AOE) in lung tissue from animals exposed to hyperoxia. We propose the hypothesis that the fetal type II pneumocytes (TIIP) would be resistant to oxygen toxicity by virtue of increasing AOE activity on exposure to hyperoxia. The aim of this study was to measure the activities of catalase, glutathione reductase, glutathione peroxidase (GPX), and cytosolic superoxide dismutase (SOD) in cultures of adult and fetal rat TIIP exposed to 95% oxygen for 24 h. Control cells were incubated in room air. Hyperoxia exposure resulted in 53.4 +/- 1.2% of control viability (mean +/- S.E.M.; p = 0.001) in the adult TIIP with a significant threefold increase in the activities of all the AOE. The fetal TIIP were more resistant to hyperoxia (99.4 +/- 6.1% of control viability). However, in the fetal TIIP, only SOD and GPX levels were significantly increased (fourfold and 2.3-fold, respectively) compared with fetal controls. We conclude that fetal TIIP are more resistant to hyperoxia than adult TIIP in terms of viability; other protective antioxidant factors might account for the better survival of fetal TIIP in hyperoxia.