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.