Antioxidant Enzyme Activities and Antioxidant Enzyme Gene Expression in Hyperoxia-induced Lung Injury in Premature Rat

Preterm infants exposed to high concentration oxygen are prone to develop hyperoxic lung damage, which is an importan t underly ing cause of bronchopulmonary dysplasia (BPD).1 Although the causative agent for BPD has not been conclusively identified, hyperoxia-induced lung injury i s bel ieved to be a major factor. Data from both cellu lar and whole animal models suggest that hyperoxic lung damage produces pathological changes similar to those seen in BPD. Among the principal cellular defenses against hyperoxic lung damage i s the antioxidant enzyme (AOE) system which includes the manganese superoxide dismutase (M nSOD), cop perzin c s uper ox i de d ism uta se (CuZnSOD), catalase (CAT), and glutathione peroxidase (GP).2 The SOD, CAT, GP offer pro tection against Abstract In a preterm rat model of hyperox ia-induced lung injury, we studied the lung antioxidant enzyme (AOE) activities and gene expression. After seven days of continuous exposure to >95% oxygen, severe inju ries were found in the lungs with inflammation and edema. Manganese superoxide dismutase (MnSOD) mRNA level and SOD activities in lung tissues were significantly elevated when compared to the room air controls (p=0.002, p<0.001). There was no significant increase in the levels of glutathione peroxidase (GP), catalase (CAT) or their gene expression. These findings show that in the premature rat lung, oxygen-induced damage is associated with upregulation of SOD gene expression and increased SOD activities.