Extracellular superoxide dismutase protects lung development in hyperoxia-exposed newborn mice.
We tested the hypothesis that targeted transgenic overexpression of human extracellular superoxide dismutase (EC-SOD) would preserve alveolar development in hyperoxia-exposed newborn mice. We exposed newborn transgenic and wild-type mice to 95% oxygen (O2) or air x 7 days and measured bronchoalveolar lavage cell counts, and lung homogenate EC-SOD, oxidized and reduced glutathione, and myeloperoxidase. We found that total EC-SOD activity in transgenic newborn mice was approximately 2.5x the wild-type activity. Hyperoxia-exposed transgenic mice had less pulmonary neutrophil influx and oxidized glutathione than wild-type littermates at 7 days. We measured alveolar surface and volume density in animals exposed to 14 days more of air or 60% O2. Hyperoxia-exposed transgenic EC-SOD mice had significant preservation of alveolar surface and volume density compared with wild-type littermates. After 7 days 95% O2 + 14 days 60% O2, lung inflammation measured as myeloperoxidase activity was reduced to control levels in all treatment groups.
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- Superoxide Dismutase
- Respiratory System
- Mice, Transgenic
- Mice
- Lung
- Hyperoxia
- Extracellular Space
- Chronic Disease
- Animals, Newborn
- Animals
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Superoxide Dismutase
- Respiratory System
- Mice, Transgenic
- Mice
- Lung
- Hyperoxia
- Extracellular Space
- Chronic Disease
- Animals, Newborn
- Animals