Extracellular superoxide dismutase protects lung development in hyperoxia-exposed newborn mice.

Abstract

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.

• Authors: Mohamed N Ahmed, Hagir B Suliman, Rodney J Folz, Eva Nozik-Grayck, Maria L Golson, S Nicholas Mason, Richard L Auten
• Journal: American journal of respiratory and critical care medicine (Am J Respir Crit Care Med) Vol. 167 Issue 3 Pg. 400-5 (Feb 01 2003) ISSN: 1073-449X [Print] United States
• PMID: 12406846 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Superoxide Dismutase

Topics

• Animals
• Animals, Newborn
• Chronic Disease
• Extracellular Space
• Hyperoxia (enzymology)
• Lung (growth & development)
• Mice
• Mice, Transgenic
• Superoxide Dismutase (physiology)