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Published ahead of print on October 3, 2002, doi:10.1164/rccm.200202-108OC
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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 400-405, (2003)
© 2003 American Thoracic Society

Original Article

Extracellular Superoxide Dismutase Protects Lung Development in Hyperoxia-exposed Newborn Mice

Mohamed N. Ahmed, Hagir B. Suliman, Rodney J. Folz, Eva Nozik-Grayck, Maria L. Golson, S. Nicholas Mason and Richard L. Auten

Departments of Pediatrics, Medicine, Anesthesiology, Cell Biology, Duke University Medical Center, Durham, North Carolina

Correspondence and requests for reprints should be addressed to Richard L. Auten, M.D., DUMC Box 3373, Duke University Medical Center, Durham, NC 27710. E-mail: auten{at}duke.edu

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.

Key Words: bronchopulmonary dysplasia • superoxide dismutase • hyperoxia • newborn infant • transgenic mice




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