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, Richard L. Auten

Research output: Contribution to journalArticlepeer-review

88 Scopus citations


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 × 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.

Original languageEnglish (US)
Pages (from-to)400-405
Number of pages6
JournalAmerican journal of respiratory and critical care medicine
Issue number3
StatePublished - Feb 1 2003
Externally publishedYes


  • Bronchopulmonary dysplasia
  • Hyperoxia
  • Newborn infant
  • Superoxide dismutase
  • Transgenic mice

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine


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