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Published ahead of print on October 3, 2002, doi:10.1164/rccm.200202-108OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 3, February 2003, 400-405

A more recent version of this article appeared on February 1, 2003
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Submitted on February 12, 2002
Accepted on September 30, 2002

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

Mohamed N Ahmed1, Hagir B Suliman2, Rodney J Folz3, Eva Nozik-Grayck4, Maria L Golson2, S N Mason1, and Richard L Auten1*

1 Pediatrics, Duke University Medical Center, Durham, NC, USA, 2 Medicine, Duke University Medical Center, Durham, NC, USA; Cell Biology, Duke University Medical Center, Durham, NC, USA, 3 Medicine, Duke University Medical Center, Durham, NC, USA; Cell Biology, Duke University Medical Center, Durham, NC, USA; Cell Biology, Duke University Medical Center, Durham, NC, none, 4 Pediatrics, Duke University Medical Center, Durham, NC, USA; Anesthesiology, Duke University Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: auten{at}duke.edu.

We tested the hypothesis that targeted transgenic over-expression of human extracellular superoxide dismutase would preserve alveolar development in hyperoxia-exposed newborn mice. We exposed newborn transgenic and wild-type mice to 95% oxygen or airx7 days and measured bronchoalveolar lavage cell counts, and lung homogenate extracellular superoxide dismutase, oxidized and reduced glutathione, and myeloperoxidase. We found that total EC-SOD activity in transgenic newborn mice was ~2.5 x 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% oxygen. 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: antioxidant, bronchopulmonary dysplasia, inflammation,




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