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Am J Physiol Lung Cell Mol Physiol (October 26, 2001). doi:10.1152/ajplung.00058.2001
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Articles in PresS, published online ahead of print October 24, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00058.2001
Submitted on February 13, 2001
Accepted on October 23, 2001

The role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis

Russell P Bowler1*, Micheal Nicks1, Karrie Warnick1, and James D Crapo1

1 Medicine, National Jewish Medical and Research Center, Denver, Co, USA

* To whom correspondence should be addressed. E-mail: bowlerR{at}njc.org.

Bleomycin administration results in well-described intracellular oxidative stress that can lead to pulmonary fibrosis. The role of alveolar interstitial antioxidants in this model is unknown. Extracellular superoxide dismutase (EC-SOD) is the primary endogenous extracellular antioxidant enzyme and is abundant in the lung. We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Two weeks after intratracheal bleomycin administration, we found that wildtype mice induced a 106±25% increase in lung EC-SOD. Immunohistochemical staining revealed that a large increase in EC-SOD occurred in injured lung. Using mice that overexpress EC-SOD specifically in the lung, we found a 53±14% reduction in bleomycin-induced lung injury assessed histologically and a 17±6%reduction in lung collagen content two weeks after bleomycin administration. We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration.




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