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Articles in PresS, published online ahead of print May 10, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00011.2002
Submitted on January 10, 2002
Accepted on May 3, 2002
1 Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA
2 Department of Medicine, University of Pit, Pittsburgh, PA, USA
* To whom correspondence should be addressed. E-mail: tdoury{at}imap.pitt.edu.
Extracellular superoxide dismutase (ECSOD) is highly expressed in lung tissue. ECSOD contains a heparin-binding domain that is sensitive to proteolysis. This heparin-binding domain is important in allowing ECSOD to exist in relatively high concentrations in specific regions of the extracellular matrix and on cell surfaces. ECSOD has been shown to protect the lung against hyperoxia in transgenic and knockout studies. This study tests the hypothesis that proteolytic clearance of ECSOD from the lung during hyperoxia contributes to the oxidant/antioxidant imbalance associated with this injury. 100% oxygen exposure for 72 hours resulted in a significant decrease in ECSOD levels in the lungs and BALF of mice. This correlated with a significant depletion of ECSOD from the alveolar parenchyma as determined by immunflourescence and immunohistochemistry. ECSOD mRNA was unaffected by hyperoxia. However, there was an increase in the ratio of proteolysed to uncut ECSOD after hyperoxia suggesting that hyperoxia depletes ECSOD from the alveolar parenchyma by cutting the heparin-binding domain. This may enhance hyperoxic pulmonary injury by altering the oxidant/antioxidant balance in alveolar spaces.
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