Journal of Applied Physiology AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol 97: 2006-2013, 2004. First published August 6, 2004; doi:10.1152/japplphysiol.00480.2004
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HIGHLIGHTED TOPICS
Lung Growth and Repair

Redistribution of pulmonary EC-SOD after exposure to asbestos

Roderick J. Tan ,1,* Cheryl L. Fattman,1,* Simon C. Watkins,2 and Tim D. Oury1

Departments of 1Pathology and 2Cell Biology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15261

Submitted 4 May 2004 ; accepted in final form 28 July 2004

Inhalation of asbestos fibers leads to interstitial lung disease (asbestosis) characterized by inflammation and fibrosis. The pathogenesis of asbestosis is not fully understood, but reactive oxygen species are thought to play a central role. Extracellular superoxide dismutase (EC-SOD) is an antioxidant enzyme that protects the lung in a bleomycin-induced pulmonary fibrosis model, but its role has not been studied in asbestos-mediated disease. EC-SOD is found in high levels in the extracellular matrix of lung alveoli because of its positively charged heparin-binding domain. Proteolytic removal of this domain results in clearance of EC-SOD from the matrix of tissues. We treated wild-type C57BL/6 mice with 0.1 mg of crocidolite asbestos by intratracheal instillation and euthanized them 24 h later. Compared with saline- or titanium dioxide-treated control mice, bronchoalveolar lavage fluid (BALF) from asbestos-treated mice contained significantly higher total protein levels and increased numbers of inflammatory cells, predominantly neutrophils, indicating acute lung injury in response to asbestos. Decreased EC-SOD protein and activity were found in the lungs of asbestos-treated mice, whereas more EC-SOD was found in the BALF of these mice. The EC-SOD in the BALF was predominantly in the proteolyzed form, which lacks the heparin-binding domain. This redistribution of EC-SOD correlated with development of fibrosis 14 days after asbestos exposure. These data suggest that asbestos injury leads to enhanced proteolysis and clearance of EC-SOD from lung parenchyma into the air spaces. The depletion of EC-SOD from the extracellular matrix may increase susceptibility of the lung to oxidative stress during asbestos-mediated lung injury.

extracellular superoxide dismutase; acute lung injury; antioxidants; oxidative stress; asbestosis; proteolysis; pulmonary fibrosis


Address for reprint requests and other correspondence: T. D. Oury, 7thfloor Scaife Hall, 3550 Terrace St., Univ. of Pittsburgh, Pittsburgh, PA 15261 (tdoury{at}imap.pitt.edu).




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