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Am J Physiol Lung Cell Mol Physiol (March 29, 2002). doi:10.1152/ajplung.00409.2001
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Articles in PresS, published online ahead of print March 29, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00409.2001
Submitted on October 19, 2001
Accepted on February 15, 2002

Overexpression of extracellular superoxide dismutase decreases lung injury after exposure to oil fly ash

Andrew J. Ghio1, Hagir B. Suliman2, Jacqueline D. Carter1, Amir M. Abushamaa2, and Rodney J. Folz2*

1 National Health & Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC, USA
2 Departments of Medicine & Cell Biology, Duke University Medical Center, Durham, NC, USA

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

The mechanism of tissue injury after exposure to air pollution particles is not known. Biological effect has been postulated to be mediated via an oxidative stress catalyzed by metals present in particulate matter (PM). We utilized a transgenic (Tg) mouse model that overexpresses extracellular superoxide dismutase (EC-SOD) to test the hypothesis that lung injury after exposure to PM results from an oxidative stress in the lower respiratory tract. Wild-type (Wt) and Tg mice were intratracheally instilled with either saline or 50 µg residual oil fly ash (ROFA). Twenty-four hours later, specimens were obtained and included bronchoalveolar lavage (BAL) and lung for both homogenization and light histopathology. Following ROFA exposure, EC-SOD Tg mice showed a significant reduction in BAL total cell counts (composed primarily of neutrophils) and BAL total protein compared to Wt. EC-SOD animals also demonstrated diminished concentrations of inflammatory mediators in BAL. There was no statistically significant difference in BAL lipid peroxidation, however EC-SOD mice had lower concentrations of oxidized glutathione (GSSG) in the BAL. We conclude that enhanced EC-SOD expression decreased both lung inflammation and damage after exposure to ROFA. This supports a participation of oxidative stress in the inflammatory injury after PM exposure rather than reflecting a response to metals alone.




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