Journal of Applied Physiology
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J Appl Physiol 63: 2159-2163, 1987;
8750-7587/87 $5.00
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Journal of Applied Physiology, Vol 63, Issue 5 2159-2163, Copyright © 1987 by American Physiological Society


ARTICLES

Xanthine oxidase mediates elastase-induced injury to isolated lungs and endothelium

T. C. Rodell, J. C. Cheronis, C. L. Ohnemus, D. J. Piermattei and J. E. Repine
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262.

Xanthine oxidase (XO)-generated toxic O2 metabolites appear to contribute to reperfusion injury, but the possibility that XO is involved in hyperoxic or neutrophil elastase-mediated injury has not been investigated. We found that lungs isolated from rats fed a tungsten-rich diet had negligible XO activities and after exposure to hyperoxia developed less acute edematous injury during perfusion with buffer or purified neutrophil elastase than XO-replete lungs from control rats which had been exposed to hyperoxia. In parallel, tungsten-treated XO-depleted cultured bovine pulmonary arterial endothelial cells made less superoxide anion and as monolayers leaked less 125I-labeled albumin after exposure to neutrophil elastase than XO-replete endothelial cell monolayers. Our findings suggest that XO-derived O2 metabolites contribute to acute edematous lung injury from hyperoxia directly and by enhancing susceptibility to neutrophil elastase.


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