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Am J Physiol Lung Cell Mol Physiol 279: L413-L417, 2000;
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Vol. 279, Issue 3, L413-L417, September 2000

EB2000 SYMPOSIUM REPORT
Lung redox homeostasis: emerging concepts

Marilyn P. Merker1, Bruce R. Pitt2, Augustine M. Choi3, Paul M. Hassoun4, Christopher A. Dawson1, and Aron B. Fisher5

2 Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh 15261; 5 Institute for Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104; 4 Pulmonary and Critical Care Division, Department of Medicine, New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts 02111; 3 Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06520; and 1 Departments of Anesthesiology, Pharmacology/Toxicology, and Physiology, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295

This symposium was organized to present some aspects of current research pertaining to lung redox function. Focuses of the symposium were on roles of pulmonary endothelial NADPH oxidase, xanthine oxidase (XO)/xanthine dehydrogenase (XDH), heme oxygenase (HO), transplasma membrane electron transport (TPMET), and the zinc binding protein metallothionein (MT) in the propagation and/or protection of the lung or other organs from oxidative injury. The presentations were chosen to reflect the roles of both intracellular (metallothionein, XO/XDH, and HO) and plasma membrane (NADPH oxidase, XO/XDH, and unidentified TPMET) redox proteins in these processes. Although the lung endothelium was the predominant cell type under consideration, at least some of the proposed mechanisms operate in or affect other cell types and organs as well.

endothelium; oxidation-reduction; oxidative stress


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