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The Proceedings of the American Thoracic Society 2:236-242 (2005)
© 2005 The American Thoracic Society

Nitric Oxide and Zinc Homeostasis in Acute Lung Injury

Claudette M. St. Croix, Karanee Leelavaninchkul, Simon C. Watkins, Valerian E. Kagan and Bruce R. Pitt

Department of Environmental and Occupational Health, The Graduate School Public Health and Department of Cell Biology and Physiology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

Correspondence and requests for reprints should be addressed to Claudette St. Croix, Ph.D., Department of Environmental and Occupational Health, University of Pittsburgh Graduate School Public Health, Pittsburgh, PA 15260. E-mail: CLS13{at}pitt.edu

ABSTRACT

Among putative small molecules that affect sensitivity to acute lung injury, zinc and nitric oxide are potentially unique by virtue of their interdependence and dual capacities to be cytoprotective or injurious. Nitric oxide and zinc appear to be linked via an intracellular signaling pathway involving S-nitrosation of metallothoinein—itself a small protein known to be an important inducible gene product that may modify lung injury. In the present article, we summarize recent efforts using genetic and fluorescence optical imaging techniques to: (1) demonstrate that S-nitrosation of metallothionein affects intracellular zinc homeostasis in intact pulmonary endothelial cells; and (2) reveal a protective role for this pathway in hyperoxic and LPS-induced injury.

Key Words: hyperoxia • LPS • metallothionein • nitric oxide • pulmonary endothelium • zinc




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