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United States Department of Agriculture

Agricultural Research Service

Title: Copper Deficiency Enhances Acute Lung Injury and Metalloproteinase Activity in Rats

Authors
item Schuschke, Dale - UNIVERSITY OF LOUISVILLE
item Lentsch, Alex - UNIVERSITY OF LOUISVILLE
item Kato, Atsushi - UNIVERSITY OF LOUISVILLE
item Saari, Jack

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: December 10, 2000
Publication Date: March 7, 2001
Citation: Schuschke, D.A., Lentsch, A.B., Kato, A., Saari, J.T. 2001. Copper deficiency enhances acute lung injury and metalloproteinase activity in rats [abstract]. The Federation of American Societies for Experimental Biology Journal. 15:A1097.

Technical Abstract: Dietary copper deficiency causes a number of cardiovascular defects as well as impaired immune cell function. Previous studies have shown augmented macromolecular permeability in response to inflammatory stimuli in copper-deficient rats. However, little is known regarding the role of copper in modulating acute inflammatory responses. In the current studies, we investigated the effects of dietary copper deficiency on acute lung injury induced by intrapulmonary deposition of IgG immune complexes. Weanling male Long Evans rats were fed diets either adequate (6.5 ug/g) or deficient (0.3 ug/g) for copper. I gG immune complex lung injury was greatly increased in copper-deficient rats, as indicated by enhanced vascular leakage of albumin in histopathologic changes in the lung. However, no change was observed in either the lung content of tumor necrosis factor-alpha (TNF-alpha) or lung neutrophil accumulation. Lungs from copper-deficient rats had much higher levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 than did copper adequate controls. This increased MMP activity was not attributable to alveolar macrophages or neutrophils. These data suggest that the augmented lung injury caused by copper deficiency is due to increased pulmonary MMP-2 and MMP-9 activity, and not a generalized amplification of the inflammatory response. Supported by NIH DK55030-02.

Last Modified: 10/25/2014
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