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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #128562

Title: COPPER DEFICIENCY INCREASES LUNG AND HEART ICAM-1 EXPRESSION DURING ENDOTOXEMIA

Author
item SCHUSCHKE, DALE
item PERCIVAL, SUSAN
item LOMINADZE, DAVID
item Saari, Jack
item LENTSCH, ALEX

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2001
Publication Date: 3/20/2002
Citation: Schuschke, D., Percival, S., Lominadze, D., Saari, J.T., Lentsch, A. 2002. Copper deficiency increases lung and heart ICAM-1 expression during endotoxemia [abstract]. The Federation of American Societies for Experimental Biology Journal. 16:A990.

Interpretive Summary:

Technical Abstract: We have previously shown that copper deficiency increases neutrophil accumulation (as evidenced by myeloperoxidase activity) in lungs of rats. Therefore, this study evaluated if endothelial expression of the intercellular adhesion molecule-1 (ICAM-1) is copper-dependent. Male weanling rats were fed a Cu-adequate (6.0 mg Cu/kg diet) or Cu-deficient diet (0.30 mg/kg diet) for 4 weeks. ICAM-1 expression was calculated using 125**I-anti-ICAM-1 MAb within the vasculature. Inflammation was induced by endotoxin from Salmonella abortus equi (LPS). Lung, liver, heart, kidney, and skeletal muscle were measured for 125**I Mab. There was no difference in ICAM-1 expression between unstimulated dietary groups. In LPS-stimulated rats, ICAM-1 expression was greater in the lungs and hearts of the Cu- deficient group compared to the Cu-adequate group. Similar results were seen in cultured microvascular endothelial cells that had been Cu-chelated. .These results demonstrate a tissue-specific increase in LPS-induced ICAM-1 expression during copper deficiency. The findings suggest a mechanism for the exacerbated inflammatory response seen in the lungs of copper-deficient rats. Supported by NIH DK55030-02.