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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 #88557
Title: VON WILLEBRAND FACTOR (VWF) BUT NOT SUPEROXIDE DISMUTASE (SOD) RESTORES ATTENUATED PLATELET THROMBOSIS IN COPPER-DEFICIENT RATS

Author
item SCHUSCHKE, D - UNIV. OF LOUISVILLE
item LOMINADZE, D - UNIV. OF LOUISVILLE
item Saari, Jack
item MILLER, F - UNIV. OF LOUISVILLE

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 4/18/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: We have previously shown that dietary copper restriction reduces thrombogenesis in the rat microcirculation. Because copper is a requisite for platelet function and antioxidant defense, we examined the efficacy of the adhesion molecule vWF and the antioxidant SOD in restoring the attenuated thrombogenesis. Male weanling Sprague-Dawley rats were fed purified diets which were either copper-adequate (CuA) or copper-deficient (CuD) for 4 weeks. Excitation of intravascular fluorescein isothiocyanate tagged bovine serum albumin was used to induce intravascular thrombi. Determinations of vessel occlusion time were made via in vivo video microscopy in third-order venules in the cremaster muscle. The results showed a significant delay in thrombogenesis in the CuD group which was restored to normal by i.v. vWF but was not affected by topical SOD. These results suggest that the depressed thrombogenesis seen in CuD rats is a result of reduced platelet-to-endothelium adhesion medicated by vWF but not by a compromised antioxidant defense system. Supported by USDA #95- 37200-1625.