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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 #63630
Title: PLATELET AGGREGATION AND ADHESION DURING DIETARY COPPER DEFICIENCY IN RATS

Author
item LOMINADZE, DAVID - UNIV OF LOUISVILLE
item Saari, Jack
item MILLER, FREDERICK - UNIV OF LOUISVILLE
item CATALFAMO, JAMES - CORNELL UNIVERSITY
item JUSTUS, DAVID - UNIV OF LOUISVILLE
item SCHUSCHKE, DALE - UNIV OF LOUISVILLE

Submitted to: Thrombosis and Hematosis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/12/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Prevention of blood loss from an injured blood vessel requires that platelets (cells circulating in the blood) adhere to the vessel wall at the site of injury and then adhere to one another to form a clot. This process depends on a cascade of reactions between chemical factors that reside in the blood, inside the platelets and in cells of the vessel wall. Clotting is known to be impaired in dietary copper deficiency. In examining how this impairment occurs, we found that the adhesion of copper-deficient platelets to one another is greater than for copper- adequate platelets; this fails to explain the reduced ability to clot. However, copper-deficient platelets adhere more poorly to blood vessel cells than do copper-adequate platelets. This is apparently caused by a reduction in a particular clotting factor in the blood and in platelets. This serves to explain how clotting ability is impaired by copper deficiency and further emphasizes the importance of dietary copper to the body's function. This information will be useful to scientists and consumers interested in trace element nutrition of the cardiovascular system.

Technical Abstract: The effects of dietary copper deficiency in platelet-to-endothelial cell adhesion and in platelet-to-platelet aggregation were studied in vitro. Platelets were obtained from male, weanling Sprague-Dawley rats fed purified diets which were either copper-adequate (CuA, ug copper/g of diet) or copper-deficient (CuD, 0.3 ug copper/g of diet) for 4 weeks. The platelet adhesion study was performed by adding CuA or CuD platelets either suspended in homologous plasma or in Tyrode buffer salt solution (TBSS) to cultured rat endothelial cells. After a one-hour incubation at 37 deg C non-adhered platelets were removed and counted in a microcytometer. Platelet aggregation in platelet rich plasma (PRP) samples was induced by adding ADP (2x10**-4 mol/L) and measured in a turbidometric platelet aggregometer. The content of von Willebrand factor (vWF) in platelets and in plasma and the content of fibrinogen in platelets were determined. Platelet adhesion to rat endothelial cells was significantly lower for platelets from CuD rats than for platelets from CuA rats. ADP-induced platelet aggregation from CuD rats was significantly higher than platelet aggregation from CuA rats. The content of vWF in platelets and in plasma from CuD rats was significantly lower than in platelets and plasma from CuA rats. However, the amount of fibrinogen in platelets from CuD rats was about 4-fold higher than that in platelets from CuA rats. These studies illustrate that copper-deficiency diminishes platelet adhesion to endothelial cells but increases platelet aggregability. The results suggest that these physiological alterations may be the result of decreased platelet vWF and increased platelet fibrinogen during dietary copper deficiency.