Anemia in copper-deficient rats: role of alterations in erythrocyte membrane fluidity and oxidative damage. Rock, Edmond, Elyett Gueux, Andrzej Mazur, Claude Motta*, Yves Rayssiguier. Centre de Recherche en Nutrition Humaine, Laboratoire des Maladies M[acute]etaboliques, INRA, Theix, 63122 St-Gen[grave]es-Champanelle (France) Service de Biochimie, CHU, 63000 Clermont-Ferrand (France)
APStracts 2:0212C, 1995.
This study was designed to precise the nature and the mechanism of the anemia induced by dietary copper (Cu) deficiency. Male Wistar rats were pair fed from weanling for 6 weeks either a Cu-deficient or a control diet. The reduced red blood cells (RBC) 51Chromium survival indicates an increased destruction of RBC during Cu deficiency. Diphenyl hexatriene (DPH) fluorescence polarization studies revealed an increase in the fluidity of erythrocyte membranes from deficient rats. The reduced cholesterol to phospholipids ratio was consistent with the increased fluidity. Other results indicate an increased vulnerability of RBC to hemolysis in dilute hydrogen peroxide and an increased formation of lipid peroxidation products. Before exposure to free radical stress, electron spin resonance studies in intact RBC revealed decreased correlation time of 16-doxyl stearic acid confirming a more fluid membrane in RBC from Cu-deficient rats. After in vitro peroxidation, RBC from Cu-deficient rats showed a more ordered state of membrane lipids as compared to controls. Together, these studies demonstrate the hemolytic nature of the anemia. The shortened survival of erythrocytes apparently results from changes in membrane fluidity and enhanced susceptibility to peroxidation. 

Received 17 March 1995; accepted in final form 17 May 1995.
APS Manuscript Number C150-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.