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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 #68133
Title: COPPER DEFICIENCY CAUSES IN VIVO OXIDATIVE MODIFICATION OF ERYTHROCYTE MEMBRANE PROTEINS IN RATS

Author
item SUKALSKI, KATHERINE - U NORTH DAKOTA
item LABERGE, THOMAS - U NORTH DAKOTA
item Johnson, William

Submitted to: Free Radicals in Biology and Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/7/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Oxidants, which are chemicals capable of damaging cellular molecules such as lipids, DNA and proteins, are continuously produced as by-products from the metabolism of the oxygen we breath. Accumulation of damage caused by oxidants contributes to the development of a variety of degenerative diseases, including cardiovascular disease, cancer, degenerative brain diseases, and cataracts. Because oxidants are a serious threat to the health of an organism, a variety of mechanisms have evolved to defend against them. An important component of the antioxidant defense system is a copper-containing enzyme called superoxide dismutase (SOD). During dietary copper deficiency, the activity of SOD decreases in several tissues and red blood cells. Thus, it is possible that copper deficiency increases the occurrence of oxidant damage to cellular components. The red blood cell in particular may be a good target for oxidant damage during copper deficiency because its SOD activity is markedly reduced and it constantly produces the oxidant, superoxide. It was found that the membranes of red blood cells obtained from copper-deficient rats contained proteins that were oxidatively modified. Spectrin, a protein that is important for maintaining the structural integrity of the red cell membrane, was specifically damaged by copper deficiency. Because spectrin-like proteins are found in a variety of tissues, their oxidation may be important to the development of pathologies associated with copper deficiency. In a larger sense, these studies suggest that copper is an important nutrient that can help retard the oxidation process and slow the development of degenerative disease.

Technical Abstract: Oxidative stress has been postulated to contribute to the pathology associated with dietary copper deficiency. In vivo, erythrocytes are probable targets of oxidative damage as they are exposed to high concentrations of oxygen and contain heme iron that can autoxidize, which results in the formation of superoxide. Activity of the important antioxidant enzyme, copper-zinc superoxide dismutase, decreases markedly in erythrocytes during copper deficiency. The effect of dietary copper deficiency on indicators of oxidative stress was examined in erythrocyte membranes of rats maintained on a purified copper-deficient diet for 35 days after weaning. Erythrocytes were separated into young and old populations in a Percoll gradient prior to membrane isolation and quantification of lipid peroxides and protein carbonyls. Protein carbonyls, determined by Western blot immunoassay, were detected predominantly in both the alpha and beta chains of spectrin. Alpha spectrin of erythrocyte membranes from copper-deficient rats contained higher amounts of carbonyls than controls, regardless of the population of erythrocytes studied.