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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #121904


item Klevay, Leslie

Submitted to: Journal of Molecular and Cellular Cardiology
Publication Type: Abstract Only
Publication Acceptance Date: 7/6/2001
Publication Date: 10/1/2001
Citation: Klevay, L.M. 2001. Impaired oxidative defense in ischemic heart disease from diets low in copper [abstract]. Journal of Molecular and Cellular Cardiology. 33:A59.

Interpretive Summary:

Technical Abstract: Free radical damage and impaired defense against oxidative stress are implicated in the atherosclerosic process leading to myocardial infarction. Copper, which contributes to oxidative defense in vivo via some superoxide dismutases, often is low in the Western diet so closely associated with these illnesses. Nearly one fourth of 849 diets analyzed chemically in Belgium, Canada, the U.K. and U.S. do not contain the 0.9 mg daily suggested by the new Recommended Dietary Allowance for copper (from Klevay, J Am Coll Nutr 17:322, 1998). Low superoxide dismutase in patients with a history of myocardial infarction (Wang, Arteriolscler Thromb Vasc Biol 18:1915, 1998) and coronary artery disease (Landmesser, Circulation 101:2264, 2000) is consonant with low copper in leukocytes of men with coronary atherosclerosis (Kinsman, Biochem Soc Trans 18:1186, 1990) and with low dietary intakes of copper. Many anatomical, chemical and physiological similarities between people with ischemic heart disease and animals deficient in copper (Klevay, J Nutr 130:489S, 2000) such as arterial smooth muscle cell migration and proliferation, increased malondialdehyde and thiobarbituric acid reactive substances, low cardiac copper, hypercholesterolemia, impaired glucose tolerance and thrombosis support the conclusion that low copper status is important in the etiology and pathophysiology of ischemic heart disease.