Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: December 1, 2003
Publication Date: March 24, 2004
Citation: Klevay, L.M. 2004. Copper deficiency decreases paraoxonase activity in rats [abstract]. Federation of American Societies for Experimental Biology Journal. 18:A915. Technical Abstract: Decreased paraoxonase (PON1) predicts coronary heart disease and is found in smokers, in diabetes mellitus and in familial hypercholesterolemia. The enzyme is located on the HDL molecule and is largely responsible for its antioxidant ability (Durrington, et al. Arterio Thromb Vasc Biol 22:1248, 2002). In view of the numerous similarities between animals deficient in copper and people with ischemic heart disease, the hypothesis that copper deficiency can modify PON1 activity was tested. Male, weanling rats (15/group) were given purified diet based on sucrose (62%), egg white (20%) and corn oil (10%), adequate in minerals and vitamins, and either deficient (0.3) or adequate (5.6mg/kg) in copper. Analyses: copper by spectroscopy, lipids and PON1 by colorimetry, statistics by 't'. After 33 days, animals were anesthetized and samples were collected. Data are mean±SE. Cholesterol Liver Cu PON1 PON1/HDL mg/dl mg/kg U/ml U/mmole Adequate 113±4.7 10.6±0.4 146±4.2 208±10.5 Deficient 131±5.5 1.5±0.1 114±4.1 137±5.4 p <0.020 <0.00001 0.0001 <0.00002 Deficiency was verified by increased plasma cholesterol and decreased liver copper. The decreased activity of PON1, both absolutely and relative to HDL, identifies a new impairment of oxidative defense in copper deficiency and a potential nutritional intervention in low PON1 states. The PON1/HDL ratio may be a sensitive, and accessible, index of copper deficiency.