Abstract

Severely copper deficient animals manifest hypertriglyceridemia, hyperuricemia, glucose intolerance, decreased hemoglobin concentration, abnormalities of the electrocardiogram and sudden death due to rupture of the heart. In addition, experimental copper deficiency in animals is also characterized by central nervous system disorders such as ataxia, motor incoordination, and brain and spinal cord degeneration. Further, feeding high levels of dietary fructose or sucrose as compared to starch has been reported to produce a more severe copper depletion syndrome in rats. Serum ceruloplasmin and superoxide dismutase activity in erythrocytes are also decreased in copper deficiency and these parameters are used as markers of copper status. Decreases in plasma enkephalins levels have also been suggested as markers of copper deficiency1. Recently, significant differences in symptoms of copper deficiency have been observed between male and female rats fed low copper diets2. Only male rats fed a copper deficient diet with fructose died of cardiac rupture. Females were protected against this syndrome, indicating sex hormones may be involved. Atrial natriuretic peptides (ANP) have been shown to play a role in cardiac function, where, their levels in plasma are higher in patients with congestive heart failure and in hypertensive subjects. It is possible that in copper deficiency, atrial peptides may be differently regulated in male and female rats. We therefore studied the effect of copper deficiency and of sex hormones on ANP from plasma and atria.

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