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Serum Copper Elevation Promotes Hepatic Ceruloplasmin Production and Excretion in Rat Model of Myocardial Infarction

Ceruloplasmin (Cp) is a major copper‐binding protein in blood, regulating copper homeostasis. High levels of serum copper and Cp are both risk factors for coronary artery disease, particularly in patients with acute myocardial infarction. However, the relationship between the changes in serum copper and Cp levels in response to myocardial ischemia remains unknown. It is known that myocardial ischemia causes copper efflux from the heart leading to copper elevation in the blood. The present study was undertaken to test the hypothesis that the elevation of serum copper leads to an increase in hepatic Cp production and excretion. Adult male Sprague‐Dawley rats were subjected to left anterior descending (LAD) coronary artery ligation to induce myocardial infarction. Serum copper and Cp levels, as well as changes in hepatic Cp and copper‐transporting P‐type ATPase (ATP7B), were determined from blood and liver samples harvested on day 1, 4, or 7 after the operation. Serum copper concentrations were significantly increased on day 4 after LAD ligation, accompanied by an increase in serum Cp levels and activities. Concomitantly, the protein levels of Cp and copper exporter, ATP7B, were also significantly increased in the liver. Taken together, these results indicate that the elevated serum Cp levels mostly likely result from the increase in Cp production and excretion in the liver in response to the elevated serum copper levels following myocardial ischemia.