Abstract

Copper (Cu) deficiency, induced in rats by suckling from Cu-deficient dams and by offering a semisynthetic low-Cu diet from weaning, resulted in cardiac enlargement. This enlargement was not due to accumulation of excess fluid in the heart but was characterized by mitochondrial hypertrophy as demonstrated by electron microscopy and biochemical studies. Administration of reserpine limited the extent of cardiac enlargement; however, heart total noradrenaline (NA), unchanged by Cu deficiency, was significantly reduced by reserpine. It was concluded that cardiac enlargement in Cu deficiency was not directly related to NA concentration. An alteration in cardiac energy status, however, was suggested by reduction in activity of the nonheme iron-dependent enzyme, succinic dehydrogenase.

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