CARDIAC-HYPERTROPHY IN COPPER-DEFICIENT RATS IS OWING TO INCREASED MITOCHONDRIA

Dietary copper depletion results in cardiac hypertrophy and ultrastruc tural alterations. The objective of this study was to determine the co mponents that contribute to cardiac enlargement. Two groups (n = 4) of male, weaning, Sprague-Dawley rats were fed ad libitum with copper-ad equate or copper-deficient diets for five weeks. Cross sectional trans mission electron micrographs from both groups were evaluated using ima ge analysis to quantify absolute area occupied by myocyte, mitochondri a, myofibril, and other intracellular material. Copper-deficient rats had larger myocytes, increased area of mitochondria, and increased rat io of mitochondria:myofibril as well as mitochondria:myocyte. Copper d eficiency did not change the absolute area occupied by myofibrils. The se data suggested that increase in the absolute mitochondria area is t he major contributory factor to the cardiac hypertrophy in copper defi ciency. Under the conditions used, myofibril has minimal role toward c ontributing to the hypertrophic state. The pathology reported resemble s human forms of genetic mitochondrial cardiomyopathies. The copper-de ficient rat may be a useful model to investigate the underlying bioche mical or molecular responses when peptides of enzymes are deleted.