Cardiac hypertrophy in copper-deficient rats is owing to increased mitochondria

Dietary copper depletion results in cardiac hypertrophy and ultrastructural alterations. The objective of this study was to determine the components that contribute to cardiac enlargement. Two groups (n = 4) of male, weaning, Sprague-Dawley rats were fed ad libitum with copper-adequate or copper-def...

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Bibliographic Details
Published in:Biological trace element research 1998-06, Vol.64 (1/3), p.175-184
Main Authors: Mao, S. (The Ohio State University, Columbus, OH.), Medeiros, D.M, Wildman, E.C
Format: Article
Language:English
Subjects:
Animals
Cardiomegaly - etiology
CARENCE EN SUBSTANCE NUTRITIVE
COBRE
COEUR
COPPER
Copper - deficiency
CORAZON
CUIVRE
DEFICIENCIAS NUTRITIVAS
Dietary minerals
HEART
HIPERTROFIA
HYPERTROPHIE
HYPERTROPHY
Male
Microscopy, Electron
Mitochondria
Mitochondria, Heart - ultrastructure
NUTRIENT DEFICIENCIES
Peptides
RAT
RATA
RATS
Rats, Sprague-Dawley
Rodents
ULTRAESTRUCTURA
ULTRASTRUCTURE
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Summary:Dietary copper depletion results in cardiac hypertrophy and ultrastructural alterations. The objective of this study was to determine the components that contribute to cardiac enlargement. Two groups (n = 4) of male, weaning, Sprague-Dawley rats were fed ad libitum with copper-adequate or copper-deficient diets for five weeks. Cross sectional transmission electron micrographs from both groups were evaluated using image analysis to quantify absolute area occupied by myocyte, mitochondria, myofibril, and other intracellular material. Copper-deficient rats had larger myocytes, increased area of mitochondria, and increased ratio of mitochondria:myofibril as well as mitochondria:myocyte. Copper deficiency did not change the absolute area occupied by myofibrils. These data suggested that increase in the absolute mitochondria area is the major contributory factor to the cardiac hypertrophy in copper deficiency. Under the conditions used, myofibril has minimal role toward contributing to the hypertrophic state. The pathology reported resembles human forms of genetic mitochondrial cardiomyopathies. The copper-deficient rat may be a useful model to investigate the underlying biochemical or molecular responses when peptides of enzymes are deleted.
ISSN:0163-4984
1559-0720
DOI:10.1007/bf02783334