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Mitochondrial respiration in hearts of copper-deficient rats

Conference · · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)
OSTI ID:5373136
;  [1]
  1. Univ. of North Dakota, Grand Forks (United States) USDA/ARS, Grand Forks, ND (United States)

Morphological observations indicate that dietary copper deficiency causes structural damage of cardiac mitochondria. The purpose of this study was to determine whether mitochondrial function is impaired as well. Male, weanling Sprague-Dawley rats were fed diets deficient or sufficient in copper for 4 wks. Copper deficiency was verified by measurement of plasma (ND (CuD) vs 0.46 {plus minus} 0.15 {mu}g/ml (CuS)) and kidney copper. Mitochondria were isolated and P/O ratio, state 3 and state 4 respiration rate and acceptor control index (ACI) were determined using succinate or pyruvate/malate as substrate. Determinations were made polarographically at 30C in a reaction medium consisting of 0.25 M sucrose, 0.1 mM EDTA, 200 mM MgCl and 200 mM sodium phosphate buffer. State 3 respiration rate in mitochondria from CuD hearts was 30% lower than in CuS mitochondria when succinate was used as substrate and 28% lower when pyruvate/malate was used. Copper deficiency reduced state 4 respiration rate by 31% when succinate was used and 16% when pyruvate/malate was used. P/O ratio and ACI were not significantly affected by copper deficiency. The observed decreases in respiration rates are consistent with decreased cytochrome c oxidase activity shown by others to occur in mitochondria isolated from hearts of copper-deficient rats.

OSTI ID:
5373136
Report Number(s):
CONF-9104107--
Journal Information:
FASEB Journal (Federation of American Societies for Experimental Biology); (United States), Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Vol. 5:4; ISSN FAJOE; ISSN 0892-6638
Country of Publication:
United States
Language:
English

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