Mitochondrial respiration in heart, liver, and kidney of copper-deficient rats

Ann M. Bode, Lisa A. Miller, Jeannine Faber, Jack T. Saari

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Morphological observations in some tissues indicate that dietary copper deficiency results in structural damage to 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 weeks. Mitochondria were isolated from heart, liver, kidney cortex, and kidney medulla. P/O ratio, state 3 and state 4 respiration rates (oxygen consumed in the presence and absence of ADP, respectively), and acceptor control index (ratio of state 3:state 4) were determined using succinate or pyruvate/malate as substrate. State 3 respiration rate in mitochondria from copper-deficient hearts and livers was lower than in mitochondria from copper-sufficient hearts. Copper deficiency reduced the state 4 respiration rate only in cardiac mitochondria. Neither respiration rate was affected by copper deficiency in mitochondria from kidney medulla or cortex. P/O ratio was not significantly affected by copper deficiency in any tissue examined. Acceptor control index was reduced only in liver mitochondria. The observed decreases in respiration rates are consistent with decreased cytochrome c oxidase activity, shown by others to occur in mitochondria isolated from hearts and livers of copper-deficient rats.

Original languageEnglish (US)
Pages (from-to)668-672
Number of pages5
JournalThe Journal of Nutritional Biochemistry
Issue number12
StatePublished - Dec 1992
Externally publishedYes


  • cardiac mitochondria
  • copper deficiency
  • mitochondrial respiration


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