Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/2/2002
Publication Date: 3/14/2003
Citation: Saari, J.T. 2003. Differential effects of dietary copper deficiency on respiration via cardiac mitochondrial complexes I and II [abstract]. The Federation of American Societies for Experimental Biology Journal. 17:A1128.
Technical Abstract: Respiration of isolated rat heart mitochondria is reduced by dietary copper (Cu) deficiency. We examined 1) whether the reduced respiration could be confirmed in a tissue-slice model, 2) the relative importance of mitochondrial complexes I and II to this reduction and 3) whether nitric oxide (NO) has a role in the reduced respiration. Young male rats were fed Cu-adequate (6 mg/kg) or Cu-deficient (0.3 mg/kg) diets for 5 wks. O**2 uptake of heart slices was measured with an O**2 electrode. Heart slices were 1) untreated, 2) treated with malonate and provided with pyruvate-malate (testing the complex I-III-IV pathway) or 3) treated with rotenone and provided with succinate (complex II-III-IV pathway). O**2 uptake was depressed by Cu deficiency in untreated tissue. O**2 uptake of malonate-treated tissue, using either endogenous stores of NADH or that generated by pyruvate-malate addition, was depressed by Cu deficiency. O**2 uptake of rotenone-treated tissue was unaffected by Cu deficiency when endogenous substrate was relied upon, but increased by Cu deficiency when succinate was provided. Acute NO synthase inhibition showed no interactions with diet except for a small exaggeration of the Cu effect on malonate-treated tissue. These findings indicate that depression of heart mitochondrial respiration by dietary Cu deficiency results from a balance of decreased respiration by complex I and increased respiration by complex II.