FUNCTIONAL-ASPECTS OF OXIDATIVE-PHOSPHORYLATION AND ELECTRON-TRANSPORT IN CARDIAC MITOCHONDRIA OF COPPER-DEFICIENT RATS

Although dietary copper deficiency causes physiological, morphological , and biochemical abnormalities in cardiac mitochondria, the relations hip observed between abnormalities of mitochondrial structure and func tion have been inconsistent in previous studies. The purpose of the pr esent study was to re-evaluate the respiration rates of cardiac mitoch ondria from copper-deficient rats and to use several drugs that uncoup le and inhibit mitochondrial respiration in order to clarify the mecha nisms of mitochondrial dysfunction found in several laboratories. Copp er deficiency reduced state 4 and state 3 cardiac mitochondrial respir ation rates with all substrates tested. However, neither the ratio of ADP/oxygen consumed nor the acceptor control index was affected by cop per deficiency. Cardiac mitochondria of copper-deficient rats showed a resistance to respiratory blockade by oligomycin and an increased abi lity to hydrolyze ATP in the presence of oligomycin compared with mito chondria of copper-adequate rats. This suggests that copper deficiency affects the function of the cardiac mitochondrial ATP synthase.