Impaired cardiac mitochondrial membrane potential and respiration in copper-deficient rats.
Cardiac mitochondrial respiration, ATP synthase activity, and membrane potential and intactness were evaluated in copper-deficient rats. In the presence of NADH, both copper-deficient and copper-adequate mitochondria had very low oxygen consumption rates, indicating membrane intactness. However copper-deficient mitochondria had significantly lower oxygen consumption rates with NADH than did copper-adequate mitochondria. Copper-deficient mitochondria had significantly lower membrane potential than did copper-adequate mitochondria using fluorescent dyes. Copper-deficient mitochondria had significantly lower state 3 oxygen consumption rates and were less sensitive to inhibition by oligomycin, an ATP synthase inhibitor. Copper-deficient and copper-adequate mitochondria responded similiarly to CCCP. No difference was observed in mitochondrial ATPase activity between copper-deficient and copper-adequate rats using submitochondrial particles. We conclude that cardiac mitochondrial respiration is compromised in copper-deficient rats, and may be related to an altered ATP synthase complex and/or a decreased mitochondrial membrane potential.
Chen
Xiulian
X
Department of Human Nutrition, Kansas State University, Manhattan, Kansas 66506, USA.
Jennings
Dianne B
DB
Medeiros
Denis M
DM
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003300:Copper / Q000172:deficiency*; D007700:Kinetics; D008099:Liver / Q000201:enzymology; D008564:Membrane Potentials / Q000502:physiology; D008929:Mitochondria, Heart / Q000502:physiology* / Q000648:ultrastructure; D025261:Mitochondrial Proton-Translocating ATPases / Q000378:metabolism*; D010101:Oxygen Consumption; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism
D003300:Copper; D000255:Adenosine Triphosphate; D013482:Superoxide Dismutase; D025261:Mitochondrial Proton-Translocating ATPases