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Altered nucleotide content and changes in mitochondrial energy states associated with copper deficiency in rat platelets

Johnson, W. Thomas, Dufault, Steven N., Newman, Samuel M. Jr.
Journal of nutritional biochemistry 1995 v.6 no.10 pp. 551
copper, mitochondria, liver, blood plasma, hemoglobin, experimental diets, adenosine monophosphate, adenosine diphosphate, adenosine triphosphate, guanosine triphosphate, purine nucleotides, energy, rats, blood platelets, nutrient deficiencies, hematocrit, ferroxidase
Dietary copper deficiency severely reduces platelet cytochrome c oxidase activity, but the effect of this perturbation on platelet energy metabolism is unknown. In this study, the effect of copper deficiency on platelet adenine nucleotide and GTP content was determined. Structural changes in platelet mitochondria during copper deficiency also were examined. Copper deficiency caused a 24% reduction in adenosine triphosphate (ATP) content, a 113% increase in adenosine monophosphate (AMP) content, and a 36% reduction in GTP content. Because the secretory pool of ATP was not affected by copper deficiency, the changes observed in platelet nucleotide content most likely reflect an effect on the metabolic nucleotide pool. Furthermore, the number of platelet mitochondria exhibiting swollen cristae and high matrical density, characteristics suggesting that mitochondria are engaged in oxidative phosphorylation, was increased by copper deficiency. These findings indicate that copper deficiency can alter energy metabolism in platelets in a manner that is consistent with partial blockage of mitochondrial electron transport and reduced ATP production.