Annals of Nutrition and Metabolism · 1990 · 17 citations · 14 references
Life SciencesNutritionNutritional SciencesCellular MetabolismMineral MetabolismNutritional BiochemistryCopper DeficiencyCopper MetabolismCopper NutritionGlutathione MetabolismCeruloplasmin BiologyEnzymesGlutathione S-transferase ActivityGlutathione S-transferase-mediated MetabolismHepatic Copper MetabolismMethionine MetabolismSuperoxide Dismutase 1
Two groups (n = 5) of male weanling Wistar rats were housed individually and fed copper (Cu)-deficient (0.5 mg Cu/kg) diets either with or without methionine supplementation (18 g/kg) for 49 days. Plasma caeruloplasmin (EC 1.16.3.1) and erythrocyte superoxide dismutase (EC 1.15.1.1, CuSOD) activities were measured in blood. Tissue Cu levels and the activities of cytochrome c oxidase (EC 1.9.3.1, CCO) and CuSOD were measured in the heart and liver. Hepatic activities of the sulfhydryl-sensitive enzymes, creatine kinase (EC 2.7.3.2), fumarase (EC 4.2.1.2) glutathione S-transferase (EC 2.5.1.18) and lipoamide dehydrogenase (EC 1.6.4.3) were also measured. Apart from cardiac CCO activity all of the measured indices of Cu status were found to be significantly (p less than 0.05) decreased in the methionine supplemented rats. Although fumarase activity was significantly (p less than 0.05) decreased in the methionine-supplemented animals compared with controls, the activities of the other sulfhydryl-sensitive enzymes were not significantly decreased. These results suggest that some of the toxic effects of excess dietary methionine may be mediated through interference with copper metabolism rather than through the previously postulated inhibition of sulfhydryl-sensitive enzymes by metabolites of methionine.
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William H. Habig, M. Pabst, William B. Jakoby · Journal of Biological Chemistry · 1974 · 18.1K citations · Full text
Trace Elements in Human Nutrition
Michael Golden · JAMA · 1963 · 231 citations