Excess Dietary Methionine Decreases Indices of Copper Status in the Rat

Abstract

Two groups (n = 5) of male weanling Wistar rats were housed individually and fed copper (Cu)-defιcient (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 < 0.05) decreased in the methionine supplemented rats. Although fumarase activity was significantly (p < 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.

Disturbances of micronutrient and antioxidant status in diabetes

“…1981;Lynch & Strain, 1989;Wachnik eta/. 1989: Strain & Lynch, 1990 while Lawrence & Jenkinson (1987) have found that Cu deficiency in the rat resulted in increased carbon tetrachloride-induced lipid peroxidation as indicated by expired ethane. Similarly Saari et a/.…”

Methionine Supplementation Did Not Augment Oxidative Stress, Atherosclerotic Changes and Hepatotoxicity Induced by High Cholesterol Diet in C57BL/6J Mice

“…However, in rats, an HM diet did not alter cholesterol and triglyceride levels in the plasma and did not produce atherosclerotic changes in the aorta (11,12). An HM diet has been reported to induce the production of oxidative metabolites resulting from methionine metabolism and to cause defects in the enzymatic antioxidant system as well as iron accumula tion in tissues (3,7,(13)(14)(15). Therefore, oxidative stress has been proposed to play a role in the development of hepatic lesions (3,13), atherosclerotic disturbances (5 -8) and erythrocyte hemolysis (4) induced by an HM diet.…”

Preliminary study on the behavioral response of zebrafish to the presence of methionine and polypropylene residues in water

“…On the other hand, methionine is one of the essential aminoacids of the body [3], due to its involvement in angiogenesis and its antioxidant properties. Nowadays, it is also used as a treatment for copper and acetaminophen poisoning [4], liver disorders and viral infections amongst other things [5]. Increased levels of methionine may lead to oxidative lesions, apoptosis and oxidative stress [6].…”