Abstract
To investigate the effect of copper deficiency on folate and homocysteine metabolism, we measured plasma, red-cell and hepatic folate, plasma homocysteine and vitamin B-12 concentrations, and hepatic methionine synthase activities in rats. Two groups of male Sprague-Dawley rats were fed semi-purified diets containing either 0.1 mg (copper-deficient group) or 9.2 mg (control group) of copper per kg. After 6 weeks of dietary treatment, copper deficiency was established as evidenced by markedly decreased plasma and hepatic copper concentrations in rats fed the low-copper diet. Plasma, red-cell, hepatic folate, and plasma vitamin B-12 concentrations were similar in both groups, whereas plasma homocysteine concentrations in the copper-deficient group were significantly higher than in the control group (P<0.05). Copper deficiency resulted in a 21% reduction in hepatic methionine synthase activity as compared to the control group (P<0.01). This change most likely caused the increased hepatic 5-methyltetrahydrofolate and plasma homocysteine concentrations in the copper-deficient group. Our results indicate that hepatic methionine synthase may be a cuproenzyme, and plasma homocysteine concentrations are influenced by copper nutriture in rats. These data support the concept that copper deficiency can be a risk factor for cardiovascular disease. Copyright (C) 1999 Elsevier Science B.V.
Original language | English (US) |
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Pages (from-to) | 351-356 |
Number of pages | 6 |
Journal | Biochimica et Biophysica Acta - General Subjects |
Volume | 1427 |
Issue number | 3 |
DOIs | |
State | Published - May 24 1999 |
Keywords
- Copper deficiency
- Folate
- Homocysteine
- Methionine synthase
- Rat
- Vitamin B-12
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology