Folate and homocysteine metabolism in copper-deficient rats

Tsunenobu Tamura, Kyu H. Hong, Yasuharu Mizuno, Kelley E. Johnston, Carl L Keen

Research output: Contribution to journalArticle

21 Scopus citations

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 languageEnglish (US)
Pages (from-to)351-356
Number of pages6
JournalBiochimica et Biophysica Acta - General Subjects
Volume1427
Issue number3
DOIs
StatePublished - May 24 1999

Keywords

  • Copper deficiency
  • Folate
  • Homocysteine
  • Methionine synthase
  • Rat
  • Vitamin B-12

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Fingerprint Dive into the research topics of 'Folate and homocysteine metabolism in copper-deficient rats'. Together they form a unique fingerprint.

  • Cite this