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American Journal of Clinical Nutrition, Vol 59, 631-635, Copyright © 1994 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
MA Mansoor, PM Ueland and AM Svardal
Department of Pharmacology and Toxicology, University of Bergen, Haukeland Hospital, Norway.
We determined reduced, oxidized, and protein-bound homocysteine, cysteine, and cysteinylglycine in plasma from 13 patients with hyperhomocysteinemia (total homocysteine in the range 30.6-159.8 mumol/L) due to cobalamin deficiency. Reduced homocysteine (means +/- SD: 1.87 +/- 2.06 mumol/L) was markedly above normal (0.24 +/- 0.12 mumol/L) in most patients, and the reduced fraction increased as an exponential function of the total homocysteine concentration. The ratio of reduced homocysteine to total homocysteine was positively correlated with the reduced-total ratio for cysteine and cysteinylglycine, suggesting redox equilibrium between different aminothiol species. The free oxidized and the protein-bound forms of homocysteine account for most of the homocysteine in plasma of these patients. The amount of protein-bound homocysteine was negatively correlated with the concentrations of both protein-bound cysteine and cysteinylglycine, indicating displacement of these aminothiols by homocysteine.
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