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Effect of Riboflavin Status on the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype
Author(s) -
Stuart J. Moat,
Pauline AshfieldWatt,
Hilary J. Powers,
Robert G. Newcombe,
I.F.W. McDowell
Publication year - 2003
Publication title -
clinical chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.705
H-Index - 218
eISSN - 1530-8561
pISSN - 0009-9147
DOI - 10.1373/49.2.295
Subject(s) - methylenetetrahydrofolate reductase , riboflavin , homocysteine , medicine , endocrinology , thermolabile , b vitamins , vitamin , chemistry , reductase , genotype , biochemistry , enzyme , gene
Riboflavin (vitamin B(2)) is the precursor for FAD, the cofactor for methylenetetrahydrofolate reductase (MTHFR). MTHFR catalyzes the formation of 5-methyltetrahydrofolate, which acts as a methyl donor for homocysteine remethylation. Individuals with the MTHFR 677C-->T mutation have increased plasma total homocysteine (tHcy) concentrations, particularly in association with low folate status. It has been proposed that riboflavin may act together with folate to lower plasma tHcy, particularly in individuals with the thermolabile MTHFR T variant.

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