Vitamin B6 Deficiency, Genome Instability and Cancer

Abstract

Vitamin B6 functions as a coenzyme in >140 enzymatic reactions involved in the metabolism of amino acids,carbohydrates, neurotransmitters, and lipids. It comprises a group of three related 3-hydroxy-2-methyl-pyrimidinederivatives: pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM) and their phosphorylated derivatives [pyridoxal5’-phosphate (PLP) and pyridoxamine 5’-phosphate (PMP)], In the folate metabolism pathway, PLP is a cofactorfor the mitochondrial and cytoplasmic isozymes of serine hydroxymethyltransferase (SHMT2 and SHMT1),the P-protein of the glycine cleavage system, cystathionine β-synthase (CBS) and γ-cystathionase, and betainehydroxymethyltransferase (BHMT), all of which contribute to homocysteine metabolism either through folatemediatedone-carbon metabolism or the transsulfuration pathway. Folate cofactors carry and chemically activatesingle carbons for the synthesis of purines, thymidylate and methionine. So the evidence indicates that vitaminB6 plays an important role in maintenance of the genome, epigenetic stability and homocysteine metabolism.This article focuses on studies of strand breaks, micronuclei, or chromosomal aberrations regarding protectiveeffects of vitamin B6, and probes whether it is folate-mediated one-carbon metabolism or the transsulfurationpathway for vitamin B6 which plays critical roles in prevention of cancer and cardiovascular disease.

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