The main form of vitamin B6 in foods is pyridoxal phosphate, bound as a Schiff base to lysine in dietary proteins. There is also a small amount of pyr-idoxamine phosphate. In plant foods a significant amount of the vitamin is present as pyridoxine, and a number of plants contain pyridoxine glyco-sides, which have limited availability. Heating foods can lead to the formation of (phospho)pyridoxylly-sine, which has antivitamin activity.
Pyridoxal phosphate bound to proteins is released on digestion of the protein. The phosphorylated vitamers are dephosphorylated by membrane-bound alkaline phosphatase in the intestinal mucosa; all three vitamers are absorbed by carrier-mediated diffusion, followed by oxidation and phos-phorylation, so there is accumulation of pyridoxal phosphate, which does not cross cell membranes, by metabolic trapping.
Both pyridoxal and the phosphate circulate in the bloodstream; the phosphate is dephosphorylated by extracellular alkaline phosphatase, and tissues take up pyridoxal by carrier-mediated diffusion, followed by metabolic trapping as phosphate esters. Pyrid-oxine and pyridoxamine phosphates are oxidized to pyridoxal phosphate (Figure 1).
Tissue concentrations of pyridoxal phosphate are controlled by the balance between phosphorylation and dephosphorylation. The activity of the phospha-tases is greater than that of the kinase in most tissues so that pyridoxal phosphate that is not bound to enzymes will be dephosphorylated. Free pyridoxal either leaves the cell or is oxidized to 4-pyridoxic acid by aldehyde dehydrogenase, which is present in all tissues, and also by hepatic and renal aldehyde oxidase. 4-Pyridoxic acid is the main excretory product.
Approximately 80% of total body vitamin B6 is in muscle, associated with glycogen phosphorylase. This does not seem to function as a true reserve of the vitamin and is not released from muscle in times of deficiency.
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