Six compounds have vitamin B6 activity (Figure 1): pyridoxine, pyridoxal, pyridoxamine, and their 5′-phosphates. The active coenzyme is pyridoxal 5′-phosphate. Some 80% of the body’s total vitamin B6 is pyridoxal phosphate in muscle, mostly associated with glycogen phosphorylase. This is not available in deficiency, but is released in starvation, when glycogen reserves become depleted, and is then available, especially to liver and kidney, to meet increased requirement for gluconeogenesis from amino acids.

Fig1. Interconversion of the vitamin B6 vitamers.

Vitamin B6 Has Several Roles in Metabolism

Pyridoxal phosphate is a coenzyme for many enzymes involved in amino acid metabolism, especially transamination and decarboxylation. It is also the cofactor of glycogen phosphorylase, where the phosphate group is catalytically important. In addition, it is important in steroid hormone action. Pyridoxal phosphate removes the hormone-receptor complex from DNA binding, terminating the action of the hormones. In vitamin B6 deficiency, there is increased sensitivity to the actions of low concentrations of estrogens, androgens, cortisol, and vitamin D.

Vitamin B6 Deficiency Is Rare

 Although clinical deficiency disease is rare, there is evidence that a significant proportion of the population has marginal vitamin B6 status. Moderate deficiency results in abnormalities of tryptophan and methionine metabolism. Increased sensitivity to steroid hormone action may be important in the development of hormone-dependent cancer of the breast, uterus, and prostate, and vitamin B6 status may affect the prognosis.

Vitamin B6 Status Is Assessed by Assaying Erythrocyte Transaminases

The most widely used method of assessing vitamin B6 status is by the activation of erythrocyte transaminases by pyridoxal phosphate added in vitro, expressed as the activation coefficient. Measurement of plasma concentrations of the vitamin is also used.

In Excess, Vitamin B6 Causes Sensory Neuropathy

The development of sensory neuropathy has been reported in patients taking 2 to 7 g of pyridoxine per day for a variety of reasons. There was some residual damage after withdrawal of these high doses; other reports suggest that intakes in excess of 100 to 200 mg/d are associated with neurological damage.

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