A number of different vitamers share the activity of vitamin B6, which is structurally a pyridine ring with differing substituent molecules on the carbon atom at position 4. Pyridoxine, pyridoxal and pyridoxamine represent the alcohol, aldehyde and amine forms of vitamin B6, respectively. While unphosphoryated pyridoxine is found in plants foods, pyridoxamine phosphate and pyridoxal phosphate are found in animal tissues. Absorption of vitamin B6 vitamers is in their unphosphorylated form, and hydrolysis of any vitamin B6 phosphates occurs in the small intestine to produce the free form of the vitamin. Once absorbed vitamin B6 compounds must be phosphorylated to form a 5’-phosphate derivative for biological activity, and this can occur in the enterocytes of the small intestine. Any vitamin B6 not phosphorylated by the enterocytes is phosphorylated in the liver. In the liver, pyridoxamine phosphate and pyridoxine phosphate are converted to pyridoxal phosphate, the main form of the vitamin found in humans. Despite being water soluble, the liver can store a small amount of vitamin B6.
Vitamin B6 in its phosphorylated form is required as a co-factor by a large number of enzymes, most of which are involved in amino acid metabolism. Pyridoxal phosphate is useful in this regard because it can interact with the α-carbon on amino acids, causing it to become labile, which facilitates reactions. Transamination, decarboxylation, transulfhydration, desulfhydration, cleavage, synthesis and racemisation reactions all require pyridoxal phosphate. Porphyrin synthesis, and the metabolism of glycogen and tryptophan also require vitamin B6, and vitamin B6 may be needed for the action of steroid hormones. Vitamin B6 deficiency shows species variation amongst mammals. In humans, vitamin B6 deficiency causes fatigue in adults and neurological problems in infants, but is very rare and hard to induce experimentally. Insufficiency of vitamin B6 raises homocysteine levels because pyridoxal phosphate is required as a co-factor in the metabolism of homocysteine to cystathionine. Cellular increases in homocysteine as a result of vitamin B6 insufficiency spill over into the plasma, and high circulating levels oh homocysteine are a risk factor for cardiovascular disease.