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7.3E: Vitamin B₆ (Pyridoxine)

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    Vitamin B6 refers to a group of chemically similar compounds which can be interconverted in biological systems. Vitamin Bis part of the vitamin B group of essential nutrients. Its active form, pyridoxal 5′-phosphate, serves as a coenzyme in some 100 enzyme reactions in amino acid, glucose, and lipid metabolism. Several forms 

    • Pyridoxine 5′-phosphate (P5P)
    • Pyridoxal (PL)
    • Pyridoxal 5′-phosphate (PLP), the metabolically active form (sold as P-5-P vitamin supplement)
    • Pyridoxamine (PM)
    • Pyridoxamine 5′-phosphate (PMP)
    • 4-Pyridoxic acid (PA), the catabolite which is excreted in urine
    • Pyritinol, a semi-synthetic derivative of pyridoxine, where two pyridoxine moieties are bound by a disulfide bridge.

    All forms except pyridoxic acid and pyritinol can be interconverted. Absorbed pyridoxamine is converted to PMP by pyridoxal kinase, which is further converted to PLP by pyridoxamine-phosphate transaminase or pyridoxine 5′-phosphate oxidase which also catalyzes the conversion of PNP to PLP. Pyridoxine 5′-phosphate oxidase is dependent on flavin mononucleotide (FMN) as a cofactor which is produced from riboflavin (vitamin B2) i.e. in this biochemical pathway, dietary vitamin B6 cannot be used without vitamin B2.

    1224px-Pyridoxal-phosphate.svg.png

    Pyridoxine and Pyridoxamine

    PLP, the metabolically active form of vitamin B6, is involved in many aspects of mcronutrient metabolism, neurotransmitter synthesis, histamine synthesis, hemoglobin synthesis and function, and gene expression. PLP generally serves as a coenzyme (cofactor) for many reactions including decarboxylation, transamination, racemization, elimination, replacement, and beta-group interconversion. The liver is the site for vitamin B6 metabolism.Amino acid metabolism PLP is a cofactor in the biosynthesis of five important neurotransmitters: serotonin, dopamine, epinephrine, norepinephrine, and gamma-aminobutyric acid (GABA). PLP is also involved in the synthesis of histamine.

    Dietary Sources

    Vitamin B6 is widely distributed in foods in both its free and bound forms. Cooking, storage, and processing losses of vitamin B6 vary and in some foods may be more than 50%, depending on the form of vitamin present in the food. Plant foods lose the least during processing, as they contain mostly pyridoxine, which is far more stable than the pyridoxal or pyridoxamine found in animal foods. For example, milk can lose 30–70% of its vitamin B6 content when dried. Vitamin B6 is found in the germ and aleurone layer of grains, and milling results in the reduction of this vitamin in white flour. The heating that occurs before most freezing and canning processes are other methods that may result in the loss of vitamin B6 in foods.

    Foods that contain large amounts of vitamin B6 include:

    • fortified breakfast cereals
    • pork
    • turkey
    • beef
    • bananas
    • chickpeas
    • potatoes
    • pistachios

    Dietary Reference Intake

    The Food and Nutrition Board (FNB) of the U.S. Institute of Medicine updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for vitamin B6 in 1998. The current EARs for vitamin B6 for women and men ages 14 and up increase with age from 1.0 to 1.3 mg/day and from 1.1 to 1.4 mg/day, respectively; the RDAs increase with age from 1.2 to 1.5 and from 1.3 to 1.7 mg/day, respectively. RDAs are higher than EARs so as to identify amounts that will cover people with higher than average requirements. RDA for pregnancy equals 1.9 mg/day. RDA for lactation equals 2.0 mg/day. For infants up to 12 months the Adequate Intake (AI) is 0.1–0.3 mg/day. and for children ages 1–13 years the RDA increases with age from 0.5 to 1.0 mg/day. As for safety, the FNB sets Tolerable Upper Intake Levels (known as ULs) for vitamins and minerals when evidence is sufficient. In the case of vitamin B6 the UL is set at 100 mg/day. The European Food Safety Authority reviewed the same safety question and set its UL at 25 mg/day. Safety issues are presented at length in the Toxicity section.

    For U.S. food and dietary supplement labeling purposes the amount in a serving is expressed as a percent of daily value (%DV). For vitamin B6 labeling purposes 100% of the Daily Value was 2.0 mg, but as of May 2016 it has been revised to 1.7 mg. Food and supplement companies have until July 28, 2018 to comply with the change.

    Absorption and excretion

    Vitamin B6 is absorbed in the jejunum and ileum by passive diffusion. With the capacity for absorption being so great, animals are able to absorb quantities much greater than necessary for physiological demands. The absorption of pyridoxal phosphate and pyridoxamine phosphate involves their dephosphorylation catalyzed by a membrane-bound alkaline phosphatase. Those products and nonphosphorylated forms in the digestive tract are absorbed by diffusion, which is driven by trapping of the vitamin as 5′-phosphates through the action of phosphorylation (by a pyridoxal kinase) in the jejunal mucosa. The trapped pyridoxine and pyridoxamine are oxidized to pyridoxal phosphate in the tissue.

    The products of vitamin B6 metabolism are excreted in the urine, the major product of which is 4-pyridoxic acid. An estimated 40–60% of ingested vitamin B6 is oxidized to 4-pyridoxic acid. Several studies have shown that 4-pyridoxic acid is undetectable in the urine of vitamin B6-deficient subjects, making it a useful clinical marker to assess the vitamin B6 status of an individual. Other products of vitamin B6metabolism excreted in the urine when high doses of the vitamin have been given include pyridoxal, pyridoxamine, and pyridoxine and their phosphates. A small amount of vitamin B6 is also excreted in the feces.

    Deficiencies

    The classic clinical syndrome for vitamin B6 deficiency is a seborrhoeic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy (due to impaired sphingosine synthesis) and sideroblastic anemia (due to impaired heme synthesis).

    Less severe cases present with metabolic disease associated with insufficient activities of the coenzyme PLP. The most prominent of the lesions is due to impaired tryptophan–niacin conversion. This can be detected based on urinary excretion of xanthurenic acid after an oral tryptophan load. Vitamin B6 deficiency can also result in impaired transsulfuration of methionine to cysteine. The PLP-dependent transaminases and glycogen phosphorylase provide the vitamin with its role in gluconeogenesis, so deprivation of vitamin B6 results in impaired glucose tolerance.

    A deficiency of vitamin B6 alone is relatively uncommon and often occurs in association with other vitamins of the B complex. The elderly and alcoholics have an increased risk of vitamin B6 deficiency, as well as other micronutrient deficiencies. Evidence exists for decreased levels of vitamin B6 in women with type 1 diabetes and in patients with systemic inflammation, liver disease, rheumatoid arthritis, and those infected with HIV. 

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