Vitamin B6 refers to a group of three compounds: pyridoxol (pyridoxine), pyridoxal and pyridoxamine. Pyridoxine is the predominant form in plants, whereas pyridoxal and pyridoxamine are vitamin forms generally found in animal products. These three forms have equal activity when administered to animals, but are not equivalent when administered to various microorganisms. Two additional vitamin B6 forms found in foods are the coenzyme forms of pyridoxal phosphate (PLP) and pyridoxamine phosphate. Various forms of vitamin B6 found in animal tissues are interconvertible, with vitamin B6metabolically active mainly as PLP and to a lesser degree as pyridoxamine phosphate. Vitamin B6 has been shown to be stable to heat, acid and alkali; however, exposure to light, especially in neutral or alkaline media, is highly destructive. The free base and the commonly available hydrochloride salt are soluble in water and alcohol (Illus. 9-1).
There are several vitamin B6 antagonists, which either compete for reactive sites of apoenzymes or react with PLP to form inactive compounds. The presence of a vitamin B6 antagonist in linseed meal is of particular interest to animal nutritionists. This substance was identified in 1967 as hydrazic acid and was found to have antibiotic properties (Parsons and Klostermann, 1967). Pesticides (e.g., carbaryl, propoxur or thiram) can be antagonistic to vitamin B6. Feeding a diet enriched with vitamin B6 prevented disturbances in the active transport of methionine in rats intoxicated with pesticides (Witkowska et al., 1992). Digestion of vitamin B6 would first involve splitting the vitamin, as it is bound to the protein portion of foods. Vitamin B6 is absorbed mainly in the jejunum but also in the ileum by passive diffusion. Absorption from the colon is insignificant, even though colon microflora synthesize the vitamin. However, Durst et al. (1989) administered vitamin B6 in the cecum of sows and concluded that the vitamin was absorbed at this location. Little information is available on digestion and absorption of vitamin B6in ruminants; however, large quantities of the vitamin are synthesized in the rumen. Vitamin B6 compounds are all absorbed from the diet in the dephosphorylated forms. The small intestine is rich in alkaline phosphatases for the dephosphorylation reaction. Sakurai et al. (1992) reported that a physiological dose of pyridoxamine was rapidly transformed to pyridoxal in the intestinal tissues and then released in the form of pyridoxal into the portal blood. After absorption, B6 compounds rapidly appear in liver, where they are mostly converted into PLP, considered to be the most active vitamin form in metabolism. Under normal conditions, most of the vitamin B6 in blood is present as PLP that is linked to proteins, largely albumin in the plasma and hemoglobin in the red blood cells (McCormick, 2006). Pyridoxal phosphate is the major B6 form in goat milk, accounting for 75% of the vitamin B6 activity (Coburn et al., 1992). Both niacin (as nicotinamide adenine dinucleotide phosphate [NADP]-dependent enzyme) and riboflavin (as the flavoprotein pyridoxamine phosphate oxidase) are important for conversion of vitamin B6forms and phosphorylation reactions (Kodentsova et al., 1993).at these specific sites under physiological conditions (DeLuca, 2008).
Although other tissues also contribute to vitamin B6 metabolism, the liver is thought to be responsible for forming PLP found in plasma. Pyridoxal and PLP found in circulation are associated primarily with plasma albumin and red blood cell hemoglobin (Mehansho and Henderson, 1980). Pyridoxal phosphate accounts for 60% of plasma vitamin B6. Researchers do not agree on whether pyridoxal or PLP is the transport form of B6 (Driskell, 1984).
Only small quantities of vitamin B6 are stored in the body. The vitamin is widely distributed in various tissues, mainly as PLP or pyridoxamine phosphate. Vitamin B6 readily passes the placenta. Pyridoxal crosses the human placenta readily in both directions (Delport et al., 1991; Schenker et al., 1992). Pyridoxic acid is the major excretory metabolite of the vitamin, eliminated via the urine. Also, small quantities of pyridoxol, pyridoxal and pyridoxamine, as well as their phosphorylated derivatives, are excreted in urine (Henderson, 1984). Vitamin B6 metabolism is altered in renal failure, as observed in rats exhibiting plasma pyridoxal phosphate 43% lower than controls (Wei and Young, 1994).
Picture on left shows inflamed edema of the eyelid in vitamin B6 deficiency. Picture on right shows vitamin B6 deficiency: rough deficient plumage, weaknes and incoordination of movements.
Courtesy of L.R. McDowell, University of Florida
A more specific sign of B6 deficiency is the nature of the nervous condition that develops. Deficient chicks are abnormally excitable. As deprivation continues, nervous disorders become increasingly severe (Bräunlich, 1974). There is trembling and vibration of the tip of the tail, with movement stiff and jerky. Chicks run aimlessly about with lowered head and drooping wings (Illus. 9-4). Finally, convulsions develop, during which chicks fall on their side or back, with the legs scrabbling. Violent convulsions cause complete exhaustion and may lead to death (Leeson and Smmers, 2001). These clinical signs may be distinguished from those of encephalomalacia by the greater intensity of activity during a B6deficiency seizure, which results in complete exhaustion and often death (Scott et al., 1982
Neuritis and “squatting position.”
Courtesy of L.R. McDowell, University of Florida
Blood alterations are also typical of vitamin B6 inadequacy in chicks. An extreme deficiency leads to microcytic, polychromatic, hypochromic anemia in conjunction with atrophy of the spleen and thymus (Asmar et al., 1968). Marginal deficiencies provoke microcytic, normochromic polycythemia (Blalock and Thaxton, 1984), and deficient chicks show a decreased immunoglobulin M and immunoglobulin G response to antibody challenge (Blalock et al., 1984). Similar signs of a vitamin B6 deficiency have been observed in turkey poults: loss of appetite, poor growth (Illus. 9-5), oversensitivity, cramps and eventually death. Ducklings not receiving enough vitamin B6 grow slowly, and development of plumage is poor. At five days of age, ducklings showed retarded growth (Yang and Jeng, 1989). Clinical signs, which were first observed at seven days of age, were characterized by decreased appetite, extreme weakness, hyperexcitability, convulsions and death. Hematologic examination at three weeks of age indicated that vitamin B6 deficiency in ducklings resulted in microcytic, hypochromic anemia.
Note poor growth in a vitamin B6- deficient turkey poult (about four weeks old) compared with a normal poult at right.
Courtesy of T.W. Sullivan, University of Nebraska.
Signs of B6 deficiency in chicks appear very rapidly after introduction of a B6-deficient feed. Fuller and Kifer (1959) reported that signs of a deficiency appeared on the eighth day. Chronic borderline B6 deficiency produces perosis; usually one leg is severely crippled, and one or both of the middle toes may be bent inward at the first joint (Gries and Scott, 1972). Vitamin B6 deficiency in growing chicks affected biomechanical properties of tibial bone, with reduced dry weight and cortical thickness (Masse et al., 1994; 1996). A marked increase in gizzard erosion was found in vitamin B6-deficient chicks (Daghir and Haddad, 1981). For adult poultry, vitamin B6 deficiency results in reduced egg production and hatchability as well as decreased feed consumption, weight loss and death. A severe deficiency [levels of vitamin B6below 0.5 mg per kg (0.23 mg per lb)] of diet causes rapid involution of the ovary, oviduct, comb and wattles in mature laying hens. Involution of testes, comb and wattles occurs in vitamin B6-deficient adult cockerels (Scott et al., 1982).
Vitamin B6 is one of the B vitamins that receives the least amount of attention when poultry rations are formulated. Because of its wide distribution in feedstuffs, nutritionists generally expect adequate levels in typical poultry diets. Evidence to date indicates that corn, soybean meal and other ingredients used to supply energy and protein in practical poultry diets provide the minimum requirement of vitamin B6. However, the bioavailability in corn and soybean meal ranges from only 45% to 65% (Hoffmann-La Roche, 1979). Under certain conditions, vitamin B6 supplementation is warranted for practical growing and breeding diets for poultry and other monogastrics. Fuller et al. (1961) believe that while breeder diets containing corn-soybean meal probably provide the minimum requirement for vitamin B6 to support hatchability, there is little margin of safety. In turkey breeders, there is decreasing deposition of vitamins B6 and B12 in the egg with aging (Robel, 1983). Hatchability of turkey eggs decreased with increasing age of the breeder hen. This maybe related to the decreasing nutrient deposition in the egg that occurs as the hen ages. The amount of supplemental vitamin B6 recommended for monogastric species varies from 1 to 10 mg per kg (0.45 to 4.5 mg per lb) of diet depending on species, age, activity, stress level and field conditions (Bauernfeind, 1974). Reasons for needed supplementation of vitamin B6 include the following (Perry, 1978): (1) great variations in amounts of B6 in individual ingredients; (2) variable bioavailability of this vitamin in feed; (3) losses reported during processing of feed ingredients; (4) discrepancies between activity for test organisms and those for animals; (5) a higher vitamin B6requirement due to a marginal level of methionine in the diet; and (6) high-protein diets. Variability of vitamin B6 in feeds depends on the sample origin, conditions of growth, climate, weather and other local factors. Yen et al. (1976) determined available vitamin B6 in corn and soybean meal using a chick growth assay. Vitamin B6 in corn was found to be 38% to 45% available, and B6 in soybean meal, 58% to 62% available. There was little difference in availability between corn samples not heated and those heated to 120°C (248°F). However, corn heated to 160°C (320°F) contained significantly less available B6. Levels of vitamin B6 contained in feedstuffs are also affected by processing and subsequent storage. In one report, a loss of 30% of B6 was observed in alfalfa meal during the coarse milling and pelleting processes (Bräunlich, 1974). Bioavailability of feedstuffs can be as low as 40% to 50% after heating.
Predominant losses of vitamin B6 activity in feedstuffs occur in the pyridoxal and pyridoxamine forms, with pyridoxine the more stable form. Supplemental vitamin B6 is reported to have higher bioavailability and stability than the naturally occurring vitamin. Naturally occurring vitamin B6 in retorted milk products exhibited only 50% of the bioavailability of synthetic B6 or B6 in formulas fortified with the vitamin prior to thermal processing (Tomarelli et al., 1955).
Insufficient data are available to support estimates of the maximum dietary tolerable levels of vitamin B6 for poultry. It is suggested, primarily from dog and rat data, that dietary levels of at least 50 times the nutritional requirements are safe for most species (NRC, 1987). Vitamin B6 toxicity causes ataxia, muscle weakness and incoordination at levels approaching 1,000 times the requirement (Leeson and Summers, 2001). Large doses of vitamin B6 can produce detrimental effects in experimental animals and humans. Signs of toxicity, which occur most obviously in the peripheral nervous system, include changes in gait and peripheral sensation (Krinke and Fitzgerald, 1988). Changes in central nervous system function were detected in rats fed excessive vitamin B6 using measurement techniques of startle behavior (Schaeffer, 1993).
Ask a question about our products & solutions or subscribe to our newsletter..