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DSM in Animal Nutrition & Health

Vitamin B6

Properties and Metabolism

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 parenterally 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, although exposure to light, especially in neutral or alkaline media, is highly destructive. Forms of vitamin B6 are colorless crystals soluble in water and alcohol both as free bases and the commonly available hydrochloride salt of the alcohol form, pyridoxine hydrochloride (Illus. 9-1). There are vitamin B6 antagonists that either compete for reactive sites of apoenzymes or react with PLP to form inactive compounds. Presence of a vitamin B6 antagonist in linseed is of particular interest to animal nutritionists. In 1967 this substance was identified as hydrazic acid and was found to have antibiotic properties (Parsons and Klostermann, 1967).


Illustration 9-1


Digestion of vitamin B6 first involves 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. Large quantities of the vitamin are synthesized in the rumen. Vitamin B6compounds 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. 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 red blood cells (McCormick, 2006). After absorption, B6compounds rapidly appear in the liver, where they are mostly converted into PLP, considered to be the most active vitamin form in metabolism. 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. 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. Russell et al. (1985) investigated B6 metabolism in swine muscle. Excess dietary vitamin B6 increased whole-muscle total PLP. Russell et al. (1985) indicated that under the conditions of their study, muscle tissue acts as an immobile reservoir of PLP and 60% to 95% of muscle PLP was bound to muscle glycogen phosphorylase. 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 into the urine (Henderson, 1984).



Vitamin B6 in the form of PLP and to a lesser degree pyridoxamine phosphate play an essential role in the interaction of amino acid, carbohydrate and fatty acid metabolism and the energy-producing tricarboxylic acid (TCA) cycle. Over 50 enzymes are already known to depend on vitamin B6coenzymes. Pyridoxal phosphate functions in nearly all reactions involved in amino acid metabolism, including transamination, decarboxylation, deamination and desulfhydration, as well as the cleavage or synthesis of amino acids. Vitamin B6 participates in functions that include the following (Braunlich, 1974; Marks, 1975; Driskell, 1984; McCormick, 2006; Dakshinamurti and Daskshinamurti, 2007):

  • Deaminases for serine, theonine and cystathionine.
  • Desulfhydrases and transulfhydrases interconversion.
  • Synthesis of niacin from tryptophanase hydroxykynurenine is not converted to hydroxyanthranilic acid but rather to xanthurenic acid due to lack of the B6-dependent enzyme kynureninase.
  • Formation of delta-aminolevulinic acid from succinyl coenzyme A and glycine, the first step in porphyrin synthesis.
  • Conversion of linoleic to arachidonic acid in the metabolism of essential fatty acids (this function is controversial).
  • Glycogen phosphorylase catalyzes glycogen breakdown to glucose-1-phosphate. Pyridoxal phosphate appears not to be a coenzyme for this enzyme, but rather to affect the enzyme’s conformation.
  • Synthesis of epinephrine and norepinephrine from either phenylalanine or tyrosinease. Both norepinephrine and epinephrine are involved in carbohydrate metabolism as well as in other body reactions.
  • Racemases—PLP-dependent racemases enable certain microorganisms to utilize d-amino acids. Racemases have not yet been detected in mammalian tissues.
  • Transmethylation by methionine.
  • Incorporation of iron in hemoglobin synthesis.
  • Amino acid transport—all three known amino acid transport systems, (1) neutral amino acids and histidine, (2) basic amino acids and (3) proline and hydroxyproline, appear to require PLP.
  • Formation of antibodies—B6 deficiency results in inhibition of the synthesis of globulins that carry antibodies.
  • Inflammation—higher vitamin B6 levels were linked to protection against inflammation (Morris et al., 2010).


McDowell (2000) reported that the decarboxylation of tryptophan to serotonin is also B6-dependent. Matte et al. (1997a) investigated the relationship of B6 in metabolism of tryptophan in weanling piglets. Matte et al. (1997a) were unable to detect an effect on the oxidation of the tryptophan pathway but suggested that B6 may stimulate another pathway in tryptophan metabolism. Matte et al. (1997b) investigated the importance of pyridoxine and tryptophan on glucose tolerance and insulin response to glucose in weanling piglets receiving a liquid diet through surgically inserted gastric tubes. Matte et al. (1997b) detected an interaction between parenteral pyridoxine and duodenal infusion on changes in plasma insulin concentration. The greatest response was observed in the piglets that received 3 ml of pyridoxine HCl (5 gm per L) intramuscularly and then an infusion of glucose. The insulin response was increased by approximately 55% in this group. Matte et al. (1997b) concluded that tryptophan and pyridoxine probably have different modes of action on the sensitivity and release of insulin. Matte et al. (1997b) suggested that the effect of vitamin B6 on insulin response to a glucose load was perhaps linked to its role in decarboxylation of tryptophan to serotonin. However, Matte (1997) indicated that results from his own research have been inconsistent with regard to the effect of pyridoxine supplementation on insulin metabolism and that further studies will be required.

Neurological disorders, including states of agitation and convulsions, result from reduction of B6 enzymes in the brain, including glutamate decarboxylase and gamma-aminobutyric acid transaminase. With a vitamin B6 deficiency, dopamine release is delayed, which may contribute to motor abnormalities (Tang and Wei, 2004). Maternal restriction of B6 in rats adversely affected synaptogenesis, neurogenesis and neuron longevity, and differentiation of the progeny (Groziak and Kirksey, 1990,1987). Recent work in animal models suggests that vitamin B6 deficiency during gestation and lactation alters the function of N-methyl-D-aspartate receptors, a subtype of receptors of the glutamatergic neurotransmitter system thought to play an important role in learning and memory (Guilarte, 1993).

Animal and human studies suggest that a vitamin B6 deficiency affects both humoral and cell-mediated immune responses. In humans, vitamin B6 depletion significantly decreased percentage and total number of lymphocytes, mitogenic responses of peripheral blood lymphocytes to T-and B-cell mitogens and interleukin 2 production (Meydani et al., 1991). The role of PLP in effecting one-carbon metabolism is important in nucleic acid biosynthesis and immune system function. The PLP is also needed for gluconeogenesis by way of transaminases active on glucogenic amino acids and for lipid metabolism that involves several aspects of PLP function. For example, for production of carnitine needed to act as a vector for long-chain fatty acids for mitochondrial β-oxidation and of certain bases for phospholipid biosynthesis (McCormick, 2006).



The requirement for vitamin B6 has been found generally to depend on species, age, physiologic function, dietary components, the intestinal flora and other factors that are not yet fully understood. Vitamin B6 is produced by microorganisms of the intestinal tract in swine, but whether significant quantities are absorbed and utilized is in doubt. Animals practicing coprophagy would obviously be receiving vitamin B6 from this source. In early studies, Hughes and Squibb (1942) estimated the pyridoxine requirement to be between (0 and 2.3 mg per lb) body weight daily for pigs with an average beginning body weight of 30 pounds. Vitamin B6 requirements for swine generally vary from 1 to 2 mg per kg (0.5 to 0.9 mg per lb) of diet (NRC, 1998). In early-weaned pigs, Kosters and Kirchgessner (1976a) indicated that lower levels of B6 are required for satisfactory feed efficiency than for optimum growth. Feed required per kg of weight gain in their experiment was increased only at the lowest vitamin B6 supplementation level, 0.5 ppm. For maximum weight gain, Kosters and Kirchgessner (1976a) suggested that 2 ppm was sufficient from 3.5 to 10 kg (1.6 to 4.5 lb) body weight, while only 1.2 ppm was required from 10 to 21 kg (4.5 to 9.5 lb) body weight. Using the same weight ranges, Kosters and Kirchgessner (1976b) reported similar requirements for optimum feed intake in early-weaned piglets. Furthermore, feed consumption was stated to be as sensitive a criterion of B6 supply as was growth rate. Milleret al. (1957) evaluated the pyridoxine requirements of baby pigs and determined that between 0.75 to 1 mg pyridoxine per kg (0.34 to 0.45 lb) dry matter of a synthetic milk diet was needed for the pigs’ total well-being under the conditions of their studies. Sewell et al. (1964) found a slightly higher vitamin B6 requirement for early-weaned pigs than the values reported by Miller et al. (1957). Under the conditions of their experiment, Sewell et al. (1964) recommended 0.9 to 3.5 mg vitamin B6 per kg (0.4 to 1.6 mg per lb) of feed and estimated that 1.8 mg vitamin B6 per kg (0.8 mg per lb) of feed would be required for pigs 3 to 8 weeks of age. Data by Woodworth et al. (1997) supported the addition of 2 to 3 gm pyridoxine per ton of diet for maximum average daily gain and average daily feed intake on days 0 through 14 after weaning. Matte (1995) suggested that the recommendations for water-soluble vitamins in swine are in many cases based on research that was reported decades ago and on deficiency syndromes. Furthermore, he emphasized that today’s pigs are raised in different housing and under different feeding conditions and vary greatly in genetics from the pigs used in many of the early research studies. Matte (1995) indicated that the optimum pyridoxine level is probably twice the Agricultural Research Council (1981) level. Pigs weighing 1 to 5 kg (2.2 to 11 lbs) require 2 mg vitamin B6 per kg (0.9 mg per lb) of feed, while pigs greater than 20 kg (44 lbs) and breeding animals require 1 mg per kg (0.5 mg per lb) of vitamin B6 in feeds (NRC, 1998). Recent data using growth (Woodworth et al., 2000) or metabolic (Matte et al., 2001) criteria suggest optimal responses at dietary and parenteral daily levels, two and 10 times higher, respectively, than those currently recommended (NRC 1998). Breed of animal and environmental temperature have been shown to influence vitamin B6 requirements for some species (i.e., poultry and rats). Regarding ambient temperature, when rats were housed at 33°C, they needed twice as much vitamin B6as when they were housed at 19°C (Braunlich, 1974) Quantity of dietary protein affects requirement for vitamin B6 in both animals and humans. The vitamin B6requirement is increased when high-protein diets are fed. For example, when feed contained 60% casein instead of 20%, the level of pyridoxine required by mice was three times as high (Miller and Baumann, 1945). A number of studies have suggested that amino acid imbalance has an adverse effect on vitamin B6 status, in that weight gain was depressed and survival was decreased when large amounts of a single amino acid were added to rat diets limited in the vitamin. High tryptophan, methionine and other amino acids increase the need for vitamin B6 (Scott et al., 1982). Matte et al. (1998) indicated that based on pyridoxine status and data concerning glycemia and insulinemia stimulated by enteric glucose in pyridoxine-supplemented early-weaned pigs, the optimal daily parenteral pyridoxine was 15 mg. However, in their study, a decrease in riboflavin status was pronounced in the piglets with the highest gastric tube feeding amount and greatest pyridoxine supply. Matte et al.(1998) therefore concluded that the optimal dietary level of pyridoxine that reproduces the effects of the parenteral pyridoxine should be determined, and in addition, effects on riboflavin status should be taken into consideration. Certain feed antagonists, bioavailability of B6 in feeds and nutrients other than protein influence the B6 requirement. Niacin and riboflavin are needed for interconversions of different forms of vitamin B6, with an overdose of thiamin reported to produce vitamin B6 deficiency in rats (Driskell, 1984).



Vitamin B6 is widely distributed in foods and feeds. In general, muscle meats, liver, vegetables, nuts and whole-grain cereals and their by-products are among the best sources; few feedstuffs except fruits are really poor sources. The bioavailability of two common swine feeds is 65 percent for soybean meal and 45 to 56 percent for corn (McDowell and Ward, 2008).

Unfortunately, sow milk is a poor dietary source of vitamin B6 (Benedikt et al. 1996) with approximately 0-4 µg/ml. This is believed to cover less than half the amount required to sustain the piglet growth rate (Coburn, 1994). The reduced quality and increased quantity of protein in the post-weaning feed, as opposed to dam’s milk, would further increase the B6 needs, because of an increased interconversin and oxidation of amino acids. Those metabolic pathways are, in many cases, B6-dependent (Matt et al., 2005).

The vitamin in cereal grains is concentrated mainly in bran; the rest contains only small amounts. Many analytical figures for vitamin B6, especially older ones, were too low because assays that did not measure all of the biologically active forms used (Scott et al., 1982). Matte (1997) indicated that the number of forms and possible inter-conversion among these forms interfere with the determination of B6 content in feed. In biologic samples of several forms, pyridoxine is far more stable than either pyridoxal or pyridoxamine. The level of vitamin B6 in all feeds is affected by processing and subsequent storage. Vitamin B6 loss during cooking, processing, refining and storage has been reported to be as high as 70% (Shideler, 1983) or in the range of 0% to 40% (Birdsall, 1975). Losses may be caused by heat, light and various agents that can promote oxidation. Two-hour sunlight exposure may destroy half of this vitamin’s activity in milk. Irradiation as a potential method for microbial control of poultry feed results in a loss of 15% vitamin B6potency (Leeson and Marcotte, 1993).

Pyridoxine-5’-beta-D-glucoside (PNG), a conjugated form of vitamin B6, has been shown to be abundant in various plant-derived foods (McCormick, 2006). This form of B6 may account for up to 50% of the total vitamin B6 content of oilseeds such as soybeans and sunflower seeds. The utilization of dietary PNG relative to pyridoxine has been shown to be 30% in rats and 50% in humans (Gregory et al., 1991). In suckling rats, the availability of vitamin B6 derived from PNG is only 25% compared with pyridoxine (Trumbo and Gregory, 1989). The glycosylated PNG can quantitatively alter the metabolism of pyridoxine in vivo. Therefore, it partially impairs the metabolic utilization of co-ingested non-glycosylated forms of vitamin B6 (Nakano and Gregory, 1995; Nakano et al., 1997).

Data on vitamin B6 content of feeds are generally insufficient, and information on the vitamin’s bioavailability is lacking. Matte (1997) summarized the methods available for determining pyridoxine concentration, including microbial bioassay, fluorometric measurements without separation by high pressure liquid chromatography (HPLC) and fluorometric detection after HPLC separation, in addition to other direct techniques, such as activation of pyridoxal phosphate-dependent enzymes. Bioavailability of B6 was found to be greater in beef than in cornmeal, spinach or potatoes (Nguyen and Gregory, 1983). LeKlem et al. (1980) reported that in young adult men. The vitamin B6bioavailability in whole wheat bread was lower than in white bread enriched with pure pyridoxine, suggesting a difference in bioavailability between pyridoxine hyrdrochloride and naturally occurring sources of vitamin B6.

Commercially, vitamin B6 is available as crystalline pyridoxine hydrochloride and various dilutions. Pyridoxine hydrochloride contains 82.3% vitamin B6 activity. Dry premixes are used in feeds, and the crystalline product is used in parenteral and oral pharmaceuticals.



Characteristics of vitamin B6 deficiency in most species are retarded growth, dermatitis, epileptic-like convulsions, anemia and partial alopecia (Illus. 9-2). Due to the predominant function of the vitamin in protein metabolism, during a deficiency a fall in nitrogen retention is observed, feed protein is not well utilized, nitrogen excretion is excessive and impaired tryptophan metabolism may result.


Illustration 9-2: Vitamin B6 Deficiency in Growing Swine


Pig on left is vitamin B6 deficient. Pig on right received a vitamin B6-fortified diet.


An indication of a vitamin B6 deficiency is elevated urinary levels of xanthurenic acid and kynurenic acid, indicating incomplete conversion of tryptophan. For status evaluation, Driskell (1984) concluded that the best assessment parameter for vitamin B6status in clinical cases is measurement of either the coenzyme stimulation of erythrocyte alanine aminotransferase activity or PLP level.In growing pigs, clinical signs of vitamin B6 deficiency include a poor appetite, slow growth (Illus. 9-3), microcytic hypochromic anemia, epileptic-like fits or convulsions (Illus. 9-4), fatty infiltration of the liver, diarrhea, rough hair coat, scaly skin, a brown exudate around the eyes, demyelination of peripheral nerves and subcutaneous edema (Bauernfeind, 1974; Braunlich, 1974; Cunha, 1977). Hughes and Squibb (1942) reported many of these deficiency symptoms and also an unsteady gait in pyridoxine-deficient pigs. Almost identical symptoms of B6 deficiency were reported in baby pigs (Lehrer et al., 1951). Follis and Wintrobe (1945) reported specifically on the effects of pyridoxine deficiency on the nervous tissues. Myelin degeneration of the peripheral portion of the sensory nerve was observed to be the initial neural change in pyridoxine-deficient animals. Based on morphologic data, the preliminary site of injury in pyridoxine-deficient animals is in the myelin sheath and axon. Like some other vitamins, vitamin B6 deficiency reduces the immune responses of the pig (Harmon et al., 1963). The first and most conspicuous sign in baby pigs that vitamin B6 is insufficient is a loss of appetite. This may appear in less than two weeks if the deficiency is severe and may be accompanied by reduced growth, vomiting, diarrhea, and a peculiar compulsion to lick.


Illustration 9-3: Vitamin B6 Deficiency


Courtesy of R.W. Luecke and E.R. Miller, Michigan Agricultural Experimentation Stationand J. Nutrition


Illustration 9-4: Vitamin B6 Deficiency


Courtesy of E.H. Hughes and H. Heltman,California Agriculture Experimentation Station


When deficiency of vitamin B6 reaches an advanced stage (probably due to degeneration of the peripheral nerves), disordered movement and ataxia appear. Finally, convulsions develop at irregular intervals but are apparently stimulated by excitement, as they are most often observed at feeding time. Between these convulsions, pigs lie down and are apathetic and unresponsive (Braunlich, 1974). Braunlich (1974) suggested that a vitamin B6 deficiency may go unnoticed in swine because of a lack of visible signs associated specifically with the deficiency. Metabolic disorders may be revealed only by poor appetite, slow growth, and inefficient feed utilization. In some experiments with vitamin B6, protein retention by pigs deficient in the vitamin was reduced to less than half of that shown in animals receiving sufficient amounts of the vitamin. During reproduction and lactation, sows fed a corn-sorghum-soybean meal diet responded to vitamin B6 supplementation of 4.4 mg per kg (2 mg per lb) of feed (Adams et al., 1967). Vitamin B6supplementation of 11 mg per kg (5 mg per lb) of feed produced a slightly superior daily weight gain, more piglets born alive, and a smaller number of resorbed fetuses as compared with control sows that received only 1 mg per kg (0.45 mg per lb) of vitamin B6 (Ritchie et al., 1960). Knights et al. (1998) observed a tendency for reduced weaning-to-estrus intervals and increased nitrogen retention in Yorkshire and Hampshire sows. These researchers also observed an increased litter size in Yorkshire sows following feeding of 16 ppm pyridoxine daily to sows from weaning through the next gestation. In rats, Roth-Maier et al. (1996) concluded that adequate levels of B6 during lactation did not compensate for a lack of B6 during gestation and vice versa, as a high dose of B6 during gestation was unable to alleviate all effects of a suboptimal supply of B6 during lactation. These conclusions were based on data assessing rat liver B6 status.


Fortification Considerations

Vitamin B6 is one of the B vitamins that is least likely to be deficient in swine. Because of its wide distribution in feedstuffs, nutritionists generally expect adequate levels in typical swine diets. Evidence to date indicates that corn, soybean meal and other ingredients used to supply energy and protein in practical swine diets provide the minimum requirement of vitamin B6. However, the bioavailability of vitamin B6in corn and soybean meal ranges from only 45% to 65% (Hoffmann-La Roche, 1979). Vitamin B6 concentration of corn, soybean meal and dried whey, the principal ingredient in most diets of weanling pigs, range from 4 to 6.4 mg per kg (1.8 to 2.9 mg per lb) (NRC, 1998). This compares to a vitamin B6 requirement (NRC, 1998) for 5 to 20 kg (2.3 to 9.1 lb) pigs of 1.5 mg per kg (0.68 mg per 1b) of feed. Woodworth et al. (2000) fed weanling pigs, that were receiving a corn, whey and soybean meal based diet, supplemental vitamin B6 for 35 days. From day 0 to 14 after weaning, pigs fed 3.3 mg per kg (1.5 mg per lb) of added vitamin B6 maximized average daily gain and feed intake. This corresponds to an analyzed total vitamin B6concentration of 7.1 to 7.9 mg per kg (3.2 to 3.6 mg per lb) of diet. The authors suggest that earlier requirement studies may not be applicable today due to advances in genetic selection and production systems that result in fast-growing, lean pigs weaned at an early age. Under certain conditions, vitamin B6 supplementation is warranted for practical growing and breeding diets for swine. 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 age, activity, stress of performance and field use experience (Bauernfeind, 1974). Reasons for needed supplementation of vitamin B6 include the following (Perry, 1978): (1) great variations in amounts of B6 in individual feed ingredients, (2) variable bioavailability of this vitamin in ingredients, (3) losses reported during processing of ingredients, (4) discrepancies between activity for test organisms and those for animals, (5) a higher vitamin B6 requirement due to a marginal level of methionine in the diet and (6) high-protein diets. Matte (1997) indicated that pyridoxine requirements increase with more rapid growth rates. He reported that for weaned piglets, the dietary levels of B6 optimal for growth performance are two to five times greater than the requirements for growing-finishing pigs based on a variety of data (Kosters and Kirchgessner, 1976a; Bretzinger, 1991; NRC, 1998). Matte (1997) also stated that as early-weaning practices increase, optimum B6 levels may be even higher. Based on pyridoxal-5-phosphate measurements in plasma and red blood cells, Matte (1997) indicated that a high post-weaning requirement for B6 in piglets may be related to the reduced quality and increased quantity of protein in feed versus sows’ milk. This in turn would cause more interconversion and oxidation of amino acid reactions, which depend on pyridoxal phosphate. Matte et al. (2005) fed early weaned pigs from 0 to 100 mg per kg (0 to 45.5 mg per lb) of supplemental vitamin B6. There was no growth benefit found from supplemental vitamin B6, however 50 mg per kg (22.7 mg per lb) of vitamin B6saturated red blood cells with thevitamin. 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 grow assay. Vitamin B6 was found to be 38% to 45% available in corn, and 58% to 62% available in soybean meal. It is probably equally available for the pig. There was little difference in availability between corn samples not heated and those heated to 120°C. However, corn heated to 160°C contained significantly less available vitamin B6. The level of vitamin B6 in feedstuffs is also affected by processing and subsequent storage. In one report a loss of 30% of vitamin B6 in alfalfa meal during the coarse-milling and pelleting processes was observed (Braunlich, 1974). Bioavailability can be as low as 40% to 50% after heat processing of feedstuffs. Sewell et al. (1964) investigated the effect of corn oil on vitamin B6 requirements and found no measurable influence of corn oil on the requirement. Roth-Maier and Kirchgessner (1997) examined the effects of wheat bran and alfalfa meal supplements on vitamin B6 metabolism in sows provided with a suboptimal vitamin B6 supply. In comparison with cellulose, bacterially fermentable substrates from wheat bran induced higher bacterial vitamin B6 synthesis. Fecal vitamin B6 excretion was linearly increased with increasing fibrous supplementation.

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 a higher bioavailability and stability than the naturally occurring vitamin. Naturally occurring vitamin B6 in retorted milk products exhibited only 50% of the bioavailability of synthesized vitamin B6 or vitamin B6 in formulas that were fortified with the vitamin prior to thermal processing (Tomarelli et al., 1955).

The recovery of vitamin B6, as pyridoxine hydrochloride, in a multivitamin premix not containing trace minerals was 100%, even after three months of storage at 37°C. However, stability in a premix containing trace minerals was poor, with only 45% recovery after three months at 37°C (Adams, 1982). Verbeeck (1975) found vitamin B6 to be stable in premixes with minerals as sulfates. However, if minerals in the form of carbonates and oxides are used, 25% of the vitamin can be lost over a three-month period. Stress agents such as choline chloride help catalyze this destruction. Gadient (1986) considers pyridoxine to be very sensitive to heat, slightly sensitive to moisture and light, and insensitive to oxygen. Retention of B6 activity in pelleted feeds after three months at room temperature should be 80% to 100% as a general rule.


Vitamin Safety

Insufficient data are available to support estimates of the maximum tolerable dietary levels of vitamin B6 for swine. 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, 1998). Vitamin B6 toxicity causes ataxia, muscle weakness and uncoordination at levels approaching 1000 times the requirement (Leeson and Summers; 2001).