Vitamin B6 Activity Research Articles

A Randomized Pilot Trial to Evaluate the Bioavailability of Natural versus Synthetic Vitamin B Complexes in Healthy Humans and Their Effects on Homocysteine, Oxidative Stress, and Antioxidant Levels

The vitamin B complex comprises 8 different water-soluble constituents that humans must sequester from the diet. This pilot study compared natural versus synthetic vitamin B complexes for their bioavailability, accumulation, and their impact on antioxidants, homocysteine levels, and oxidative stress. We conducted a double-blind randomized clinical trial with thirty healthy participants. They were randomly assigned to group N (natural) and group S (synthetic). Vitamin B was ingested daily for 6 weeks in the range of about 2.5 times above the recommended daily allowance. Blood samples were taken at baseline, 1.5 h, 4 h, 7 h (diurnal), 6 w (discontinuation of supplements), and 8 w (washout). Blood levels of thiamine (B1), riboflavin (B2), pyridoxine (B6), folic acid (B9), cobalamin (B12), homocysteine, total antioxidants, peroxidase activity, polyphenols, and total peroxides were determined. Compared to initial values, serum levels of each B vitamin increased at the end of the supplementation period: i.e., B1 (+23% N; +27% S), B2 (+14% N; +13% S), B6 (+101% N; +101% S), B9 (+86% N; +153% S), and B12 (+16% N) (p < 0.05). Homocysteine (-13% N) decreased, while peroxidase activity (+41% S) and antioxidant capacity increased (+26% N). Short-term effects were already observed after 1.5 h for B9 (+238% N; +246% S) and after 4 h for vitamin B2 (+7% N; +8% S), B6 (+59% N; +51% S), and peroxidase activity (+58% N; +58% S). During the washout period, serum levels of B vitamins decreased except for thiamine and peroxidase activity, which increased further. This clinical pilot study revealed comparable bioavailability for both natural and synthetic B vitamins but did not show statistically noticeable differences between groups despite some favourable tendencies within the natural vitamin group, i.e., sustained effects for cobalamin and endogenous peroxidase activity and a decrease in homocysteine and oxidative stress levels.

Vitamins, phenolics and antioxidant activity of culinary prepared Suillus luteus (L.) Roussel mushroom

Unblanched and blanched Suillus luteus (L.) Roussel mushrooms were braised to consumption consistency with rape seed oil (100 g/kg) and NaCl (5 g/kg) and 2 types of culinary product were obtained. Evaluation was carried out on fresh mushrooms, as well as mushroom products as follows: unstored; stored at 20 °C for 48 h; and stored at 4 °C for 48 and 96 h. Braising led to increases in dry matter, basic nutritional components and tocopherols, and decreases in: total polyphenols (46–61%), total flavonoids (71–81%), vitamin C (71–81%), thiamine (71–81%), riboflavin (78%), vitamin B3 (0–13%), vitamin B6 (13–70%) and antioxidant activity using ABTS, DPPH and FRAP assays (70–77%). Storage led to further losses of vitamin C and B-group vitamins. Products stored for 48 h at room temperature showed high total viable counts as well as the presence of yeasts, lactic acid bacteria and Bacillus strains; however, cold-stored products showed no microbiological contamination.

The effect of vitamin B6 on cognition.

Micronutrient status can affect cognitive function at all ages. Vitamin deficiencies could influence memory function and might contribute to age-associated cognitive impairment and dementia. Vitamin B6, comprising three chemically distinct compounds pyridoxal, pyridoxamine, and pyridoxine, is involved in the regulation of mental function and mood. Vitamin B6 is also an essential homocysteine re-methylation cofactor, and deficiency is associated with increase in blood homocysteine levels. Homocysteine is a risk factor for cerebrovascular disease and may also have directly toxic effects on neurons of the central nervous system. Neuropsychiatric disorders including seizures, migraine, chronic pain and depression have been linked to vitamin B6 deficiency. Epidemiological studies indicate that poor vitamin B6 status is common among older people. Hyperhomocysteinaemia has been suggested as a cause or mechanism in the development Alzheimer's disease and other forms of dementia. Supplementation with B vitamins including vitamin B6 has been shown to reduce blood homocysteine levels. To assess the efficacy of vitamin B6 supplementation in reducing the risk of developing cognitive impairment by older healthy people, or improving cognitive functioning of people with cognitive decline and dementia, whether or not vitamin B6 deficiency has been diagnosed. The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group was searched on 20 May 2003 using the terms: vitamin B6, pyridoxine, pyridoxamine, pyridoxal. For relevant trials on healthy elderly people MEDLINE, EMBASE and CENTRAL were searched using the previously mentioned terms as well as the term cognit * All unconfounded, double-blind randomized controlled trials in which the intervention with vitamin B6 was compared with placebo for healthy older people or people with cognitive decline or dementia. The primary outcome of interest was the efficacy of vitamin B6 supplementation on cognitive function. The two reviewers independently evaluated all studies identified as possibly meeting the criteria for inclusion. One reviewer independently extracted the data. Studies were rated for their overall quality. The weighted mean differences between treatment and placebo groups, with 95% confidence intervals, were calculated for each outcome. Review Manager version 4.2 was used to analyse the variance. No trials of vitamin B6 involving people with cognitive impairment or dementia were found. The two trials included in the review (Bryan 2002; Deijen 1992) used a double-blind, randomized, placebo-controlled design and involved 109 healthy older people. One trial restricted enrolment to women and the other to men. Vitamin B6 supplementation and healthy older women: Bryan 2002 enrolled 211 healthy women from various age groups into a 5-week study. The trial was of multifactorial design with folic acid, vitamin B12, vitamin B6 and placebo in its four arms. Twelve healthy women aged 65 to 92 years received 75 mg vitamin B6 orally per day and were compared with 21 healthy women who were allocated to placebo. No statistically significant benefits from vitamin B6 on mood or cognition were observed. Vitamin B6 supplementation and healthy older men: Deijen 1992 recruited 76 healthy men aged 70 to 79 years. They were divided into 38 matched pairs, one member of each pair randomly allocated to 20 mg of vitamin B6 (pyridoxine hydrochloride) per day for 12 weeks the other to placebo. No statistically significant differences between treatment and placebo were found in their effects on cognition or mood. Effect of vitamin B6 supplementation on vitamin B6 status: Deijen 1992 reported that 20 mg of pyridoxine hydrochloride per day for 12 weeks increased blood vitamin B6 activity as assessed as by plasma pyridoxal-5'-phosphate (WMD 238, 95%CI 211.58 to 264.42, P<0.00001) and erythrocyte enzyme asparate aminotransferase (WMD 0.43, 95%CI 0.30 to 0.56, P<0.00001). Effect of vitamin B6 supplementation on blood homocysteine concentration: Neither of the included trials measured homocysteine levels. Drop-outs: All participants allocated to vitamin B6 or placebo completed the trial protocol. Adverse Events: No adverse effects were reported. Effect of vitamin B6 on carer burden, care costs and institutionalization rate: We found no trials in which these outcomes were assessed. This review found no evidence for short-term benefit from vitamin B6 in improving mood (depression, fatigue and tension symptoms) or cognitive functions. For the older people included in one of the two trials included in the review, oral vitamin B6 supplements improved biochemical indices of vitamin B6 status, but potential effects on blood homocysteine levels were not assessed in either study. This review found evidence that there is scope for increasing some biochemical indices of vitamin B6 status among older people. More randomized controlled trials are needed to explore possible benefits from vitamin B6 supplementation for healthy older people and those with cognitively impairment or dementia.

Regulation of calcium influx into vascular smooth muscle by vitamin B6.

In the vitamin B6 deficiency-induced hypertensive (B6DHT) rat there is an increased influx of calcium into the vascular smooth muscle. Vitamers which possess vitamin B6 activity blocked the in vitro calcium influx into the caudal artery of B6DHT rats and the BAY K 8644-induced influx into artery segments from vitamin B6-supplemented (control) rats. BAY K 8644 did not increase further the calcium influx into caudal artery segments from B6DHT rats. However, when this influx was partly decreased by Nifedipine or by pyridoxal phosphate, BAY K 8644 antagonized their effects indicating that calcium influx mediated by the dihydropyridine-sensitive calcium channel is a site of the calcium influx defect in the B6DHT rat.

Functionalized Bilayer Membranes as Artificial Tryptophan Synthase. Characterization of Catalytic Efficiency, Substrate Specificity, and Reaction Selectivity

Abstract Functionalized bilayer membranes having vitamin B6 activity effectively catalyzed β-replacement reactions of serine with indoles to afford the corresponding tryptophan derivatives in aqueous media under mild conditions. Catalytic capability of the present artificial enzyme was subjected to change by changing a combination of molecular components constituting the catalyst system. The structural mode of a hydrophobic pyridoxal derivative as the coenzyme model, the catalytic ability of an amino acid residue placed in a peptide lipid which forms single-walled bilayer vesicles as the apoenzyme model, and the coordination property of added metal ions were found to be responsible for the overall catalytic performance. Multifunctional assistance was observed in the β-replacement reaction of serine with indole, and the reaction proceeded in preference to other side reactions, such as β-elimination, dealdolation, and transamination reactions. Substrate selectivity was found to be primarily dependent on the nucleophilicity of indole derivatives.

Lack of Vitamin B6 Activity of 6‐Hydroxypyridoxine

ABSTRACTHydroxylation of the C‐6 position of pyridoxine has been described recently as a mechanism for the degradation of vitamin B6 in foods. The nutritional properties of the resulting 6‐hydroxypyridoxine in mammals have not been previously evaluated. 6‐Hydroxypyridoxine was synthesized and its structure confirmed by UV and NMR spectroscopy. A rat bioassay with multiple dose levels was conducted to compare the vitamin B6 activity of pyridoxine and 6‐hydroxypyridoxine with respect to a variety of indices of vitamin B6 metabolism. By all criteria employed, 6‐hydroxypyridoxine exhibited neither vitamin B6 nor antivitamin B6 activity and, thus, is nutritionally inert.

Functionalised bilayer membranes having vitamin B6 activity as artificial tryptophan synthase

Synthetic bilayer vesicles having vitamin B6 activity markedly enhanced the β-replacement reaction of serine with indole to afford tryptophan, showing turnover behaviour, in aqueous media under mild conditions.

Vitamin B 6 activity as determined by erythrocyte AST measurement on the RA-1000

Vitamin B 6 activity as determined by erythrocyte AST measurement on the RA-1000

Conversion of pyridoxine into 6-hydroxypyridoxine by food components, especially ascorbic acid.

In experiments designed to examine interactions between pyridoxine (PN) and food components, PN was found to be converted into an unidentified compound in the presence of the homogenates of various plant foods under mild conditions. The formation of the compound tended to be higher when food samples had a higher ascorbic acid (AsA) content. The reaction was neither thermal decomposition nor photodecomposition. This compound was also formed by incubating PN with AsA in the dark. Conversion of PN into the compound proceeded with oxidation of AsA, and was negligible under anaerobic conditions. The pH optimum for the reaction was between 4 and 7, and the temperature optimum was between 30 and 50 degrees C. The compound was purified by ion-exchange chromatography, isolated as colorless needles, and identified as 6-hydroxypyridoxine from UV, PMR, IR and MS spectral data. 6-Hydroxypyridoxine had neither vitamin B6 nor antivitamin B6 activity for Saccharomyces carlsbergensis 4228 (ATCC 9080). From these results, we inferred that hydroxylation of PN in the presence of food components, especially AsA, caused loss of vitamin B6 in plant foods during food processing, storage and cooking.

Effects of thiamin on vitamin B6 synthesis in yeasts.

The effects of exogenous thiamin on the growth yield and vitamin B6 content of 18 strains of yeasts and a few strains of bacteria were examined. The addition of thiamin hardly affected the growth yield of the yeasts tested, except for two strains Saccharomyces uvarum strain 4228 and Saccharomyces uvarum IFO 0751. In contrast, the vitamin B6 content of all the yeasts tested, except Pichia membranaefaciens IFO 0189, decreased markedly in the presence of thiamin. In S. uvarum IFO 1265, the synthesis of vitamin B6 was maximally inhibited by the addition of thiamin (1.5 nmol ml-1) to the growth medium without affecting cell growth, whereas the amounts of cellular vitamin B6 increased in the presence of the thiamin antagonist, pyrithiamin or oxythiamin, at concentrations that did not affect growth. When [4'-14C]pyridoxine. HCl (0.5 micrograms ml-1) was added to the growth medium at least 54% of the added isotope was incorporated into the cells during 24 h incubation. In the presence of thiamin (15 nmol ml-1), at least 32% of the added isotope was incorporated. The metabolism of [4'-14C]pyridoxine. HCl to inactive forms having no vitamin B6 activity was not stimulated by the addition of thiamin. Thus, vitamin B6 synthesis in many yeasts was affected by thiamin, whereas, in bacteria, growth yield and vitamin B6 content were not affected by thiamin.

Thermal Degradation Kinetics of Pyridoxine Hydrochloride in Dehydrated Model Food Systems

ABSTRACTThe thermal degradation kinetics of pyridoxine hydrochloride were examined using a dehydrated model food system designed to simulate a ready‐to‐eat breakfast cereal. This study was carried out to provide information useful in estimating the thermal losses of pyridoxine hydrochloride in the processing of breakfast cereals and other low moisture dehydrated food systems. Portions of the model system which were fortified with pyridoxine hydrochloride were toasted in a conduction oven at 155°, 170°, 185°, and 200°C for a minimum of six heating times at each temperature. Pyridoxine (PN) content was determined in the heat treated model systems by high performance liquid chromatography (HPLC). For each heat treatment, the loss of pyridoxine could be described by a first order kinetics model. The first order rate constants for 155°, 170°, 185°, and 200°C were 1.74 × 10−2 min−1, 5.22 × 10−2 min−1, 16.88 × 10−2 min−1, and 48.95 × 10−2 min−1, respectively. The calculated Arrhenius activation energy was 29.8 Kcal/mol. In comparing the HPLC method to the standard microbiological assay, the HPLC assay gave lower PN values for the toasted model system. To explain this discrepancy, HPLC fractions were collected and analyzed by the microbiological assay. No significant vitamin B6 activity was found in any fraction other than that containing the PN peak. It is possible that the milder extraction procedure used in the HPLC assay is less capable of recovering forms of PN which may become bound during the toasting process. These potentially bound forms may or may not be biologically available.

Stability, bactericidal activity, vitamin B6 activity and gastrointestinal absorption of benzoic acid esters of pyridoxine.

alpha 4-O-Benzoyl-pyridoxine (PN-4'MB) and alpha 5-O-benzoyl-pyridoxine (PN-5'MB) were hydrolyzed in 10% aqueous solution of acetone at pH 1-4. They were hydrolyzed obeying apparent first-order kinetics. In the pH range of 1-7, PN-4'MB was hydrolyzed 10 times faster than PN-5'-MB. At pH 7-12, an interconversion between the two derivatives was observed. They were bactericidal against Escherichia coli and Bacillus subtilis and prevented severe convulsions induced in mouse by 4'-methoxypyridoxine, a potent antagonist of vitamin B6. PN-4'MB was hydrolyzed with the homogenate of rat liver more easily than PN-5'MB. The metabolite of PN-MBs in man was identified as 4'-pyridoxic acid, i.e., a principal metabolite of PN, using high-performance liquid chromatography. The amount of urinary excretion of 4'-pyridoxic acid in 10 hr after oral administration of PN-4'MB or PN-5'MB was as large as that of PN.

Vitamin B6 metabolism in idiopathic sideroblastic anaemia and related disorders.

Patients with idiopathic anaemias associated with abnormal sideroblasts were defined according to morphologic and ferrokinetic criteria and the haematologic and biochemical effects of vitamin B6 therapy were evaluated. While all patients presented similar clinical pictures, peripheral blood changes and bone marrow abnormalities, two distinct groups were identified by sideroblast morphology and ferrokinetics. Patients with more than 5% true ring sideroblasts in the marrow (IRSA) uniformly had marked ineffective erythropoiesis, while those with abnormal sideroblasts but few true ring forms were hypoproliferative. Measurements of red cell pyridoxine kinase (PnK) and intracellular pyridoxal 5-phosphate availability (PLP) as assessed by the activity of the PLP-dependent enzyme asparate aminotransferase (EGOT), revealed slightly decreased PnK levels in IRSA subjects but normal intracellular PLP activities in both groups. Furthermore, when treated with pyridoxine, all patients showed increases in both red cell PnK and EGOT activities which were similar to those seen in normal subjects. Treatment with PLP also effectively increased erythrocyte vitamin B6 activity. Even so, neither pyridoxine nor intramuscular PLP improved erythropoiesis as determined by serial haematocrits, reticulocyte counts and erythron iron turnover measurements.However, since both therapies increased red cell protoporphyrin levels and the excretion of urinary coproporphyrin in a number of subjects, the possibility that impaired haem synthesis in the sideroblastic anaemias is associated with abnormal vitamin B6 metabolism at the level of the mitochondrion must still be considered.

Inhibition of the interaction between the complement component Clq and immune complexes.

Several groups of compounds were examined for their ability to inhibit in vitro the binding of Clq to insoluble immune complexes. As expected from previous studies, polyinosinic acid, liquoid, sodium pentosan polysulfate, aliphatic diamines and heparin are good inhibitors. This study shows that compounds with much lower toxicity, such as certain amino acids and substances with vitamin B6 activity (pyridoxal-5-phosphate:P5P) were also capable of decreasing the binding of Clq. Using methods of equilibrium dialysis and difference spectra, it was shown that this compound binds to both, Clq und IgG antibody by forming Schiff bases. Clq binds approximately 10 times more P5P when compared to IgG. Immune complexes prepared with IgG antibody modified by P5P and stabilized with sodium borohydride had the same complement-fixing and Clq-binding capacity as normal immune complexes. This suggests that the inhibition of Clq-binding to immune complexes by P5P is due to a modification of lysyl resides in Clq. Collagen and IgG fragments derived from Fc were also found to inhibit Clq binding to immune complexes, but at higher concentrations than the above small-molecular compounds and with a different mode of action.

Effects of penicillamine on distribution of B6 vitamens in rat urine.

The antivitamin B6 effect of DL- and D-penicillamine has been studied in rats. A considerable elevation in the urinary excretion of vitamin B6 activity (pyridoxal and its thiazolidine derivative) has been shown as a parameter of B6 antagonism. Both DL- and D-pencillamine have been shown to have an antivitamin B6 effect in rats, although that induced by the DL-form is considerably greater, as would be expected from previous studies. We suggest that B6 supplementation should be included in any long term penicillamine therapy, regardless of the isomer that is employed.

Zum Vitamin B6-Zerfall bei der Lagerung von Lebensmitteln

In a study of the effect of storage on the vitamin B6 activity of foods, the vitamin B6 content of different foods of plant and animal origin and also of a mixed feed with added pyridoxine were analyzed microbiologically using Saccharomyces carlsbergensis as test organism. Vitamin B6 activity was determined initially, in some of the specimens after storage for 10 months and again in all foods after 40 months. The storage period of 10 months caused a loss of the natural vitamin B6 content of about 25--30%. This loss increased to more than 50% after 40 months storage. The diet containing the high level of synthetic pyridoxine lost 85% of its vitamin B6 content.

Relationships between Vitamin B6-vitamer Content and the Activities of Two Transaminase Enzymes in Rat Tissues at Varying Intake Levels of Vitamin B6

To study relationships between the vitamin B6-vitamer content of rat tissues to the activities of 2 transaminase enzymes in those tissues, and the relative biological activity of 3 vitamin B6-vitamers in the rat, we arranged to study, in depth 7 groups of rats that were fed diets containing (µg/g diet) 0, 0.5, 1.0, 2.0, and 10.0 of pyridoxol·HCl and 1.0 of pyridoxal·HCl or pyridoxamine·2HCl. Although a dietary level of 2.0 µg/g diet of pyridoxol was adequate to support maximal growth, higher tissue levels of total vitamin B6 and of the individual vitamers were reached at the 10.0 µg/g diet level, in liver, kidney, brain, muscle, and heart. Of the 3 vitamin B6 vitamers, pyridoxamine was depleted to the greatest extent, as percentage, at lower levels of dietary pyridoxol. In studies on glutamic-pyruvic (GPT) and glutamic-oxalacetic transaminase (GOT) activities in the above tissues plus plasma and red blood cells, enzyme activity increased with increased dietary pyridoxol and with increased tissue vitamin B6 content. GPT was depleted to a greater extent than, and GOT to a lesser extent than, the percentage depletion for tissue vitamin B6 at lower levels of pyridoxol intake. It appeared from studies on growth, tissue content of vitamin B6 and vitamers, and tissue transaminase activity, that at the level of 1.0 µg/g diet, pyridoxal was essentially equivalent to pyridoxol for vitamin B6 activity; the study on pyridoxamine required re-evaluation. A simplified medium was used for the microbiological portion of the assay of the vitamin B6 vitamers.

Nutritive properties of freshly prepared and stored evaporated milks manufactured by a normal commercial procedure or by reduced thermal processes in the presence of nisin

SummaryFrom a batch of raw milk, evaporated milk was prepared commercially by 3 procedures:A, a normal commercial procedure involving holding the filled cans at a maximum temperature of 113 °C for 15 min;B, with nisin added and holding at a maximum temperature of 105 °C for 15 min;C, with nisin added and holding at a maximum temperature of 113 °C for 3 min. The content ofBvitamins in the raw and evaporated milks was measured microbiologically; the nutritive value of the proteins was determined in rat tests.In milkA, 83% of the vitamin B12, 38% of the vitamin B6and 20% of the thiamine were destroyed during processing. In milkB, the losses were 67, 30 and 19%, respectively, only the loss of vitamin B12being significantly lower than in milkA. In milkC, the losses were 67, 23 and 14%, respectively, each of them being significantly lower than in milkA. There was no further loss of thiamine on storage of the milks for 12 months at 4 °C, but at room temperature and at 37 °C further losses occurred in all the milks. Similarly, the vitamin B6activity of the milks decreased on storage, the loss being greatest at 37 °C, but also detectable at 4 °C. No change in the vitamin B12content occurred on storage, and no losses of biotin, nicotinic acid, pantothenic acid or riboflavin were detected during manufacture or storage of the evaporated milks.The biological value and true digestibility of the proteins of the evaporated milks were slightly lower than for the raw milk. Neither nisin treatment nor storage at room temperature for a year affected these characteristics.

The occurrence of pyridoxamine phosphate in milk

SummaryThe presence of pyridoxamine phosphate in extracts of freeze-dried raw and evaporated milks has been demonstrated by separation and identification of the vitamin B6active compounds by chromatography and electrophoresis on paper. Its presence in the milk extracts is the cause of the higher values for vitamin B6activity measured withStreptococcus faecalisas compared with those obtained withStr. faeciumorSaccharomyces carlsbergensis. This is becauseStr. faecaliscan utilize the phosphate for growth as readily as free pyridoxamine, whereasStr. faeciumandS. carlsbergensiscannot. The mild acid treatment used for extracting the vitamin B6active compounds from the milk samples for microbiological assay was found to be insufficient to hydrolyse the pyridoxamine phosphate. Further treatment of the acid extracts with intestinal phosphatase released the pyridoxamine from its phosphate and increased the vitamin B6activity measured withS. carlsbergensisandStr.faeciumso that the total vitamin B6activities of the freeze-dried raw and evaporated milks measured microbiologiclly, were then in agreement with the values found in previous tests with chicks and rats.Pyridoxamine phosphate could only be detected in small amounts in a sample of fresh milk. The possibility that more of it was formed during the processing and storage of the freeze-dried samples is discussed.

Comparative Vitamin B6 Activity of Frozen, Irradiated and Heat-Processed Foods

Comparative Vitamin B6 Activity of Frozen, Irradiated and Heat-Processed Foods