Vitamin B6 deficiency decreases the glucose utilization in cognitive brain structures of rats

The effects of vitamin B(6) deficiency on metabolic activities of brain structures were studied. Male Sprague-Dawley weanling rats received one of the following diets: (1) 7 mg pyridoxine HCl/kg (control group); (2) 0 mg pyridoxine HCl/kg (vitamin B(6)-deficient group); or (3) 7 mg pyridoxine HCl/kg with food intake restricted in quantity to that consumed by the deficient group (pair-fed control group). After 8 weeks of dietary treatment, rats in all three groups received an intravenous injection of 2-deoxy-[(14)C] glucose (100 microCi/kg). Vitamin B(6) status was evaluated by plasma pyridoxal 5'-phosphate concentrations. The vitamin B(6)-deficient group had significantly lower levels of plasma pyridoxal 5'-phosphate than did the control and pair-fed groups. The local cerebral glucose utilization rates in structures of the limbic system, basal ganglia, sensory motor system, and hypothalamic system were determined. The local cerebral glucose utilization rates in each of the four brain regions in the deficient animals were approximately 50% lower (P < 0.05) than in the control group. Results of the present study suggest that serious cognitive deficit may occur in vitamin B(6)-deficient animals.     

Dietary vitamin B6 intake modulates colonic inflammation in the IL10−/− model of inflammatory bowel disease

Pyridoxal-5-phosphate, the biologically active form of vitamin B₆, is a cofactor for over 140 biochemical reactions. Although severe vitamin B₆ deficiency is rare, mild inadequacy [plasma pyridoxal 5’-phosphate (PLP) <20 nmol/L] is observed in 19–27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B₆ intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10^?/? (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNFα, IL-6, IFN-γ, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation.     

Folate and homocysteine metabolism in copper-deficient rats.

To investigate the effect of copper deficiency on folate and homocysteine metabolism, we measured plasma, red-cell and hepatic folate, plasma homocysteine and vitamin B-12 concentrations, and hepatic methionine synthase activities in rats. Two groups of male Sprague-Dawley rats were fed semi-purified diets containing either 0. 1 mg (copper-deficient group) or 9.2 mg (control group) of copper per kg. After 6 weeks of dietary treatment, copper deficiency was established as evidenced by markedly decreased plasma and hepatic copper concentrations in rats fed the low-copper diet. Plasma, red-cell, hepatic folate, and plasma vitamin B-12 concentrations were similar in both groups, whereas plasma homocysteine concentrations in the copper-deficient group were significantly higher than in the control group (P<0.05). Copper deficiency resulted in a 21% reduction in hepatic methionine synthase activity as compared to the control group (P<0.01). This change most likely caused the increased hepatic 5-methyltetrahydrofolate and plasma homocysteine concentrations in the copper-deficient group. Our results indicate that hepatic methionine synthase may be a cuproenzyme, and plasma homocysteine concentrations are influenced by copper nutriture in rats. These data support the concept that copper deficiency can be a risk factor for cardiovascular disease.     

Effect of vitamin B6 availability on serine hydroxymethyltransferase in MCF-7 cells

Folate-activated one-carbon units are derived from serine through the activity of the pyridoxal-phosphate (PLP)-dependent isozymes of serine hydroxymethyltransferase (SHMT). The effect of vitamin B(6) availability on the activity and expression of the human mitochondrial and cytoplasmic SHMT isozymes was investigated in human MCF-7 cells. Cells were cultured for 6 months in vitamin B(6) replete (4.9 microM pyridoxine) minimal essential medium (alphaMEM) or vitamin B(6)-deficient medium containing 49, 4.9 or 0.49 nM pyridoxine. Total cellular PLP levels and SHMT activity were reduced 72% and 7%, respectively, when medium pyridoxine was decreased from 4.9 microM to 49 nM. Cells cultured in medium containing 4.9 nM pyridoxine exhibited 75%, 27% and 60% reduced levels of PLP, SHMT activity and S-adenosylmethionine, respectively, compared to cells cultured in alphaMEM. Cytoplasmic SHMT activity and protein levels, but not mRNA levels, were decreased in cells cultured in vitamin B(6) deficient medium, whereas mitochondrial SHMT activity and protein levels were less sensitive to vitamin B(6) availability. PLP bound to cytoplasmic SHMT with a K(d)=850 nM, a value two orders of magnitude lower than previously reported for the bovine cytoplasmic SHMT isozyme. Collectively, these data indicate that vitamin B(6) restriction decreases the activity and stability of SHMT, and that the cytoplasmic isozyme is more sensitive to vitamin B(6) deficiency than the mitochondrial isozyme in MCF-7 cells.     

Antitumor effect of vitamin B6 and its mechanisms

Epidemiological studies have reported an inverse association between vitamin B(6) intake and colon cancer risk. Our recent study has been conducted to examine the effect of dietary vitamin B(6) on colon tumorigenesis in mice. Mice were fed diets containing 1, 7, 14 or 36 mg/kg pyridoxine for 22 weeks, and given a weekly injection of azoxymethane (AOM) for the initial 10 weeks. Compared with the 1 mg/kg pyridoxine diet, 7, 14 and 35 mg/kg pyridoxine diets significantly suppressed the incidence and number of colon tumors, colon cell proliferation and expressions of c-myc and c-fos proteins. Supplemental vitamin B(6) lowered the levels of colonic 8-hydroxyguanosine (8-OHdG), 4-hydroxy-2-nonenal (4-HNE, oxidative stress markers) and inducible nitric oxide (NO) synthase protein. In an ex vivo serum-free matrix culture model using rat aortic ring, supplemental pyridoxine and pyridoxal 5'-phosphate (PLP) had antiangiogenic effect. The results suggest that dietary vitamin B(6) suppresses colon tumorigenesis by reducing cell proliferation, oxidative stress, NO production and angiogenesis.     

Response of blood serum constituents to production of and recovery from a kwashiorkor-like syndrome in the young pig.

Twenty-six 3-week-old genetically obese pigs were fed in two experiments to determine the serum chemistry profile during severe protein malnutrition and repletion. Severe protein deficiency was produced in pigs fed the high-fat, low-protein diet (growth failure, rough hair, low serum total protein and albumin). In Experiment 1, blood was sampled from the anterior vena cava of each pig five times during depletion and three times during repletion to determine serum total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides, total protein, albumin, glucose, Ca, inorganic P, Mg, Na, K, Cl, total bilirubin, urea N, creatinine, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase. In Experiment 2, blood was sampled weekly for 8 weeks for serum total cholesterol, HDL-cholesterol, triglycerides, albumin, glucose, Ca, P, Mg and alkaline phosphatase. HDL-cholesterol was increased (P less than 0.01) and albumin was decreased (P less than 0.01) in protein-deficient pigs in both experiments. Creatinine, total bilirubin, gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase were elevated in protein-deficient pigs compared with controls after 7 weeks of depletion. Inorganic P (P less than 0.01), Ca (P less than 0.01), and Mg (P less than 0.05) concentrations were depressed in protein-depleted pigs compared with controls in both experiments. After 8 weeks of repletion in Experiment 1, all elements except inorganic P were similar in the two groups. Short-term, severe, protein malnutrition affected lipid, electrolyte, and structural mineral metabolism and indices of liver function in the absence of parasites, diarrhea, and infection. The effects were reversed after 8 weeks of repletion. We conclude that the elevated serum cholesterol in protein deficiency is related primarily to an increase in the HDL fraction.     

Separation and quantification of the B6 vitamers in plasma and 4-pyridoxic acid in urine of adolescent girls by reversed-phase high-performance liquid chromatography

The vitamin B₆ status of seemingly healthy adolescent girls was determined using several accepted and proposed parameters in an effort to establish guidelines for status evaluation. High-performance liquid chromatography-derived plasma B₆ vitamers (pyridoxal phosphate, PLP; pyridoxine phosphate, PNP; pyridoxamine phosphate, PMP; pyridoxal, PL; pyridoxine, PN; and pyridoxamine, PM) and 4-pyridoxic acid (4-PA) concentrations and urinary 4-PA levels of 28 white adolescent females, 12–15 years, having radiomonitored plasma PLP concentrations and coenzyme stimulation of erythrocyte alanine aminotransferase activities indicative of adequate status were determined. Mean vitamin B₆ and protein intakes were 1.48 mg and 78.3 g. Ranges for plasma B₆ vitamer and 4-PA concentrations (nmol/1) were: PLP, 40.9–122.2; PNP, non-detectable (ND)—16.1; PMP, ND—8.1; PL, ND—15; PN, ND—21.9; PM, ND—17.8; and 4-PA, ND—55.7. PLP was the only vitamer found in plasma of all subjects. Urinary 4-PA concentrations ranged from 0.11 to 2.50 μmol/mmol of creatinine. B₆ vitamer values of these girls should be of use in the establishment of normal ranges for vitamin B₆ status parameters.     

Vitamin B6 metabolism in microbes and approaches for fermentative production

Vitamin B6 is a designation for the six vitamers pyridoxal, pyridoxine, pyridoxamine, pyridoxal 5′-phosphate (PLP), pyridoxine 5′-phosphate, and pyridoxamine. PLP, being the most important B6 vitamer, serves as a cofactor for many proteins and enzymes. In contrast to other organisms, animals and humans have to ingest vitamin B6 with their food. Several disorders are associated with vitamin B6 deficiency. Moreover, pharmaceuticals interfere with metabolism of the cofactor, which also results in vitamin B6 deficiency. Therefore, vitamin B6 is a valuable compound for the pharmaceutical and the food industry. Although vitamin B6 is currently chemically synthesized, there is considerable interest on the industrial side to shift from chemical processes to sustainable fermentation technologies. Here, we review recent findings regarding biosynthesis and homeostasis of vitamin B6 and describe the approaches that have been made in the past to develop microbial production processes. Moreover, we will describe novel routes for vitamin B6 biosynthesis and discuss their potential for engineering bacteria that overproduce the commercially valuable substance. We also highlight bottlenecks of the vitamin B6 biosynthetic pathways and propose strategies to circumvent these limitations.     

Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis

Patients with rheumatoid arthritis have subnormal vitamin B6 status, both quantitatively and functionally. Abnormal vitamin B6 status in rheumatoid arthritis has been associated with spontaneous tumor necrosis factor (TNF)-α production and markers of inflammation, including C-reactive protein and erythrocyte sedimentation rate. Impaired vitamin B6 status could be a result of inflammation, and these patients may have higher demand for vitamin B6. The aim of this study was to determine if daily supplementation with 50 mg of pyridoxine for 30 days can correct the static and/or the functional abnormalities of vitamin B6 status seen in patients with rheumatoid arthritis, and further investigate if pyridoxine supplementation has any effects on the pro-inflammatory cytokine TNF-α or IL-6 production of arthritis. This was a double-blinded, placebo-controlled study involving patients with rheumatoid arthritis with plasma pyridoxal 5'-phosphate below the 25th percentile of the Framingham Heart Cohort Study. Vitamin B6 status was assessed via plasma and erythrocyte pyridoxal 5'-phosphate concentrations, the erythrocyte aspartate aminotransferase activity coefficient (αEAST), net homocysteine increase in response to a methionine load test (ΔtHcy), and 24 h urinary xanthurenic acid (XA) excretion in response to a tryptophan load test. Urinary 4-pyridoxic acid (4-PA) was measured to examine the impact of pyridoxine treatment on vitamin B6 excretion in these patients. Pro-inflammatory cytokine (TNF-α and IL-6) production, C-reactive protein levels and the erythrocyte sedimentation rate before and after supplementation were also examined. Pyridoxine supplementation significantly improved plasma and erythrocyte pyridoxal 5'-phosphate concentrations, erythrocyte αEAST, urinary 4-PA, and XA excretion. These improvements were apparent regardless of baseline B6 levels. Pyridoxine supplementation also showed a trend (p < 0.09) towards a reduction in post-methionine load ΔtHcy. Supplementation did not affect pro-inflammatory cytokine production. Although pyridoxine supplementation did not suppress pro-inflammatory cytokine production in patients with rheumatoid arthritis, the suboptimal vitamin B6 status seen in rheumatoid arthritis can be corrected by 50 mg pyridoxine supplementation for 30 days. Data from the present study suggest that patients with rheumatoid arthritis may have higher requirements for vitamin B6 than those in a normal healthy population.     

家蚕体内维生素B6的存在形态和转换代谢

采用不含桑叶粉末、以去维生素牛乳酪蛋白为蛋白源的准合成饲料饲育家蚕Bombyx mori幼虫,探讨了家蚕体内维生素B（VB₆）化合物的存在形态和转换代谢途经。随饲料中盐酸吡哆醇（PN-HCl）添加量的增加,幼虫体内吡哆醇(PN)含量相应变化,其次是吡哆醛(PL);而辅酶型磷酸吡哆醛(PLP)和磷酸吡哆胺(PMP)含量存在稳定性。饲料中的吡哆醇以单纯扩散的形式进入体液;体液中的吡哆醇被各种组织吸收后,在各自的吡哆醛激酶和PNP/磷酸吡哆胺氧化酶的作用下,转变成辅酶型磷酸吡哆醛。家蚕不同于哺乳动物,没有特定的辅酶型磷酸吡哆醛形成组织和辅酶型磷酸吡哆醛的转送机制。同时家蚕体内缺乏具储存VB₆功能的辅酶型磷酸吡哆醛结合蛋白,推测这是用缺乏VB₆的饲料饲育各龄起蚕,幼虫当龄死亡的主要原因。     

Depression-like and anxiety-related behaviour of rats fed with magnesium-deficient diet

The aims of this study were to estimate of psychomotor activity, emotional status and magnesium (Mg) content in blood of rats fed with Mg-deficient diet for 49 days; and to find out whether the combination of vitamin B6 with Mg will reveal antidepressant- and anxiolytic-like activity and reduce the length of the treatment needed to recover rats from Mg-deficient condition. To induce hypomagnesemia, seventy-nine rats were placed on a Mg-deficient diet (Mg content < or = 15 mg/kg) and demineralized water for 7 weeks. Eight control rats were fed a basal control diet. On the forty-ninth day of Mg-deficient diet, rats were treated one of the six supplementations: Mg L-aspartate alone and in combination with pyridoxine, MgCl2 x 6H2O alone and in combination with pyridoxine, Magne B6 (Mg lactate with pyridoxine) and Mg sulfate (50 mg Mg and 5 mg vitamin B6 per kg). In our study Mg-deficiency was associated with depleted intraerythrocytic (0.748 +/- 0.036 vs. 1.83 +/- 0.026 mmol/l, p < 0.001) and plasma (0.567 +/- 0.029 vs. 1.20 +/- 0.030 mmol/l, p < 0.001) Mg level compared to control rats. It was shown Mg deficiency resulted in depression-like and anxiety-related behavior in rats. Open field test result in rats including locomotor activity (number of crossed squares) and vertical activity (number of standing on hind paws), number of visiting in central squares were decreased significantly. In the elevated plus maze test, the number of visiting open arms (by 63.6%) and residence time (by 78.5%) of rats were significantly less as compared with the control group. In the forced swimming test, time immobile was significantly increased (by 70.2%) and time of swimming was decreased (by 15%) compared to control. Mg salts alone and in combination with vitamin B6 administered to Mg-deficient rats increased the Mg level in plasma and erythrocytes. Furthermore, this increase was in relation to vitamin B6 given to the animal. It was established, that the application of Mg L-aspartate and MgCl2 x 6H2O in combinations with pyridoxine led to correction of behavioural disturbances of Mg-deficient animals. Antidepressant- and anxiolytic-like activity of studied salts was comparable with those observed in Magne B6 treatment and significantly higher than in Mg sulfate treatment.     

Zinc-deficient rats have more limited bone recovery during repletion than diet-restricted rats

The objective of this study was to investigate the effects of dietary zinc deficiency and diet restriction on bone development in growing rats, and to determine whether any adverse effects could be reversed by dietary repletion. Weanling rats were fed either a zinc-deficient diet ad libitum (ZD; <1 mg zinc/kg) or nutritionally complete diet (30 mg zinc/kg) either ad libitum (CTL) or pair-fed to the intake of the ZD group (DR; diet-restricted) for 3 weeks (deficiency phase) and then all groups were fed the zinc-adequate diet ad libitum for 3, 7, or 23 days (repletion phase). Excised femurs were analyzed for bone mineral density (BMD) using dual-energy x-ray absorptiometry, and plasma was analyzed for markers of bone formation (osteocalcin) and resorption (Ratlaps). After the deficiency phase, ZD had lower body weight and reduced femur BMD, zinc, and phosphorus concentrations compared with DR; and these parameters were lower in DR compared with CTL. Femur calcium concentrations were unchanged among the groups. Reduced plasma osteocalcin in ZD and elevated plasma Ratlaps in DR suggested that zinc deficiency limits bone formation while diet restriction accelerates bone resorption activity. After 23 days of repletion, femur size, BMD, and zinc concentrations remained lower in ZD compared with DR and CTL. Body weight and femur phosphorus concentrations remained lower in both ZD and DR compared with CTL after repletion. There were no differences in plasma osteocalcin concentrations after the repletion phase, but the plasma Ratlaps concentrations remained elevated in DR compared with CTL. In summary, both ZD and DR lead to osteopenia during rapid growth, but the mechanisms appear to be due to reduced modeling in ZD and higher turnover in DR. Zinc deficiency was associated with a greater impairment in bone development than diet restriction, and both deficiencies limited bone recovery during repletion in growing rats.     

Metabolomic Analysis Reveals Extended Metabolic Consequences of Marginal Vitamin B-6 Deficiency in Healthy Human Subjects

Marginal deficiency of vitamin B-6 is common among segments of the population worldwide. Because pyridoxal 5′-phosphate (PLP) serves as a coenzyme in the metabolism of amino acids, carbohydrates, organic acids, and neurotransmitters, as well as in aspects of one-carbon metabolism, vitamin B-6 deficiency could have many effects. Healthy men and women (age: 20-40 y; n = 23) were fed a 2-day controlled, nutritionally adequate diet followed by a 28-day low-vitamin B-6 diet (<0.5 mg/d) to induce marginal deficiency, as reflected by a decline of plasma PLP from 52.6±14.1 (mean ± SD) to 21.5±4.6 nmol/L (P<0.0001) and increased cystathionine from 131±65 to 199±56 nmol/L (P<0.001). Fasting plasma samples obtained before and after vitamin B6 restriction were analyzed by ¹H-NMR with and without filtration and by targeted quantitative analysis by mass spectrometry (MS). Multilevel partial least squares-discriminant analysis and S-plots of NMR spectra showed that NMR is effective in classifying samples according to vitamin B-6 status and identified discriminating features. NMR spectral features of selected metabolites indicated that vitamin B-6 restriction significantly increased the ratios of glutamine/glutamate and 2-oxoglutarate/glutamate (P<0.001) and tended to increase concentrations of acetate, pyruvate, and trimethylamine-N-oxide (adjusted P<0.05). Tandem MS showed significantly greater plasma proline after vitamin B-6 restriction (adjusted P<0.05), but there were no effects on the profile of 14 other amino acids and 45 acylcarnitines. These findings demonstrate that marginal vitamin B-6 deficiency has widespread metabolic perturbations and illustrate the utility of metabolomics in evaluating complex effects of altered vitamin B-6 intake.     

Vitamin B6 in Plasma and Cerebrospinal Fluid of Children

Background

Over the past years, the essential role of vitamin B6 in brain development and functioning has been recognized and genetic metabolic disorders resulting in functional vitamin B6 deficiency have been identified. However, data on B6 vitamers in children are scarce.

Materials and Methods

B6 vitamer concentrations in simultaneously sampled plasma and cerebrospinal fluid (CSF) of 70 children with intellectual disability were determined by ultra performance liquid chromatography-tandem mass spectrometry. For ethical reasons, CSF samples could not be obtained from healthy children. The influence of sex, age, epilepsy and treatment with anti-epileptic drugs, were investigated.

Results

The B6 vitamer composition of plasma (pyridoxal phosphate (PLP) > pyridoxic acid > pyridoxal (PL)) differed from that of CSF (PL > PLP > pyridoxic acid > pyridoxamine). Strong correlations were found for B6 vitamers in and between plasma and CSF. Treatment with anti-epileptic drugs resulted in decreased concentrations of PL and PLP in CSF.

Conclusion

We provide concentrations of all B6 vitamers in plasma and CSF of children with intellectual disability (±epilepsy), which can be used in the investigation of known and novel disorders associated with vitamin B6 metabolism as well as in monitoring of the biochemical effects of treatment with vitamin B6.     

Intrauterine growth restriction leads to changes in sulfur amino acid metabolism, but not global DNA methylation, in Yucatan miniature piglets

Intrauterine growth restriction (IUGR), in both animals and humans, has been linked to metabolic syndrome later in life. There has been recent evidence that perturbations in sulfur amino acid metabolism may be involved in this early programming phenomenon. Methionine is the precursor for cellular methylation reactions and for the synthesis of cysteine. It has been suggested that the mechanism behind the "fetal origins" of adult diseases may be epigenetic, involving DNA methylation. Because we have recently demonstrated the fetal origins phenomenon in Yucatan miniature swine, we hypothesized that sulfur amino acid metabolism is altered in IUGR piglets. In this study, metabolites and the activities of sulfur amino acid cycle enzymes were analyzed in liver samples of 3- to 5-day-old runt (IUGR: 0.85±0.13 kg) and large (1.36±0.21 kg) Yucatan miniature pig littermates (n=6 pairs). The IUGR piglets had significantly lower specific and total activities of betaine-homocysteine methyltransferase (BHMT) and cystathionine γ-lyase (CGL) than larger littermates (P<.05). Expression of CGL (but not BHMT) mRNA was also lower in IUGR piglets (P<.05). This low CGL reduced cysteine and taurine concentrations in IUGR pigs and led to an accumulation of hepatic cystathionine, with lower homocysteine concentrations. Methylation index and liver global DNA methylation were unaltered. Reduced prenatal growth in Yucatan miniature piglets impairs their remethylation capacity as well as their ability to remove cystathionine and synthesize cysteine and taurine, which could have important implications on long-term health outcomes of IUGR neonates.     

Nonradioactive enzymatic assay for plasma and serum vitamin B(6)

Pyridoxal-5'-phosphate (PLP) is the biologically active form of vitamin B(6). Clinical studies suggest that low PLP concentrations are an independent risk factor for cardiovascular and other diseases. However, PLP concentrations are not routinely used for diagnosis because of the lack of a homogeneous, nonradioactive assay. We describe a homogeneous, nonradioactive, enzymatic PLP assay that uses the apo form of the recombinant PLP-dependent enzyme, homocysteine-alpha,gamma-lyase (rHCYase). The restoration of enzymatic activity by reconstitution of the holoenzyme is linearly dependant on the amount of PLP bound to the enzyme. Nanomolar concentrations of PLP can then be measured by the conversion (by reconstituted holo-rHCYase) of millimolar concentrations of homocysteine (HCY) to H(2)S. H(2)S combines with DBPDA (N,N-dibutylphenylenediamine) to form 3,7-Bis(dibutylamino)-phenothiazine-5'-ium chloride and the absorbance of this compound is read at 675 nm. The PLP enzymatic assay has a lower limit of detection of 14.8 nmol l(-1) and is linear to 300 nmol l(-1) and requires only 10 microl plasma or serum. This PLP assay is the first homogeneous, nonradioactive method for diagnosing vitamin B(6). The procedure takes approximately 2 h to complete.     

A Combination of Zinc and Pyridoxine Supplementation to the Diet of Laying Hens Improves Performance and Egg Quality

The objective of this study was to investigate whether zinc, along with pyridoxine, is effective in improving performance and egg quality of laying hens. One hundred and twenty, 28-week-old Hy-Line laying hens were assigned to four treatment groups, 30 hens each. The birds were fed a basal diet or the basal diet supplemented with either 30 mg of zinc/kg of diet, 8 mg of pyridoxine/kg of diet, or 30 mg of zinc plus 8 mg of pyridoxine/kg of diet. Feed conversion (P < 0.01) and egg production (P < 0.01) improved most when both zinc and pyridoxine were supplemented to the diet. Eggshell weights were also greatest (P < 0.01) when the diet was supplemented with both pyridoxine and zinc. Egg-shape index was, however, greatest with zinc-supplemented diet (P < 0.004). Haugh unit was greatest in eggs of hens fed a diet supplemented with both zinc and pyridoxine (P < 0.01). Dietary zinc and pyridoxine supplementations together increased plasma calcium and phosphorous concentrations (P < 0.002). The results of the present study suggested that zinc (30 ppm) and pyridoxine (8 ppm) supplements, when used together, are recommended in terms of a better performance and egg quality in laying hens.     

Vitamin B6 deficiency alters tissue iron concentrations in the Wistar rat

PurposeWe investigated the effect of a vitamin B6 deficiency and pair-feeding on tissue trace element status.MethodTissue zinc, copper and iron concentrations were measured in 3 groups of young, male Wistar rats receiving a diet of 3.5 mg/kg (control group), 0 mg/kg (deficient group) and a pair-fed group over 8 weeks. The pair-fed group received the same diet consumed by the control. Tissue trace element analysis was performed using atomic absorption spectrophotometry and plasma vitamin B6 status was determined using HPLC.ResultsDeficiency resulted in elevation in liver iron concentration and reduction in muscle iron concentration. Muscle copper concentrations were reduced in the pair-fed and deficient groups vs. the control group. Tissue zinc concentrations remained unaffected by the deficiency. Kidney iron and heart copper levels were elevated in the pair-fed group.ConclusionsThe liver and muscle iron changes were due to the deficiency and not to reduced calorie intake and the latter may be due to impaired heme synthesis. The differences in copper between the groups were due to reduced food intake. Zinc seems to form a fixed pool in these animals. A dietary deficiency of vitamin B6 impacts on the trace element status of certain tissues in key metabolic tissues and hence needs to be factored into the amelioration of the condition.     

Maternal Vitamin C Deficiency during Pregnancy Persistently Impairs Hippocampal Neurogenesis in Offspring of Guinea Pigs

While having the highest vitamin C (VitC) concentrations in the body, specific functions of VitC in the brain have only recently been acknowledged. We have shown that postnatal VitC deficiency in guinea pigs causes impairment of hippocampal memory function and leads to 30% less neurons. This study investigates how prenatal VitC deficiency affects postnatal hippocampal development and if any such effect can be reversed by postnatal VitC repletion. Eighty pregnant Dunkin Hartley guinea pig dams were randomized into weight stratified groups receiving High (900 mg) or Low (100 mg) VitC per kg diet. Newborn pups (n = 157) were randomized into a total of four postnatal feeding regimens: High/High (Control); High/Low (Depleted), Low/Low (Deficient); and Low/High (Repleted). Proliferation and migration of newborn cells in the dentate gyrus was assessed by BrdU labeling and hippocampal volumes were determined by stereology. Prenatal VitC deficiency resulted in a significant reduction in postnatal hippocampal volume (P<0.001) which was not reversed by postnatal repletion. There was no difference in postnatal cellular proliferation and survival rates in the hippocampus between dietary groups, however, migration of newborn cells into the granular layer of the hippocampus dentate gyrus was significantly reduced in prenatally deficient animals (P<0.01). We conclude that a prenatal VitC deficiency in guinea pigs leads to persistent impairment of postnatal hippocampal development which is not alleviated by postnatal repletion. Our findings place attention on a yet unrecognized consequence of marginal VitC deficiency during pregnancy.     

Production of pyridoxal phosphate by a mutant strain of Schizosaccharomyces pombe

Conditions for extracellular production of vitamin B6 compounds (B6), especially pyridoxal 5'-phosphate (PLP) by Schizosaccharomyces pombe leul strain were examined. The productivity was dependent on concentration of L-leucine in the culture medium: 30 mg/l gave the highest concentrations of total B6 and PLP. The viable cells harvested at different growth phases showed different productivity: middle and late exponential phase cells showed the highest productivity of total B6 and PLP, respectively. D-Glucose (1%, w/v) among other sugars gave the best productivity. Supplementation of air and ammonium sulfate significantly increased extracellular production of PLP. Superoxide anion producers, menadione and plumbagin, and H202 increased the productivity of PLP. Cycloheximide inhibited the increase of PLP by the oxidative stress and, in contrast, increased pyridoxine.