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PubMed2000

Added dietary pyridoxine, but not thiamin, improves weanling pig growth performance.

We conducted two trials to determine the effects of added dietary pyridoxine (vitamin B6) or thiamin (vitamin B1) on growth performance of weanling pigs. In Exp. 1, weanling pigs (n = 180, initially 5.55 +/- .84 kg, and 21 +/- 2 d of age) were fed either a control diet (no added pyridoxine or thiamin) or the control diet with added thiamin (2.8 or 5.5 mg/kg) from thiamin mononitrate or pyridoxine (3.9 or 7.7 mg/kg) from pyridoxine HC1. These five diets were fed in meal form in two phases (d0 to 14 and 14 to 35 after weaning), with identical vitamin concentrations in both phases. From d 0 to 14 after weaning, pigs fed added pyridoxine had increased (quadratic, P < .05) ADG and ADFI; pigs fed 3.9 mg/kg of added pyridoxine had the greatest improvement. From d 14 to 35 and 0 to 35, ADG and ADFI increased (linear P = .06) for pigs fed increasing pyridoxine. Growth performance was not improved by added thiamin. In Exp. 2, weanling pigs (n = 216, initially 6.08 +/- 1.13 kg, and 21 +/- 2 d of age) were fed a control diet or the control diet with 1.1, 2.2, 3.3, 4.4, or 5.5 mg/kg of added pyridoxine from pyridoxine HCl. From d 0 to 14 after weaning, increasing pyridoxine increased (quadratic, P < .05) ADG and ADFI; pigs fed 3.3 mg/kg of added pyridoxine had the greatest ADG and ADFI. Break-point analysis suggested a requirement estimate of 3.3 and 3.0 mg/kg of added pyridoxine to maximize ADG and ADFI, respectively. From d 14 to 35 or 0 to 35, increasing pyridoxine had no effect (P > .10) on pig growth performance. These results suggest that adding 3.3 mg/kg of pyridoxine (7.1 to 7.9 mg/kg of total pyridoxine) to diets fed from d 0 to 14 after weaning can improve pig growth performance.

Animal Feed↗
PubMed1994

Picrotoxin and pentylene tetrazole induced seizure activity in pyridoxine-deficient rats.

Computerized electroencephalography and thalamic ventro-posterior lateral (VPL) unit activities were recorded from pyridoxine-deficient and pair-fed pyridoxine-supplemented adult male rats. Pyridoxine-deficient animals exhibited slow electroencephalograms (EEG) represented by the dominance of delta activity and reduced seizure thresholds to local (VPL) application of either picrotoxin or pentylene tetrazole. Frequency and amplitude of thalamic VPL unit activity were significantly reduced in pyridoxine-deficient rats as compared to pyridoxine-supplemented controls. Pyridoxine-deficient rats exhibited irregular unit activity with frequent bursts and electrosilent periods in response to local (VPL) picrotoxin or pentylene tetrazole microinjections. They also exhibited severe seizure discharge activity of prolonged duration at any given dose of either picrotoxin or pentylene tetrazole. This was represented by significantly increased burst frequency, burst duration and reduced seizure latencies. Unit activity was transformed into burst discharge activity with intermittent electrosilent zones during picrotoxin or pentylene tetrazole epileptogenesis. Cerebral gamma aminobutyric acid (GABA) level was reduced and glutamate concentration increased in pyridoxine-deficient rats when compared with pyridoxine-supplemented controls. Local (VPL) microinjection of GABA or pyridoxine induced neuronal recovery in both convulsant-treated normal and pyridoxine-deficient rats. Neuronal recovery was however delayed in pyridoxine-deficient rats. Neuronal recovery was associated with a significant increase in EEG background frequency and reduction in delta frequencies in the EEG records of both normal and pyridoxine-deficient rats. Reduced seizure threshold and delayed neuronal recovery are related to the significantly reduced brain regional GABA and elevated glutamate levels in pyridoxine-deficient rats.

Animals↗
PubMed2005

Hospital pharmacy and emergency department availability of parenteral pyridoxine.

OBJECTIVES: Pyridoxine is a recommended antidote that should be available in emergency departments (EDs). A pediatric use of this preparation is the treatment of acute seizures secondary to pyridoxine dependency or responsiveness. Two cases of children with pyridoxine-dependent and pyridoxine-responsive seizures whose treatment was affected by the unavailability of pyridoxine in local EDs are presented. These cases prompted the development of a survey to ascertain the availability of parenteral pyridoxine in the pharmacies and EDs of both children's and general hospitals in the United States. METHODS: A survey of 203 pharmacy directors in 100 pediatric hospitals (42 self-governing and 58 within a hospital) and 103 general hospitals was conducted. The questionnaire asked for the number of licensed beds and whether injectable pyridoxine was on the formulary and stocked by the ED. RESULTS: The overall response rate was 73% (83% pediatric and 64% general hospitals). Injectable pyridoxine was on the formulary of 99% of pediatric hospitals and 91% of general hospitals (P = 0.044). Of those hospitals that had pyridoxine on the formulary, the availability of injectable pyridoxine in EDs was low in both pediatric (20.7%) and general hospitals (16.7%). CONCLUSIONS: Given the number of possible uses of parenteral pyridoxine in the ED, it is suggested that there is a case for all pediatric and general hospital pharmacies to have it on the formulary and further for all EDs in these hospitals to have injectable pyridoxine available for immediate use.

Emergency Service, Hospital↗
PubMed1986

Hypothyroidism of hypothalamic origin in pyridoxine-deficient rats.

Pyridoxine-deficient young rats (3 weeks old) had significantly reduced levels of pituitary TSH, serum thyroxine (T4) and tri-iodothyronine (T3) compared with pyridoxine-supplemented rats. The status of the pituitary-thyroid axis of normal, pyridoxine-supplemented and pyridoxine-deficient rats was evaluated by studying the binding parameters of [3H](3-methyl-histidine2)TRH in the pituitary of these rats. The effects of TRH and T4 injections on pituitary TSH and serum TSH, T4 and T3 of these two groups were also compared. The maximal binding of TRH receptors in the pituitary of pyridoxine-deficient rats was significantly higher than that of pyridoxine-supplemented control and normal rats, but there was no change in the binding affinity. Treatment with TRH stimulated TSH synthesis and release. It also increased serum T4 and T3 in both pyridoxine-supplemented and pyridoxine-deficient rats. Treatment with T4 decreased serum and pituitary TSH in both pyridoxine-supplemented and pyridoxine-deficient rats, compared with saline-treated rats. The increased pituitary TRH receptor content, response to TRH administration and the fact that regulation at the level of the pituitary is not affected in the pyridoxine-deficient rat indicates a hypothalamic origin for the hypothyroidism of the pyridoxine-deficient rat.

Animals↗
PubMed1993

Pyridoxine-5'-beta-D-glucoside competitively inhibits uptake of vitamin B-6 into isolated rat liver cells.

Uptake of pyridoxine-5'-beta-D-glucoside by freshly isolated rat liver cells was studied at a concentration (0.5 mumol/L) approximating the physiological range of vitamin B-6 by using a membrane filtration method. Unlabeled pyridoxine glucoside was found to competitively inhibit the uptake of [4'-3H]pyridoxine but have no detectable effect on the uptake of D-[1-3H]glucose by hepatocytes. The uptake of [3H]pyridoxine glucoside by isolated rat liver cells was very similar to the uptake of [3H]pyridoxine with Kt = 13.8 mumol/L (6.3 mumol/L for pyridoxine) and Vmax = 82 pmol/(10(6) cells.min) [28 pmol/(10(6) cells.min for pyridoxine)]. The results of this study indicate that pyridoxine glucoside uses the same transport system as does pyridoxine. Upon entry to the cell, pyridoxine glucoside undergoes hydrolysis to release pyridoxine, which is the rate-limiting step in metabolism of this beta-glucoside.

Animals↗
PubMed1996

Pyridoxine 4'-alpha- and 5'-alpha-D-glucosides are taken up and metabolized by isolated rat liver cells.

Uptake and metabolism of pyridoxine-4'-alpha-D-glucoside and pyridoxine-5'-alpha-D-glucoside by freshly isolated rat liver cells were studied using the membrane filtration method. The presence of the pyridoxine-alpha-glucosides at either 0.5 or 5.0 micromol/L had no inhibitory effect on the uptake of pyridoxine (0.5 micromol/L) by hepatocytes. The amount of pyridoxine-alpha-glucoside transported into the cells was only 10-12% of that of pyridoxine. The initial rates of uptake of the pyridoxine-alpha-glucosides were linear with concentrations up to 50 micromol/L. On entry into the cells, 78% of pyridoxine-5'-alpha-glucoside and 15% of the pyridoxine-4'-alpha-glucoside were hydrolyzed at the end of 60 min. Because pyridoxine-5'-alpha-glucoside is hydrolyzed readily and does not interfere with the transport of pyridoxine, the glucoside, if present in animal- or plant-derived foods, may be available as a source of vitamin B-6.

Animals↗
PubMed1988

Pineal indoleamine metabolism in pyridoxine-deficient rats.

Pyridoxine deficiency causes physiologically significant decrease in brain serotonin (5-HT) due to decreased decarboxylation of 5-hydroxytryptophan (5-HTP). We have examined the effect of pyridoxine deficiency on indoleamine metabolism in the pineal gland, a tissue with high indoleamine turnover. Adult male Sprague-Dawley rats were fed either a pyridoxine-supplemented or pyridoxine-deficient diet for 8 weeks. Pyridoxine deficiency did not alter the pattern of circadian rhythm of pineal 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), N-acetylserotonin (NAS), and melatonin. However the levels of these compounds were significantly lower in the pineal glands of pyridoxine-deficient animals. Pineal 5-HTP levels were consistently higher in the pyridoxine-deficient animals and a conspicuous increase was noticed at 22.00 h. Increase in pineal NAS and melatonin levels caused by isoproterenol (5 mg/kg at 17.00 h) were significantly lower (P less than 0.05) in the pyridoxine-deficient animals. Treatment of pyridoxine-deficient rats with pyridoxine restored the levels of pineal 5-HT, 5-HIAA, NAS, and melatonin to values seen in pyridoxine-supplemented control animals. These results suggest that 5-HT availability could be an important factor in the regulation of the synthesis of pineal NAS and melatonin.

Animals↗
PubMed2001

The role of L-arginine/nitric oxide pathway in the antinociceptive activity of pyridoxine in mouse.

In the present study the role of L-arginine/nitric oxide (NO)/cGMP pathway in the antinociceptive activity of pyridoxine in p-benzoquinone-induced abdominal constriction test in mouse was investigated. Pyridoxine (CAS 58-56-0) displayed dose-dependent antinociceptive activity at 0.0625-1 mg/kg (s.c.) doses. L-arginine (CAS 1119-34-2), a NO precursor, displayed a triphasic pattern as antinociception-nociception-antinociception (61.8 +/- 7.8, -36.5 +/- 12.7 and 17.0 +/- 4.3%, 5, 40 and 50 mg/kg, s.c., respectively). The antinociceptive effect of pyridoxine at ED50 dose (0.43 mg/kg, s.c.) (47.7 +/- 3.9%) was significantly decreased by L-arginine at 40 and 50 mg/kg doses (4.1 +/- 9.3 and 37.8 +/- 1.6%, respectively) while 5 mg/kg dose of L-arginine significantly potentiated the pyridoxine analgesia. On the other hand, pyridoxine reversed the L-arginine-induced nociception to antinociception (4.1 +/- 9.3%) and augmented the antinociceptive effect of L-arginine (37.8 +/- 1.6%). L-NG-nitroarginine methyl ester (CAS 51298-62-5), a NO synthase inhibitor, at 75 mg/kg, s.c. produced antinociception and significantly increased the antinociceptive effect of pyridoxine (63.7 +/- 1.2%). Methylene blue (CAS 61-73-4, MB), a guanylyl cyclase and/or NO synthase inhibitor, was antinociceptive and nociceptive at 5 and 40 mg/kg doses, respectively, 5 mg/kg dose of MB significantly increased the antinociceptive effect of pyridoxine, but did not change it at 40 mg/kg dose. On the other hand, pyridoxine significantly decreased the antinociceptive effect of MB and reversed the MB-induced nociception to antinociception. Combination of pyridoxine and morphine (CAS 57-27-2) (ED50: 0.13 mg/kg, s.c.) at 49.8 +/- 1.9% revealed a significant antinociceptive potentiation (69.1 +/- 1.8%). The findings of the present study emphasise the contribution of central and/or peripheral L-arginine/NO/cGMP nociceptive processes in pyridoxine-induced antinociception.

Analgesics↗
PubMed1976

Effects of magnesium and high dietary intakes of pyridoxine on the chick.

Day-old broiler-type male chicks were used to determine what effects magnesium and high dietary pyridoxine had on the chick's performance. The chicks were randomly assigned to 15 treatments of magnesium at 875, 1375 and 1875 mg/kg. diet and pyridoxine at 1, 4, 31, 301, and 3001 mg/kg. diet in a 3 x 5 factorial block design. A regression was used to study some of the criteria. The highest mortality of 20% occurred in chicks on the 1875 mg. magnesium-3001 mg. pyridoxine treatment. Magnesium and pyridoxine had highly significant effects on body moisture. Effects due to magnesium and pyridoxine and the interaction between the two were highly significant for weight gain and the efficiency of feed utilization (E.F.U.) At 1875 mg. magnesium/kg diet, maximum growth response and E.F.U. were predicted to occur on 10 and 39 mg pyridoxine/kg diet, respectively, Neither magnesium nor the interaction between magnesium and pyridoxine had any significant effect on carcass protein. Pyridoxine had a highly significant effect on carcass protein. Maximum response in carcass protein occurred at 31 mg. pyridoxine/kg diet irrespective of magnesium level. Serum aminotransferase activity (S.A) was significant for magnesium, pyridoxine and the interaction between the two. Pyridoxine requirement for maximum S.A. was 49 mg/kg diet at 1875 mg magnesium/kg diet. Pyridoxine requirement for maximum response was highest for S.A. and least for growth. But S.A. had the highest R2 whereas growth had the least.

Animal Feed↗
PubMed1982

Pyridoxine resistance in a rat hepatoma cell line.

The natural vitamin, pyridoxine, in the millimolar range is toxic to cultured rat hepatoma cells. A pyridoxine-resistant Fu5-5 rat hepatoma cell line was established by a stepwise increase in the concentration of pyridoxine in the medium. The newly established cell line, referred to as clone 10 (Cl.10), is resistant to killing by pyridoxine in concentrations up to 5 mM. Saturation kinetics for the uptake of [3H]pyridoxine into Fu5-5 and Cl.10 cells revealed that Fu5-5 cells take up 10 times more [3H]pyridoxine than do Cl.10 cells. Whereas the Vmax value for the uptake of [3H]pyridoxine was the same for both cell lines, the apparent Km for the Cl.10 cells was 12.5 microM compared to 0.71 microM for the Fu5-5 cells. However, intracellular levels of pyridoxal 5'-phosphate were 69% higher in Cl.10 cells than in the parental line. The resistant line is neither a permeability mutant nor deficient in pyridoxal kinase. Cl.10 cells contain 37% more adenosine 5'-triphosphate than do Fu5-5 cells and have a mitochondrial volume that is 50% greater than that of the parental line. In the absence of pyridoxine in the medium, Cl.10 cells revert to parental type with respect to pyridoxine uptake but not with respect to resistance to killing. They also maintain an enlarged mitochondrial volume. Thus, increased mitochondrial volume may be related to the development of resistance to high levels of pyridoxine.

Animals↗
PubMed1996

Activities of glycogen phosphorylase, alanine aminotransferase and aspartate aminotransferase in adult worms of Litomosoides carinii recovered from pyridoxine deficient cotton rats (Sigmodon hispidus).

This paper demonstrates that the activities of glycogen phosphorylase (GP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are reduced in adult worms of the filarial nematode Litomosoides carinii recovered from pyridoxine-deficient cotton rats when compared to worms recovered from pyridoxine-sufficient controls. GP, ALT and AST activities were determined in adult worms L. carinii recovered from cotton rat hosts over a 20-week experimental period. Activities of GP, ALT and AST in the parasite showed a direct correlation with the dietary pyridoxine intake of their host. Throughout the experiment, enzyme activities were significantly lower (P < 0.001) in worms from rats fed a pyridoxine-free diet ad libitum that in worms from rats fed either a stock colony diet, a pyridoxine-free diet ad libitum with daily supplementation of 100 micrograms pyridoxine or limited amounts of pyridoxine-free diet with daily supplementation of 100 micrograms pyridoxine. The lower than normal activity of GP, ALT, AST and other enzymes dependent on the biologically active derivative of pyridoxine, the coenzyme pyridoxal-5-phosphate (PLP), interferes with the protein, carbohydrate and lipid metabolism of L. carinii and may in part cause the reduced establishment, development and growth of the parasite in pyridoxine-deficient hosts.

Alanine Transaminase↗
PubMed1965

CONTROL OF PYRIDOXINE BIOSYNTHESIS IN ESCHERICHIA COLI.

Dempsey, Walter B. (University of Florida, Gainesville). Control of pyridoxine biosynthesis in Escherichia coli J. Bacteriol. 90:431-437. 1965.-The total pyridoxine in a culture of exponentially growing Escherichia coli was 3.6 x 10(-10) moles per mg of dry cells. One-fourth of this total was present in the medium, and was at least 90% pyridoxal 5'-phosphate. Both pyridoxol and pyridoxal, when present initially at 6 x 10(-7)m, substituted entirely for de novo synthesis of pyridoxine. The other four forms of the pyridoxine group were ineffective at this concentration. Pyridoxine biosynthesis in exponentially growing cultures of E. coli was immediately stopped by adding pyridoxol to the medium to a final concentration of 4 x 10(-7)m. Amino acid auxotrophs of E. coli suspended in minimal medium without the required amino acid produced extracellular pyridoxine for several hours at an average rate of 1.3 x 10(-10) moles per hr per mg of dry cells. The rate of production of extracellular pyridoxine by a threonine-starved threonine auxotroph was not altered by growing the culture before starvation in media containing 6 x 10(-5)m pyridoxol. The extracellular form of pyridoxine produced in these starvations required hydrolysis to be detected in the bioassay used in these measurements. The total findings suggest that pyridoxine biosynthesis is controlled by a rapidly acting mechanism but not by repression.

Amino Acids↗
PubMed1996

Pineal response after pyridoxine test in children.

To characterize the pineal response to pyridoxine, plasma melatonin was measured in one hundred and twenty children 3 hours after vitamin B6 administration. The children, aged between 1.5 and 8 years, were divided in four groups as follows: a) control day group, grouping 27 children sampled at 9:00 and at 12:00; b) control night group, grouping 29 children sampled at 21:00 and at 24:00; c) pyridoxine day group, grouping 30 children sampled at 9:00, then intravenously (i.v.) injected with 3 mg/kg of pyridoxine, and sampled at 12:00; and d) pyridoxine night group, grouping 34 children sampled at 21:00, i.v. injected with 3 mg/kg of pyridoxine, and sampled at 24:00. Melatonin concentration was measured by radioimmuno assay. The data obtained showed a significant increase in melatonin levels after pyridoxine administration in the pyridoxine night group (39.87 +/- 8.02 pg/ml basal vs 88.45 +/- 9.21 pg/ml after pyridoxine, p < 0.001). The other groups did not showed significant differences in melatonin concentrations. Statistical analysis shows that the administration of pyridoxine during the nocturnal hours represents a stimulating factor to increase the pineal production of melatonin in children.

Case-Control Studies↗