Dietary Pyridoxine Research Articles

Effects of dietary pyridoxine and protein levels on growth, vitamin B 6 content, and free amino acid profile of juvenile Penaeus japonicus

A 2 × 2 factorial design was utilized to evaluate the effects of dietary pyridoxine (0 and 200 mg kg −1 diet) and protein (49 and 64%) levels on growth, B 6 vitamer content, and free amino acid profile of juvenile Penaeus japonicus (0.17 ± 0.03 g; mean ± sd) after a 10-week feeding experiment. Pyridoxine (PN) and protein levels significantly ( P < 0.05) improved weight gain, feed intake, feed efficiency, and increased whole body protein content, muscle glutamate oxaloacetate transaminase activity, and ammonia-N excretion. Interaction between these two factors was not significant ( P > 0.05) for those mentioned variables. Weight gain of prawns fed the PN-supplemented diets was almost 2 × higher than that of prawns fed diets without supplemental PN. Significant increases in body protein, protein efficiency ratio, protein retention, and weight gain indicated that dietary protein was efficiently deposited in the body of prawns fed PN-supplemented diets. Pyridoxal phosphate and pyridoxamine phosphate were the predominant forms of vitamin B 6 in both the hepatopancreas and muscle, and their levels were significantly higher in prawns fed PN-supplemented diets. Higher levels of aspartic acid, threonine, serine, glycine, valine, and tyrosine were found in whole body of prawns fed diets without supplemental PN suggesting that catabolism of these amino acids was reduced in the prawns deficient in vitamin B 6, thereby resulting in reduced ammonia-N excretion.

Chronic Exercise Affects Vitamin B-6 Metabolism but Not Requirement of Growing Rats , ,

The effect of chronic exercise (forced swimming) on vitamin B-6 status and metabolism was studied in growing male rats fed deficient (0 mg pyridoxine-HCl/kg), suboptimal (2 mg pyridoxine-HCl/kg) or control (7 mg pyridoxine-HCl/kg) diets for 9 wk. Sedentary rats were fed the same diets. Body weight gain was lower in deficient rats than in both other dietary groups. Sedentary rats were heavier than trained rats of all diet groups. Erythrocyte aspartate aminotransferase, urinary 4-pyridoxic acid excretion, blood (plasma and erythrocytes) and tissue B-6 vitamers were measured. Urinary 4-pyridoxic acid, plasma pyridoxal 5′-phosphate and erythrocyte aspartate aminotransferase values of exercised and sedentary rats responded to changes in dietary pyridoxine but were not different from one another. After 9 wk of vitamin B-6 depletion, tissue concentrations of pyridoxal 5′-phosphate and pyridoxamine 5; 5'-phosphate were 41–66% and 26–49% lower, respectively, in the deficient groups than in the control groups. Larger percentage differences occurred in plasma than in tissues (95 vs. 22–66%). In liver, pyridoxal 5′-phosphate concentrations were lower, whereas pyridoxal concentrations were higher in trained than in sedentary rats. In gastrocnemius muscle, pyridoxal 5′-phosphate, pyridoxamine 5′-phosphate and total vitamin B-6 concentrations were higher in trained than in sedentary rats. Concentrations of vitamin B-6 compounds in heart, kidneys, brain and adrenals were not affected by training. On the basis of the vitamin B-6–dependent variables measured in this study, we conclude that prolonged exercise affects the metabolism of vitamin B-6, but does not increase the vitamin B-6 requirement in growing rats.

Activities of glycogen phosphorylase, alanine aminotransferase and aspartate aminotransferase in adult worms ofLitomosoides cariniirecovered 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.

Enhanced pyridoxine supplementation of diets for gilthead seabream (Sparus aurata L.)

AbstractUsing a high protein diet (483 g/kg), two trials were carried out to assess any potential benefit which may result from the supplementation of diets for fingerling and grower class gilthead seabream with pyridoxine at levels which were below, matched and far exceeded the minimum dietary requirement. At the level of supplementation below the minimal requirement (lowest level) the responses from the practical diet almost matched the responses from the diet containing an amount of pyridoxine corresponding to the published minimum requirement for the species and no significant improvement in performance was recorded in response to increasing supplement level. However, despite the absence of a marked effect on overall performance, a small potential for increased activity of alanine aminotransferase was recorded amongst grower class fish given diets containing the lowest supplement. The proximate composition of the grower class fish was unaffected by the level of pyridoxine supplementation though marginal increases in the lipid content of the fingerlings were observed. At the haematological level, haematocrit, total haemoglobin and the plasma concentrations of glucose and protein were also unaffected. However, on the application of an acute stressor (repeated netting), significant alterations in haematocrit and plasma glucose concentration reflecting dietary pyridoxine supplement were recorded.

Tissue B-6 Vitamer Concentrations in Rats Fed Excess Vitamin B-61

Diets containing 1, 10, 100, 175 or 250 times the NRC recommended level of pyridoxine HCl (7 mg/kg) were fed to rats (218 g, 12 per group) to evaluate the effects on tissue B-6 vitamer concentrations. After 10 wk, food intake and body weights did not differ among groups. Overt toxicity was not observed. Tissues were taken from five rats of each group after overnight food deprivation (unfed rats); the remaining seven rats in each group were allowed access to food (fed rats). In plasma of unfed rats, 4-pyridoxic acid and pyridoxal concentrations increased significantly (P < 0.05) with increasing dietary pyridoxine; pyridoxal phosphate was not affected by dietary pyridoxine. Concentrations of pyridoxal phosphate and pyridoxal increased significantly with increasing dietary pyridoxine in erythrocytes of unfed rats. Excretion of urinary B-6 vitamers and 4-pyridoxic acid in a 24-h period increased with dietary pyridoxine in fed rats. As dietary pyridoxine was increased, kidney pyridoxal concentrations increased significantly in fed rats only. Dietary pyridoxine did not affect vitamer concentration in muscle and liver of either unfed or fed rats, or in brain of unfed rats. Muscle glycogen phosphorylase, which contains pyridoxal phosphate, was not affected by dietary pyridoxine. There was a marginally significant (P = 0.058) increase in erythrocyte alanine, but not in aspartate, aminotransferase activity with increasing dietary pyridoxine. Plasma concentration of pyridoxal phosphate, which is used as a measure of vitamin B-6 status, did not reflect intake of pyridoxine in this study. Likewise, muscle pyridoxal phosphate and glycogen phosphorylase, advanced as possible reservoirs of vitamin B-6 because of positive correlations with dietary vitamin B-6 under some conditions, were unresponsive to excess dietary vitamin B-6.

Plasma Pyridoxal-5-Phosphate Levels in Vitamin B6 Deficient Cotton Rats During Infection withLitomosoides carinii

Abstract Plasma pyridoxal-5-phosphate (PLP) activity was determined over a 24-week period in uninfected cotton rats and in those infected with the nematode parasite Litomosoides carinii. Levels of PLP showed a direct correlation with dietary pyridoxine (vitamin B6) intake. PLP concentrations were significantly lower in cotton rats orally fed a pyridoxine-free diet ad libitum compared to rats fed either a vitamin B6 free diet ad libitum or a vitamin B6 diet in limited amounts and also given a 100 μg daily vitamin B6 supplement. From the onset of infection with L. carinii 8 weeks after diet commencement, PLP levels declined steadily up to the end of the experiment. PLP levels were 3 to 3.5 times lower in worms from pyridoxine-deficient cotton rats than in worms taken from cotton rats given oral vitamin B6 supplementation.

Dietary vitamin B 6 effects on the distribution of intestinal mucosal and microbial β-glucosidase activities toward pyridoxine-5′-β- d-glucoside in the guinea pig

Guinea pigs utilize dietary pyridoxine-5′-β- d-glucoside (PN-glucoside) as a source of vitamin B 6 more extensively than other species studied to date, including rats, mice, hamsters, and humans. In this study, we evaluated the sources of β-glucosidase activity involved in the hydrolysis and utilization of dietary PN-glucoside and the potential influence of vitamin B 6 nutritional status. Male guinea pigs (∼400 g, 3 to 6/diet group) were fed a sucrose/casein based diet containing 0, 1, or 3 mg/kg pyridoxine (as pyridoxine · HCl) for 4 wk. Animals fed diets containing the two lower concentrations of pyridoxine exhibited loss of body weight, although plasma pyridoxal 5′-phosphate did not vary as a function of dietary pyridoxine concentration. However, significant differences in plasma and muscle taurine and erythrocyte aspartate aminotransferase activity among diets indicated functional differences in vitamin B 6 status. β-glucosidase activity (pmol/hr/mg protein), as measured using [ 3H] pyridoxine-glucoside as the substrate, was higher in lumenal contents than mucosal cytosol. Specific activity in mucosal cytosol was significantly higher in animals fed diets containing 0 mg/kg pyridoxine than either 1 or 3 mg/kg. In contrast, the specific β-glucosidase activity of lumenal contents was significantly lower in guinea pigs fed 0 mg/kg pyridoxine versus 1 or 3 mg/kg pyridoxine diets. Although the absolute quantity of the mammalian and microbial enzyme available for in vivo small intestinal hydrolysis of dietary pyridoxine-glucoside cannot be directly determined, these data indicate that both mucosal and microbial β-glucosidase activities may contribute to the intestinal hydrolysis of pyridoxine-glucoside, and that the distribution of these activities is influenced by the concentration of dietary vitamin B 6.

Effects of pyridoxine deficiency on the metabolism of N-nitrosodimethylamine in the rat.

The alteration in the metabolic activation of N-nitrosodimethylamine (NDMA) was investigated in the rat during dietary pyridoxine deficiency. The in vitro metabolism of NDMA by demethylase system was measured in both liver and kidney microsomes. The profile of the kidney enzyme appears similar to that of the liver indicating that at least two forms of isozymes with the low and the high Km's are present. Pyridoxine deficiency significantly increased the activity of NDMA-demethylase of both organs. The increase in the activity of NDMA-demethylase induced by dietary pyridoxine deficiency can be reversed by supplementation of pyridoxine (500 micrograms), i.p., daily for two consecutive days. The increase in the NADPH cytochrome c reductase activity was observed after 6 weeks on pyridoxine-deficient diet.

Effect of Dietary Supplemental Pyridoxine Levels on the Hatchability of Turkey Eggs

Two identical experiments were conducted each with 120 Large White turkey hens in individual cages to determine the value of dietary pyridoxine supplementation for increasing hatchability. The hens were fed a basal corn and soybean meal diet. Weekly data responses were averaged across 5- to 6-wk timespans and recorded in three grouped time periods over the reproduction cycles. The hens were photostimulated at 31 wk of age and at 33 wk of age were assigned to dietary treatments containing 0, 6, 12, and 18 mg of supplemented pyridoxine/kg of diet. Thirty hens were fed each dietary treatment. In Experiment 1, eggs were collected for 4 days in the middle of each time period and egg yolk and albumen were assayed separately for vitamin B6. Although the vitamin B6 concentration in egg yolk was stable (1.9 μg/g dried basis), concentrations of vitamin B6 in egg albumen increased with incremental dietary pyridoxine levels; however, the average level of vitamin B6 in egg albumen was only 4% of the average level in egg yolk. About 37 μg of vitamin B6 per egg (82 g) was assayed in eggs from all treatments in the production periods. Incremental dietary levels of supplemented pyridoxine above the basal (unsupplemented pyridoxine) diet level did not result in increasing hatchability or egg vitamin B6 levels. Differences were not observed for 7-day or 28-day embryo deaths among treatments within the three 5- or 6-wk production periods of both experiments.

Effects of the color additive caramel color III and 2-acetyl-4(5)-tetrahydroxybutylimidazole (THI) on the immune system of rats

Administration of ammonia caramel color (AC) to rats may decrease blood lymphocyte counts, specifically in rats fed a diet low in vitamin B 6. This effect is associated with 2-acetyl-4(5)-(1,2,3,4-tetrahydroxybutyl)imidazole (THI). To characterize and compare the effects of AC and THI and to study the influence of dietary pyridoxine, two studies in rats were conducted. Weanling rats fed a diet containing 2–3 ppm pyridoxine and exposed to 4% AC or 5.72 ppm THI in drinking water for 4 weeks showed reduced cell numbers in spleen and popliteal lymph nodes, as well as in the blood. Flow cytometric analyses demonstrated a comparable reduction in B and T lymphocytes. In blood, spleen, and popliteal lymph nodes, CD4 + lymphocytes were more reduced than CD8 + cells. The number of bone marrow cells was not affected. Although thymus weight and cell number were not affected either, a decreased cortex over medulla area ratio and an increase in medullary cell density largely due to an increase in CD4 + thymocytes was observed. Decreased numbers of ED2 + macrophages were observed in the thymic cortex and in the spleen red pulp. All effects observed were either less pronounced or absent in a study with rats fed a diet containing 11–12 ppm pyridoxine. The effects of AC and THI on the immune system were similar. Whereas AC exposure was associated with changes in vitamin B 6 status, THI did not induce obvious effects on vitamin B 6 parameters. It is proposed that the effects of AC and THI on the immune system are not caused by a disturbance of vitamin B 6 metabolism, but may in fact result from a disturbance of a specific PLP-dependent process.

Seizure activity in pyridoxine-deficient adult rats.

This investigation tested the hypothesis that the degree of pyridoxine depletion rather than the status of neuronal maturity determines seizure proneness in the pyridoxine-deficient rat. Dietary pyridoxine deficiency was induced in neuronally mature rats. Seizure activity was monitored using computerized EEG analysis. Dietary pyridoxine deficiency of 10 weeks' duration induced in neuronally mature rats led to spontaneous convulsive seizure activity. Even moderately pyridoxine-deficient adult rats (on the deficient diet for less than 8 weeks) exhibited seizure-like diffuse spike and wave activity and electrocortical inhibition. Picrotoxin-, pentylenetetrazol-, or domoic acid-induced seizure thresholds were significantly reduced in pyridoxine-deficient rats when compared with normal controls. Pyridoxine-deficient rats exhibited increased dominance of delta and theta activities and increased hemispherical asymmetries in response to convulsant treatment.

Alterations in dimethylnitrosamine-induced lethality and acute hepatotoxicity in rats during dietary thiamin, riboflavin and pyridoxine deficiencies

The effects of dietary thiamin, riboflavin and pyridoxine deficiencies on dimethylnitrosamine-induced lethality and hepatotoxicity were investigated in the rat. Development of deficiencies was monitored by growth rate, food intake, ratio of liver weight to body weight and the biochemical parameters (thiamin diphosphate effects for thiamin deficiency, glutathione reductase activity coefficient for riboflavin deficiency and erythrocyte glutamate-oxaloacetate transaminase activity for pyridoxine deficiency). Thiamin deficiency slightly increased the acute toxicity of dimethylnitrosamine as observed by the lowering of the LD50 dose and the greater increase in the serum glutamate-oxaloacetate transaminase and serum glutamate-pyruvate transaminase levels. Riboflavin deficiency, on the other hand, slightly increased the LD50 dose of dimethylnitrosamine and resulted in less dimethylnitrosamine-induced damage to the liver. Pyridoxine deficiency did not affect the lethal dose nor significantly alter the transaminases levels.

Hydrolysis of Pyridoxine-5'- -d-Glucoside by a Broad-Specificity -Glucosidase from Mammalian Tissues

Research was conducted to evaluate the ability of a broad-specificity beta-glucosidase in mammalian tissues to catalyze the hydrolytic release of free pyridoxine from pyridoxine-5'-beta-D-glucoside, a naturally occurring form of vitamin B6 in plant-derived foods. Activity was detected in liver and intestinal mucosa using tritiated pyridoxine glucoside as a substrate. In the rat and guinea pig, enzyme activity was greater in intestine than in liver or kidney while even greater activity was detected in human intestinal tissue. Reaction rates were, however, low in all tissues. Hydrolysis of the synthetic substrate 4-methylumbelliferyl-beta-D-glucoside was also greatest in intestinal tissue. The characteristics of the enzymatic hydrolysis of pyridoxine glucoside to pyridoxine included: (i) most activity in the soluble tissue fraction, (ii) a pH optimum of approximately 6.0, and (iii) inhibition caused by the addition of sodium taurocholate. These characteristics are very similar to those of the broad-specificity beta-glucosidase in mammalian tissues with respect to the hydrolysis of a variety of naturally occurring and synthetic substrates. The apparent Km was greater than 2 mM for pyridoxine glucoside hydrolysis by intestinal preparations of each species, which is much greater than expected intestinal concentrations derived from dietary sources. In vivo studies have indicated that the intestine is involved in the metabolic utilization of dietary pyridoxine glucoside. The results observed here suggest that an alternate process, possibly involving intestinal microorganisms, may also be involved in the in vivo hydrolysis of pyridoxine glucoside.

Dietary Pyridoxine and Protein Intake in Kittens

Dietary Pyridoxine and Protein Intake in Kittens

Effect of pyridoxine on the disposition and lymphopenic effects of 2-acetyl-4(5)-tetrahydroxybutyl imidazole in the rat

1. 2-Acetyl-4(5)-tetrahydroxybutyl imidazole (THI) administered orally to rats markedly decreased the peripheral blood lymphocyte count within 16-24 h. The lymphopenic effect of THI was prevented by co-administration of pyridoxine. 2. 14C-THI, administered orally, was absorbed in a dose-dependent manner and excreted unmetabolized. These processes were not affected by co-administration of pyridoxine. 3. In contrast, the rate of excretion of 14C-THI administered i.v. was increased by both dietary and parenterally-administered pyridoxine, and pyridoxine decreased the amount of radiolabel associated with lymphoid tissues. 4. The results show that the lymphopenic effect of THI is not sustained once it is excreted, and indicate that pyridoxine and THI may compete for the same binding site in lymphoid tissues.

Excess dietary vitamin B6 alters water maze performance in two strains of mice

The effects of excess vitamin B6 on learning performance in a water maze were studied in progeny of two strains of mice, I strain mice which demonstrate acute sensitivity to pyridoxine depletion, and C57BL strain mice, a control strain. I strain mice fed 12 mg pyridoxine (PN)/kg diet made more errors to complete the maze than C57BL mice. When fed diets with vitamin B6 410 or 1230 times the recommended amount, water maze error scores of I strain mice decreased; but for C57BL strain mice, increased. Significant differences between dietary treatment for both strains were found, however, only when scores from third and later litters were included in the analysis. This suggests that a cumulative effect of diet was necessary in order to see an effect on water maze learning. The improvement in water maze performance demonstrated by the I strain mice with vitamin B6 intakes 410 times recommended amounts indicates that the pyridoxine requirement of the I strain is between 12 and 410 mg PN/kg diet. The detrimental effects found on learning performance of C57BL strain mice, a control strain, provides evidence of neurotoxicity with ingestion of megadose amounts of vitamin B6. In parent mice, final body weight and organ weights tended to increase in the I strain and decrease in the C57BL mice with the higher PN diets, but body weight gain was less in both strains in mice fed the higher amounts of PN. In the offspring mice, dietary PN had no effect on body weight and brain pyridoxal phosphate content.

Effect of oral and parenteral administration of B 6 vitamers on the lymphopenia produced by feeding ammonia caramel or 2-acetyl-4(5)-(1,2,3,4-tetrahydroxy)butylimidazole to rats

The ability of B 6 vitamers to prevent the lymphopenic effects of ammonia caramel fed to rats has been evaluated. Diets containing 10 ppm pyridoxine or pyridoxal prevented the lymphopenia produced in rats consuming an 8% (w/v) solution of ammonia caramel, whereas the dietary content of pyridoxamine needed to be increased to 20 ppm to have the same effect. In contrast to the results of the enteral administration of the individual B 6 vitamers, pyridoxamine was found to be the most effective vitamer in preventing the ammonia caramel-induced lymphopenia when administered parenterally. However, all the nutritionally active forms of vitamin B 6 were able to prevent the depression of the peripheral blood lymphocyte count, which resulted from ingestion of ammonia caramel by rats. The proposal that oral administration of pyridoxine may prevent the intestinal absorption of the lymphopenic constituent of ammonia caramel, 2-acetyl-4(5)-(1,2,3,4-tetrahydroxy)butylimidazole (THI), is discredited, since THI was found to reduce the lymphocyte count after parenteral administration in rats fed 0.04 ppm pyridoxone in the diet and that increased amounts of dietary pyridoxine (10 ppm) could still prevent this effect. These findings further emphasise the important relationship between dietary vitamin B 6 content and the lymphopenic effects of ammonia caramel/THI in the rat.

Dietary pyridoxine interaction with tryptophan or histidine on brain serotonin and histamine metabolism

We studied the metabolic effects of high dietary intakes of pyridoxine and of the substrate-cofactor interaction between dietary histidine or tryptophan and pyridoxine in rat brain. In the substrate-cofactor interaction study, histamine and serotonin levels were determined in rats fed elevated or requirement levels of substrate (histidine: 0.3% and 0.8%, tryptophan: 0.15% and 0.6%) and excess or requirement levels of pyrodoxine HCl (7 mg vs. 3,000 mg/kg). Excess pyridoxine intake caused a differential effect on brain histamine concentration—inhibitory with the requirement level of histidine (−29%), and stimulatory (+21%) with the elevated level of histidine. When dietary tryptophan was fed at the requirement level, excess pyridoxine caused essentially no changes in hypothalamic serotonin and 5HIAA (−2%, −2%). With elevated tryptophan intake, excess pyridoxine significantly increased serotonin and 5HIAA (+32%, +20%) in the hypothalamus. These results indicate a clear interaction between substrate and coenzyme precursor which influences brain metabolism of histamine and serotonin.

The effect of pyridoxine on the number of lymphocytes in the blood of rats fed caramel colour (III)

The effect of vitamin E, folic acid, pyridoxine (vitamin B 6) and choline on the reduction in circulating lymphocytes in the blood of rats fed Caramel Colour (III) also known as ammonia caramel colour (beer type; AC) has been examined. It was found that the reduction in the number of circulating lymphocytes in rats fed AC could be prevented by the addition of pyridoxine to the diet. The activity of AC in reducing the number of circulating lymphocytes also closely resembled that of the pyridoxine antagonist 4′-deoxypyridoxine. After the isolation and identification of 2-acetyl-4(5)-tetrahydroxybutylimidazole (THI), comparative studies indicated that THI was the component of AC responsible for reducing the number of circulating lymphocytes. Although the effect of AC was reduced or prevented by increasing dietary pyridoxine, the lymphocyte reduction associated with the administration of THI was not materially affected by the dietary level of pyridoxine.

Transport and metabolism of pyridoxine and pyridoxal in mice.

[3H]Pyridoxine or [3H]pyridoxal in physiological amounts was orally administered to mice and the distribution of isotope between the six recognized forms of vitamin B6 and pyridoxic acid was determined at different times after the administration in the intestine, liver, blood, and brain. After 7 min about 50% of the radioactivity in pyridoxine and pyridoxal had been absorbed by the intestine and transported to the blood and other organs. When [3H]pyridoxine was administered, labeled pyridoxal, pyridoxal- and pyridoxine-phosphate were found in the intestine and liver, and labeled pyridoxine could not be detected in the peripheral blood but substantial amounts of labeled pyridoxal and pyridoxal-phosphate were found in the blood. The time course of the blood [3H]pyridoxal levels following the administration of [3H]pyridoxine was similar to that following the administration of [3H]pyridoxal. These results suggest that the intestine and/or liver play a major role in converting dietary pyridoxine to circulating pyridoxal which is taken up and phosphorylated by other organs. Moreover, most of the blood [3H]pyridoxal was shown to be located in the plasma. This localization may facilitate utilization by the organs.