[Data on vitamin B6 deficiency, vitamin B6 requirements and supply of vitamin B6, with an estimation of the vitamin B6 content of the average Dutch meal in 1960].
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Food Analysis↗
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Results for “VITAMIN B6 DEFICIENCY”
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Morphological abnormalities in vitamin B6 deficient tarsometatarsal chick cartilage.
The aim of this study was to test the hypothesis that deficiency of vitamin B6 would produce morphological characteristics of osteochondral lathyrism. To accomplish this goal, morphological characteristics of chick cartilage in which lathyrism was produced by two separate dietary regimens was compared to morphological changes encountered in vitamin B6 deficiency. Vitamin B6 deficiency should reduce activity of lysyloxidase needed for producing intermolecular cross-links. The question to be addressed was: would this latter deficiency impair collagen morphological features and secondarily other structures indirectly by reducing collagen molecular assembly? Failure of cross-linking of collagen in the positive controls was related to a lack of functional aldehyde cross-link intermediates which are blocked by homocysteine and aminoacetonitrile. Day-old-male Lohmann chicks were fed adequate (6 mg/kg) or vitamin B6-deficient diets. Cross-link defects were induced by homocysteine-rich diets (0.6% w/w) or a diet containing aminoacetonitrile (0.1% w/w). Animals were sacrificed at 6 weeks of age and Ossa tarsalia articular cartilage specimens, as well as the proximal end of tarsometatarsus were dissected from the tibial metatarsal joint, a major weight-bearing site. Light microscopic observations revealed reduction of subarticular trabecular bone formation, concurrent with overexpansion of the hypertrophic cell zone. Ultrastructural electron microscopy observation of articular fibro-cartilage indicated significant thickening of collagen fibers in vitamin B6 deficient birds, as well as the positive controls in comparison to that of cage-matched control birds. It was concluded that vitamin B6 deficient cross-linking may be responsible for the observed delay in bone development and aforementioned cartilage histological alterations.
Aminoacetonitrile↗
Increased uterine uptake and nuclear retention of [3H]oestradiol through the oestrous cycle and enhanced end-organ sensitivity to oestrogen stimulation in vitamin B6 deficient rats.
Vitamin B6 deficient female rats showed a significantly earlier, greater and more prolonged uptake of a tracer dose of [3H]oestradiol into the uterus, with increased nuclear accumulation, compared with vitamin B6 supplemented animals. This was most marked at oestrus, with little difference at anoestrus. The responses to low doses of ethynyl-oestradiol were greater in ovariectomized deficient animals than in those receiving the supplemented diet, with an increased uterotrophic response and greater induction of peroxidase. In the deficient animals there was virtually complete suppression of LH secretion at doses of ethynyl-oestradiol that had no effect in controls. At high doses of ethynyl-oestradiol there was no difference between the two groups of animals. The results suggest that increased uterine uptake and accumulation of [3H]oestradiol in vitamin B6 deficiency is associated with enhanced end-organ responsiveness to sub-maximal oestrogen stimulation, and that pyridoxal phosphate may have a coenzyme role in oestrogen action.
Animals↗
A cartilage matrix deficiency experimentally induced by vitamin B6 deficiency.
A vitamin B6-deficiency-induced disorder in avian articular cartilage resembling osteoarthritis has been further characterized. We measured several parameters of proteoglycan (PG) metabolism, i.e., fixed charge density and sulfated glycosaminoglycans (S-GAG) content in PN-deficient versus control articular cartilage and synovial fluid from the knee joint. Statistically significant changes were: 1) decreased content and increased extractability of total sulfated PGs from articular cartilage with guanidine HCl; 2) elevation of S-GAG concentration in synovial fluid; 3) increased plasma cystathionine (sulfur amino acid) levels. PG synthesis as assessed by 35SO4 incorporation into S-GAGs was not impaired. A lack of cartilage swelling in 0.15 M saline and the normal water content indicated that although disturbed, the collagen network was not disrupted. This finding was in agreement with a previous microscopic study that revealed no fissures in the articular cartilage. Previous findings of a normal aggregating PG size-distribution and absence of elevated metalloproteases made a disturbance of aggregating PG metabolism unlikely. Escape into the synovial fluid of small PGs, normally bound to articular collagen, was believed to result from an alteration in collagen molecular organization that could be secondary to elevated circulating SH-compounds.
Animals↗
Influence of dietary n-3 polyunsaturated fatty acids on plasma lipemic effect of vitamin B6 deficiency.
Since many connections exist between vitamin B6 and lipid metabolism, we aim to investigate the lipemic effect of different dietary intakes of polyunsaturated fatty acids in rats fed a vitamin B6 deficient diet. Diets were either vitamin B6 deficient (-B6) or vitamin B6 sufficient, pair-fed to the deficient group (PF) and ad libitum (N). The diets were combined with normal lipid (LC: soya bean-coconut-palm oils) and fish oil (FO: soya bean-fish oil). The fish oil diet with sufficient vitamin B6 content caused an increase in n-3 long chain polyunsaturated fatty acids and a decrease in arachidonic acid. In the -B6 group fed a normal lipid diet, the arachidonic acid percentage decreased and the linoleic acid percentage increased; in the -B6 group fed fish oil these changes in fatty acid composition, already consequent upon dietary intake of n-3 long chain polyunsaturated fatty acids, did not show further variations. In the dietary condition of vitamin B6 deficiency, plasma cholesterol content increased in rats fed a lipid control diet, whereas no hypocholesterolemic effect was observed in those fed a fish oil diet. Plasma triglyceride contents were not influenced by dietary lipid quality because, in all conditions, the lower food intake of the PF groups caused a decrease and vitamin B6 deficiency caused an elevation in triglyceride contents which reached those of the ad libitum groups. The study highlights the interaction between vitamin B6 and polyunsaturated fatty acids and the opportunity of dietary intake of fish oil to counterbalance some effects of vitamin B6 deficiency.
Animals↗
Alterations of KCl- and ATP-induced increase in [Ca2+]i in cardiomyocytes from vitamin B6 deficient rats.
Although vitamin B6 deficiency is related to coronary heart disease, no information regarding changes in myocardium due to vitamin B6 deficiency is available in the literature. In view of the critical role played by Ca2+ in cellular function, we investigated alterations in [Ca2+]i induced by KCI or ATP in vitamin B6 deficient and age-matched control rats. [Ca2+]i was measured in isolated cardiomyocytes by using the Fura-2 fluorescence technique. The KC1-induced increase in [Ca2+]i was augmented in vitamin B6 deficient cardiomyocytes, whereas the ATP-induced increase in [Ca2+]i was attenuated. The specific ATP binding to sarcolemma from hearts of vitamin B6 deficient rats was decreased. A single injection of vitamin B6 (10 mg/kg) to vitamin B6 deficient animals completely reversed the KC1- or ATP-induced changes in [Ca2+]i in cardiomyocytes as well as ATP binding with sarcolemma. These results regarding altered regulation of [Ca2+]i in cardiomyocytes and sarcolemmal ATP receptors indicate myocardial abnormalities due to vitamin B6 deficiency.
Adenosine Triphosphate↗
Effects of vitamin B6 deficiency on the conversion ratio of tryptophan to niacin.
To investigate how vitamin B6 (B6) deficiency affects the whole metabolism of tryptophan-niacin, rats were fed for 19 days with each of the following four kinds of diets; a complete 20% casein diet (control diet), the control diet without B6, the control diet without nicotinic acid, and the control diet without nicotinic acid and B6, and the urinary excretion of such tryptophan metabolites as kynurenic acid, xanthurenic acid, nicotinamide, N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, and N1-methyl-4-pyridone-3-carboxamide each and the enzyme activities involved in tryptophan-niacin pathway were measured. The urinary excretion of kynurenic acid decreased while that of xanthurenic acid increased drastically in the two B6-deficient groups, when compared with the B6-containing groups. These results indicate that the rats fed with the B6-free diets were in the vitamin-deficient state. The conversion ratio was calculated from the ratio of the urinary excretion of sum of nicotinamide, N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, and N1-methyl-4-pyridone-3-carboxamide, to the Trp intake. The ratio was statistically lower in the B6-free diet than in the B6-containing diet under the niacin-free conditions.
Animals↗
A comparative study of erythrocyte oxalate flux rate and urinary oxalate excretion in hyperoxaluric rats.
The present study was carried out to investigate the relation between erythrocyte oxalate flux rate and the pathogenesis of calcium oxalate renal stone disease having hyperoxaluria as the main risk factor. Male albino rats were made hyperoxaluric by feeding them diets viz. vitamin B6 deficient, vitamin B6 deficient + 51.7% galactose or fructose (serving as a sole source of carbohydrate), along with their respective pair-fed controls for 4 weeks. After 28 days of feeding, oxalate excretion was in the order of vitamin B6 deficient + galactose > galactose control > vitamin B6 deficient + fructose > vitamin B6 deficient > fructose control/vitamin B6 control. Whereas, transmembrane oxalate flux rate was in the order of vitamin B6 deficient > vitamin B6 deficient + galactose > vitamin B6 deficient + fructose > vitamin B6 control > galactose control > fructose control. No significant correlation (r = 0.304) was found between the urinary oxalate excretion and erythrocyte oxalate flux rates of various groups of rats. The study indicates that increase in oxalate excretion does not concomitantly increase the transmembrane oxalate flux in red blood cells.
Alanine Transaminase↗
Decarboxylation of S-adenosyl-L-methionine in vitamin B6 deficiency in rat liver.
The effect of a prolonged diet deficient in B6-vitamin on the activity of adenosylmethionine decarboxylase from rat liver was investigated. In contrast to an earlier report, 12 adenosylmethionine decarboxylase activity was not found to be decreased under these restricted nutritional conditions. Moreover, the addition of pyridoxal phosphate into the standard incubation mixture did not stimulate the activity of adenosylmethionine decarboxylase from the livers of the rats fed the B6-vitamin deficient diet. It is suggested that the contradictory results of Sturman and Kremzner12 might be based on an artificial liberation of carbon dioxide from S-adenosyl-L-methionine in the presence of pyridoxal phosphate. The results of this communication do not support the view that pyridoxal phosphate acts as the prosthetic group of rat liver adenosylmethionine decarboxylase.
Adenosylmethionine Decarboxylase↗
[On the pathology of tryptophan metabolism, with a report of another family with a deficiency simulating vitamin B6 deficiency].
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Adolescent↗
Effects of vitamin B6 deficiency on cytokine levels and lymphocytes in mice.
The effects of vitamin B6 (B6) deficiency on cytokine levels and proportions of lymphocyte subsets in BALB/c mice were investigated. The proportion of lymphocytes from the thymus and spleen of mice given no B6, that were CD4+ CD8- T cells, was larger than in mice given B6, and the ratio of CD8+ to CD4+ T cells in the thymus of mice given no B6 was lower. The concentrations of interleukin-5 and -10 in spleen cells stimulated in vitro with concanavalin A were significantly higher in the mice with B6 deficiency, as was their plasma corticosterone concentrations. These results suggested that B6 is necessary to maintain cytokine levels and lymphoid function in the thymus and spleen of mice.
Animals↗
Vitamin B6 deficiency and the lymphoid system. II. Effects of vitamin B6 deficiency in utero on the immunological competence of the offspring.
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Animals↗
Effect of vitamin B6 deficiency on an antibody production in mice.
To investigate the effects of vitamin B6 (B6) deficiency on an antibody production in BALB/c mice, the production of specific immunoglobulin (Ig) E antibody against dinitrophenylated ovalbumin (DNP-OVA) were measured by the methods of enzyme linked immunosorbent assay. The mice fed on on a B6 deficient diet for 4 weeks were immunized intraperitoneally with DNP-OVA absorbed to aluminum hydroxide gel. The contents of anti DNP-IgE antibodies in sera of B6 deficient mice significantly increased compared to that of control mice fed on a diet containing B6. In addition, Interleukin-4, which was known to induce IgE production in allergic reactions from splenocytes of B6 deficient mice, was approximately four-fold higher than that in control mice. According to the recovery test to the B6 deficient mice, that is feeding the control diet for 21 days, all values in terms of the body, thymus, and spleen weight, total serum protein, IgG, and anti DNP-IgE content, regained almost the same levels as those of control. These results suggest that B6 deficiency in mice would have relation to the stimulation of specific IgE antibody production against DNP-OVA.
Animals↗
Changes of glucose metabolism and skin-collagen neogenesis in vitamin B6 deficiency.
The mechanism of pellagrous changes in skin caused by a deficiency of vitamin B6 was studied in respect to neogenesis of proline in skin collagen and glucose metabolism. In vitamin B6 deficiency the insulin/glucagon coefficient in serum decreased significantly from 3.02 to 2.32, indicating a metabolic change towards gluconeogenesis. A deficiency of vitamin B6 caused a decrease in the levels of vitamin B6-dependent enzymes, such as ornithine aminotransferase, alanine aminotransferase, and aspartate aminotransferase, which also contribute to gluconeogenesis. Because the conversion of ornithine to proline via pyrroline-5-carboxylate was suppressed due to the decrease in ornithine aminotransferase activity, the amount of proline in the skin collagen fraction also decreased significantly in vitamin B6-deficient rats compared with the pair-fed control. These results suggest that the pellagrous lesions in vitamin B6-deficiency are caused by an impaired synthesis of proline from ornithine, which results in the suppression of collagen neogenesis in the skin.
Animals↗
Hematology of chicks experiencing marginal vitamin B6 deficiency.
An economical vitamin B6-deficient ration, which was palatable to broiler chickens, was prepared and fed to 1-day-old broiler chicks. The experimental ration was a glucose-soybean meal diet. Vitamin B6 was removed by washing the soybean meal with water. Microbiological analysis revealed that the washed ration contained .45 mg vitamin B6 activity/kg. Experimental rations were formulated to contain .5, 1.0, and 3.0 mg added pyridoxine HCl/kg of ration. These supplemental levels produced total pyridoxine concentrations, as assayed, of .95, 1.48, and 3.18 mg pyridoxine HCl activity/kg of diet. Chicks were grown to 7 weeks of age and characteristic B6 deficiency traits, including increased mortality, decreased body weight gain, and increased incidence of abnormal leg conformation, were quantitated or observed. An extensive hematological evaluation at 4 weeks of age indicated that this marginal B6 deficiency resulted in increased erythrocyte numbers, decreased mean corpuscular hemoglobin levels, and increased erythrocyte fragility. No changes in hematocrits, total hemoglobin level, intracellular hemoglobin concentration, or reticulocyte number were found. These results indicate that anemia did not occur in broilers experiencing a moderate vitamin B6 deficiency. The hematological condition is described as microcytic, normochromic polycythemia.
Animals↗
Restoration of tissue antioxidants and prevention of renal stone deposition in vitamin B6 deficient rats fed with vitamin E or methionine.
Observed loss in body weight gain, increased lipid peroxidation reaction, decreased concentrations of antioxidants, ascorbic acid, alpha-tocopherol and reduced glutathione and antioxidant enzymes, glutathione peroxidase and catalase and increased concentration of hydroperoxides and hydroxyl radicals in vitamin B6 deficient rat liver [J Nutri Biochem, 2 (1991) 245] and kidney [Biochem International, 21 (1991) 599] were nearly normalized on feeding with vitamin E or methionine. Accumulation of oxalate and calcium during vitamin B6 deficiency was abolished by feeding vitamin E or methionine. Calcium oxalate deposition observed in vitamin B6 deficient kidney was completely prevented when fed along with vitamin E or methionine. However the hyperoxaluria and hypercalciuria persisted even after feeding with vitamin E or methionine.
Animals↗
Protein intake and vitamin B6 deficiency in the rat. III. The effect of supplementing a low-protein, vitamin B6 deficient diet with tryptophan and with other sulfur-free amino acids.
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Amino Acids↗
BIOCHEMICAL effects of vitamin B6 deficiency.
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Humans↗