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Results for “Vitamin B Deficiency”

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At least 19 recordsLinked to original sources
PubMed1977

Influence of norethindrone on drug-metabolizing enzymes of female rat liver in various B-vitamin deficiency states.

Ingestion of high levels of thiamin significantly decreased the activity of cytochrome P-450, NADPH cytochrome c reductase, and the metabolism of aniline and ethylmorphine. Apparent VmaxS for ethylmorphine N-demethylase and aniline hydroxylase were decreased by high levels of riboflavin even though NADPH cytochrome c reductase was elevated. High levels of dietary pyridoxine significantly decreased only the Vmax for aniline hydroxylase. Generally, norethindrone produces either no change or slight depression of cytochrome P-450 regardless or diet, whereas the administration of norethindrone produced no change or an increase in activity of c reductase and ethylmorphine N-demethylase. Norethindrone induces aniline hydroxylase in animals fed all diets except those deficient in thiamin and riboflavin. The activities of the four parameters of the drug metabolizing system measured in these studies as well as the effects of norethindrone are clearly affected by the dietary status of the animal.

Aniline Hydroxylase↗
PubMed1979

Relationship between biochemical and clinical indices of B-vitamin deficiency. A study in rural school boys.

1. A study amongst schoolboys in villages around Hyderabad, India, showed that almost all the boys had riboflavin deficiency, 61% had pyridoxine deficiency, and 9.4% had thiamin deficiency as judged by enzymic tests. 2. The prevalence of angular stomatitis was 41.3% and that of glossitis was 18.2%. Biochemical deficiency of riboflavin and pyridoxine was marginally higher in children with angular stomatitis with or without associated glossitis, than in children without oral lesions. 3. Treatment with B-complex vitamins (containing 4 mg riboflavin and 10 mg pyridoxine) daily for 1 month produced significant reduction in the prevalence of glossitis but had no effect on angular stomatitis. The latter responded to topical application of gentian violet. 4. Small but significant changes in erythrocyte enzymes occurred over the period of 1 month even without vitamin supplements. 5. Results suggest that while glossitis is a relatively early manifestation of riboflavin or pyridoxine deficiency or both, angular stomatitis has a more complex aetiology perphaps associated with infection.

Adolescent↗
PubMed1976

Interactions between malnutrition and primaquine studied on Wistar rats. II. Complex vitamin B deficiency and thiamine deficiency.

The action of primaquine was investigated on male Wistar rats depleted on the vitamin B complex (approximately 50% of their requirement for optimal growth), on thiamine (approximately 50% of their requirement for optimal growth), and pair-fed control animals. There was only a marginal increase in adverse primaquine reactions in the malnourished, especially in the thiamine deficient rats.

Animals↗
PubMed1979

Effect of vitamin B-6 deficiency on preference for several taste solutions in the rat.

The effect of dietary-induced vitamin B-6 (B-6) deficiency on the intake of the taste solutions, sodium chloride (NaCl), sodium saccharin (NaSacc), quinine sulfate (QS), and hydrochloric acid (HCl) was studied using a 48 hour, two-bottle choice technique. The B-6 deficient group demonstrated increased preference to 1.5 X 10(-1) and 3.0 X 10(-1) M NaCl compared to control ad libitum fed and control pair-fed groups. Total fluid intake on NaCl test days was also elevated in the B-6 deficient rats. There was no significant difference in the mean preference to NaSacc, QS, or HCl among the three groups. Adrenal hypertrophy was observed in the deficient rats. There was no change in the plasma level of Na and Zn but there was a reduction in urinary Na excretion. When the deficient rats were replenished by intraperitoneal injection of pyridoxine.HCl and feeding with the control diet containing adequate B-6, the increased preference for NaCl was extinguished, suggesting that the preference alteration was reversible. Urinary Na excretion also returned to normal.

Adrenal Glands↗
PubMed1978

Effects of vitamin B-6 deficiency on the developing central nervous system of the rat. Myelination.

The effects of different levels of dietary pyridoxine (1.0, 1.2, 1.4, and 20.0 mg/kg diet) fed to dams during growth, gestation and lactation on myelination in progeny were investigated. Degree of myelination at 15 days, postnatally, was determined from closely matched micrographs of the four dietary treatment groups. Electron micrographs showed markedly less myelination in the 1.0 group as compared with the 1.4 and 20.0 groups with the 1.2 group appearing intermediate in the number of myelinated axons. Some myelinated axons of the 1.0 group exhibited an "unusual" appearance of whorls of lamina separated by cytoplasmic space occupied by widely separated lamina. The results indicate that brain development, particularly myelination, was affected by a deficiency of vitamin B-6 prior to and including the period of rapid myelination.

Animals↗
PubMed1976

Deoxyribonucleoside triphosphate pools in vitamin B-12-deficient Euglenagracilis.

The size of the deoxyribonucleoside triphosphate pools of vitamin B-12-deficient cells of Euglena gracilis, and of vitamin B-12-deficient cells repleted with the vitamin, were measured. We found that the pools were very small, if they exist at all, in deficient cells but expand rapidly with the addition of the vitamin. The sizes of the pools decrease when DNA synthesis is completed, and are very small when the cells begin to divide.

DNA↗
PubMed1976

Metabolism of pyridoxine in the liver of vitamin B-6-deficient rats.

The metabolism of [6-3H]pyridoxine - HCl was investigated in the liver of vitamin B-6-deficient rats. Rats were made vitamin B-6 deficient by feeding ad libitum for 42 days a diet lacking pyridoxine but otherwise optimal. Animals were each injected intraperitoneally with 33 muCi of [6-3H] pyridoxine - HCl and killed at different time intervals afterwards up to 7 days. Radioactively labeled hepatic B-6 compounds were extracted with acid and chromatographically separated on Dowex-X8 (H+) columns and the percent radioactivity for each vitamin compound was then calculated. Maximal uptake in control and deficient animals was observed 30 and 60 min, respectively, after administration of label. Radioactivity was not retained by the control animals but decreased steadily in a linear fashion after 30 min, reaching a low level after 3 h. On the other hand, vitamin deficient animals accumulated almost twice as much radioactivity in their liver as the controls and retained it through 7 days. In vitamin B-6 deficient animals 93% of the injected radioactivity was metabolized within 2 min at which time pyridoxine 5'-P and pyridoxal 5'-P reached 36 and 44% levels, respectively. Pyridoxine 5'-P dropped to minimal values (3%) within 15 min and remained unchanged for 7 days while pyridoxal 5'-P reached a peak (79%) level at 15 min and then began to drop linearly reaching a plateau (29%) at 5 days. Further, as the level of pyridoxal 5-P was falling, pyridoxamine 5'-P was linearly synthesized reaching a platuau low level (3%). The specific activity level of pyridoxal kinase decreased 3.2 times and that of pyridoxine 5'-phosphate oxidase increased 1.5 times in the state of deficiency. The results presented show that metabolism of [3H]pyridoxine in deficiency is characterized by (a) a delayed, two-fold increase in label uptake as well as an extended label retention period, (b) a rapid pyridoxal 5'-P synthesis, and (c) a continuous synthesis (and accumulation) of pyridoxamine 5'-P which is not utilized or further metabolized.

Aging↗
PubMed1976

Stability of some pyridoxal phosphate-dependent enzymes in vitamin B-6 deficient rats.

The effects of lowering the liver pyridoxal phosphate (PLP) concentration by vitamin B-6 deficiency on the stability of several rat liver enzymes were examined. Three PLP-dependent enzymes (serine dehydratase, ornithine-delta-aminotransferase, and tyrosine aminotransferase) and two non-PLP-dependent enzymes (glucose-6-phosphate dehydrogenase and phosphoenolpyruvate carboxykinase) were induced in vitamin B-6 deficient and control rats by feeding them high-protein diets or by injecting them with glucagon or dexamethasone. The decline of each activity was followed after withdrawal of the inducer. Serine dehydratase activity declined more rapidly in vitamin B-6 deficient than in control liver; however, ornithine aminotransferase and tyrosine aminotransferase activities were equally stable in deficient and control liver. Ornithine aminotransferase was predominantly in holoenzyme form in both control and deficient rats, whereas tyrosine aminotransferase was predominantly in apoenzyme form in both groups. The proportion of serine dehydratase in apoenzyme was less stable than the holoenzyme. Activity changes of glucose-6-phosphate dehydrogenase and phosphoenolpyruvate carboxykinase in control and vitamin B-6 deficient rats were similar. The results suggest that differences in the stability of PLP-dependent enzymes in vitamin B-6 deficient rats depend upon differences in the proportions of these enzymes existing as holo- and apoenzyme.

Animals↗
PubMed1977

Effects of vitamin B-6 deficiency and tryptophan loading on urinary excretion of tryptophan metabolites in mammals.

The effect of vitamin B-6 deficiency on excretion of tryptophan metabolites was compared in rats, guinea pigs, hamsters, and humans. With adequate vitamin B-6 intake, a high percentage of the tryptophan administered was excreted as kynurenic acid and quinolinic acid in rat urine, and as acetylkynurenine and kynurenine in hamster urine. None of the tryptophan metabolites measured in normal guinea pig urine or human urine accounted for more than 1% to 2% of the tryptophan administered. During vitamin B-6 deficiency, the percentages of the tryptophan load excreted as xanthurenic acid, kynurenine, and o-hydroxykynurenine, (which precede the 3-hydroxykynureninase step in the kynurenine pathway) were increased in all four species. However, the percentages excreted as 3-hydroxyanthranilic acid and quinolinic acid, which are beyond the 3-hydroxy-kynureninase step, responded differently. The 3-hydroxyanthranilic acid percentage was not changed in rat urine, but was increased in human and guinea pig urines. The quinolinic acid percentage was decreased in rat urine, unchanged in guinea pig and hamster urine, and increased in human urine. In rats, depression of 3-hydroxykynureninase activity was apparently the major factor causing a change in the pattern. However, in hamsters, kynurenine hydroxylase and o-hydroxykynureninanse activities apparently were depressed. In humans, 3-hydroxykynureninase activity also was apparently depressed and the total amount of administered tryptophan accounted fro in the urine as metabolites of the kynurenine pathway was increased. Levels of urinary metabolites reached a maximum in guinea pigs after only 1 week of consuming the vitamin B-6 deficient diet, suggesting that the vitamin deficiency developed very rapidly in this species.

Adult↗
PubMed1977

Vitamin B-6 deficiency in germfree rats.

Germfree and conventional rats were used to investigate the influence of gut microflora upon vitamin B-6 deficiency. The body weights of conventional rats fed a vitamin B-6-deficient diet for more than 5 weeks plateaued, but the rats remained alive until the end of week 9 of deficiency. The body weights of germfree rats fed the same deficient diet decreased, andmost of rats were moribund around the end of week 9 of deficiency; three died. Urinary xanthurenic acid excretion following tryptophan load continued to rise at each experimental week in deficient germfree rats, while such a progressive increase in the level of the excretion was not observed in deficient conventional rats. Autopsy revealed that some of deficient germfree rats suffered from partial or toal lunficient conventional rats. The lung atelectasis was presumed to be the result of the respiratory muscle insufficiency which was closely related to the changes of the peripheral nerves innervating these muscles. The results may suggest that the presence of gut microflora made some contribution to improvement of the vitamin B-6 deficiency.

Animals↗
PubMed1977

Induction of pyridoxal phosphate-dependent enzymes in vitamin B-6 deficient rats.

The effectiveness of dietary and hormonal treatments in inducing several pyridoxal phosphate-(PLP)-dependent enzymes has been examined in vitamin B-6 deficient rats. Holo- and apoenzymes of serine dehydratase and ornithine aminotransferase were inducible in both control and deficient rats by feeding them 80% casein diets or by injecting them with glucagon. Holo- and apotyrosine aminotransferase were induced in both control and deficient rats by injecting them with glucagon or with dexamethasone phosphate. Phosphoenolpyruvate carboxykinase, a non-PLP-dependent enzyme, was inducible in both control and deficient rats by glucagon treatment if the rats were fed, but not if they had been starved. The degree of induction of certain enzymes depended upon whether rats were fed ad libitum, starved overnight, or fed a protein-free diet prior to the induction period. Phosphoenolpyruvate carboxykinase activities were about the same in both control and deficient rats. In vitamin B-6 deficient rats, both uninduced and induced activities of serine dehydratase, ornithine aminotransferase, and tyrosine aminotransferase assayed in the prsence of PLP, but not in its absence, either equaled or exceeded control values under most experimental conditions. Synthesis of excess of apoenzyme of PLP-dependent enzymes generally accounted for the high total enzyme activity in deficient rats. Differences between values for control and deficient rats could not be accounted for by differences in liver cyclic AMP concentrations nor were they apparently related to reduced food intake of the deficient rats. High apoenzyme concentration during depletion of coenzyme would tend to prevent depletion of active enzyme.

Animals↗
PubMed1976

Postnatal patterns of fatty acids in brain of progeny from vitamin B-6 deficient rats before and after pyridoxine supplementation.

The influence of deficient and adequate maternal intakes of pyridoxine on fatty acid profiles in brains of progeny at 5, 10, and 15 days of age was studied. The effects of two different times of initiating rehabilitation of deficient dams on the brain development of progeny at 5, 10, 15, 25, and 50 days of age were also examined. Three groups of weanling, female rats were fed diets deficient in pyridoxine (1.2 mg pyridoxine-HC1/kg diet) and a fourth group received a control diet (30.0 mg pyridoxine-HC1/kg diet) throughout growth, gestation and until 5 and 10 days postpartum. Supplementation with 30.0 mg pyridoxine-HC1/kg was begun in two deficient groups at 5 and 10 days postpartum. Fatty acids C18:2, C20:4, and C22:6 in cerebellum were significantly lower in brains of 15 day-old pups from unsupplemented deficient dams compared to values for pups of control dams. Significant reductions in the omega6 fatty acids (C18:2, C20:4, and C22:4) were evident in cerebellum of 15 day-old progeny of unsupplemented deficient dams. Fatty acids C20:1 and C24:0 were not detectable in cerebellum or cerebrum of the deficient group at 15 days but were evident in other groups. Supplementation of deficient dams with vitamin B-6 at 5 and 10 days postpartum prevented the reduction of omega6 fatty acids found in deficient progeny.

Age Factors↗