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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↗
PubMed1991

[Neuropsychological disorders in vitamin B 12 deficiency].

Vitamin B12 deficiency is often attended by neuropsychic disorders. In the geriatric population, the level of vitamin B12 is mostly reduced. However, the clinical manifestations and pathogenesis are not completely specified. The authors describe a female patients in whom vitamin B12 deficiency was coupled with manifest neuropsychic disorders. Provide a detailed depiction of the clinical status, the disease course and laboratory findings. Relate the most typical neuropsychic manifestations of vitamin B12 deficiency.

Ataxia↗
PubMed1975

Vitamin B-1, B-2 and B-6 deficiencies in geriatric patients, measured by coenzyme stimulation of enzyme activities.

The vitamin B-1, B-2 and B-6 nutritional status of 153 geriatric patients was determined by measurement of the activities of transketolase (TK), glutathione reductase (GR) and glutamic-oxaloacetic transaminase (GOT) from hemolyzed erythrocytes before and after in vitro stimulation with their respective coenzymes. The change in enzyme activity after incubation of the hemolysate with the coenzyme was used to determine the activation coefficient, which was taken as an index for the vitamin B-1, B-2 and B-6 nutritional status. Determination of the normal values in 54 healthy blood donors showed that activation coefficients of TK greater than 1.27 indicated a biochemical vitamin B-1 deficiency. Activation coefficients of GR greater than 1.29 and GOT greater than 1.86 indicated, respectively, deficiencies of vitamins B-2 and B-6. On the basis of these findings 22.9% of the geriatric patients appeared to suffer from vitamin B-1 deficiency, 11.7% from vitamin B-2 deficiency and 19.0% from vitamin B-6 deficiency. Of the total number of patients, 44% showed a deficiency of one or more of these three vitamins. Oral administration of vitamin B-1 (20 mg/day), vitamin B-2 (10 mg/day) and vitamin B-6 (20 mg/day) for twelve days normalized nearly all activation coefficients. Determination of enzyme activities without coenzyme stimulation revealed significantly lower values in the deficient patients as compared with the blood donors. However, the distribution of activities for both groups overlapped to a great extent. Oral administration of vitamins raised the enzyme activities to normal values.

Aged↗
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↗
PubMed1975

Interrelationships between the B-vitamins in B12-deficiency neuromyelopathy. A possible malabsorption-malnutrition syndrome.

Five patients presenting clinically with a form B12-deficiency neuromyelopathy, with cord involvement in all and proximal muscle weakness in two of them, were investigated for their neurologic, hematologic and vitamin status. Megaloblastosis and achlorhydria were present in all, and impaired absorption of 57Co vitamin B12 and of D-xylose was detected in four. Total cyanide extracted vitamin B12 (A) was lowered in all cases and noncyanide extractable (B) in four of the five, being zero in three. All five responded to injections of hydroxocobalamin. In two patients sequential estimations showed that both A and B, especially the latter, rose steeply initially, normalizing at 50% of A after some weeks. Moiety B is suggested to be physiologically the more active and dissociable form of vitamin B12. Markedly elevated initial serum folate levels, and their subsequent fall under treatment with B12, indicated the operation of the "methyltetrahydrofolate trap". Blood levels of thiamin, nicotinic acid and pantothenic acid were within normal limits. However, serum riboflavin (B2) total vitamin B6 and pyridoxal were reduced in all where tested. Vitamin B6 deficiency could have resulted from its own malabsorption and have contributed to be B12 deficiency. Vitamin B2 and B6 levels also corrected themselves on B12 therapy. The B-vitamin deficiencies in our patients probably resulted from intestinal malabsorption, with a possible factor of malnutrition consequent to their strictly vegetarian diet.

Achlorhydria↗
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↗
PubMed1976

Metabolic changes in golden hamsters fed vitamin B-12-deficient diets.

Various metabolic changes were observed in male hamsters fed vitamin B-12-deficient diets with or without supplements of cobalt, methionine, and a previously untested cobalt-free pseudovitamin B-12. The effects observed after 31 weeks of consuming the vitamin B-12-deficient diets included a marked increase in the urinary excretion of both methylmalonic acid and formiminoglutamic acid, slight increases in red blood cell mean corpuscular volume, and higher tissue levels of glutathione and activities of glutathione reductase and glucose-6-phosphate dehydrogenase. Vitamin B-12 in the diet prevented these changes, as did inorganic cobalt. The cobalt-free pseudovitamin B-12 showed no vitamin B-12 activity, neither did it have any potent antagonistic effect. Methionine supplementation reversed some of the metabolic changes. Addition of inorganic cobalt to the diet resulted in a significant increase in tissue stores of vitamin B-12.

Animals↗