Effect Of Vitamin B12 Research Articles

Vitamin B12Supplementation to Mink (Mustela vison) in the Prevention of Feed-Induced Iron Deficiency Anaemia: II. Effect on Haematological Parameters and Mineral Content of the Liver

Abstract An effect of oral vitamin B12 administration on growth performance and fur quality characteristics in mink kits fed an anaemiogenic diet has earlier been found. The present data confirmed that kits fed the unsupplemented anaemiogenic diet developed anaemia with low haemoglobin, haematocrit and erythrocyte counts, microcytosis, anisocytosis, and low iron and cobalt contents in the liver. Oral vitamin B12 supplementation, but not injections, partly restored iron status, documented by haemoglobin and haematocrit values not being significantly different from the control group, and increased liver cobalt content. Iron therapy alone or combined with vitamin B12 resulted in normal iron status. A mechanism for the effect of vitamin B12 in preventing anaemia is suggested.

Mechanism of vitamin B6 regulation of acetylcholine-induced currents in molluscan neurons: Pre- and postsynaptic effects

Vitamin B6 has been studied for the mechanism of its effect on acetylcholine-induced sodium-potassium and chloride currents in E16 neuron of isolated brain of the snail Helix pomatia. The results indicate that the effect of vitamin B6 on acetylcholine-induced currents in postsynaptic neuron E16 is mediated via changes in gamma-aminobutyric acid (GABA) release from a presynaptic neuron and subsequent GABA-induced and cAMP-dependent processes in E16 neuron. It is suggested that effects of vitamin and antivitamin B6 on axons of a presynaptic neuron or neurons may be connected with regulation of GABA synthesis from glutamate catalyzed by the pyridoxal-phosphate-containing enzyme.

2010 Effects of vitamin B12 on the neuronal activity of rat hypothalamic slices

2010 Effects of vitamin B12 on the neuronal activity of rat hypothalamic slices

Vitamin B12 improves cognitive disturbance in rodents fed a choline-deficient diet

The effect of vitamin B12 on learning disturbance was tested in rats. Rats were fed a choline-enriched, choline-deficient, and choline-deficient diet with vitamin B12. Concentrations of acetylcholine in the brain were significantly lower in rats fed a choline-deficient diet than rats fed a choline-enriched diet. Passive avoidance learning shows that rats on a choline-deficient diet showed significantly impaired learning compared to rats on a choline-enriched diet. However, there was no significant difference of acetylcholine in the brain or in the passive avoidance learning between rats fed a choline-enriched and a choline-deficient with vitamin B12 diet. We, therefore, suggest that vitamin B12 potentiates learning in an acetylcholine-deprived brain.

Effect of vitamin B12 (mecobalamin) on the free-running period of rat circadian behavioral rhythm.

Effect of vitamin B12 (mecobalamin) on the free-running period of rat circadian behavioral rhythm.

中枢神経障害児の睡眠・覚醒リズム障害に対するビタミンＢ１２の治療効果

中枢神経障害児の睡眠・覚醒リズム障害に対するビタミンＢ１２の治療効果

O-017 - Effect of vitamin B1, B6, B12, and a γ-orizanol compound drug on nerve conduction velocity in normal and acrylamide-treated rats.

O-017 - Effect of vitamin B1, B6, B12, and a γ-orizanol compound drug on nerve conduction velocity in normal and acrylamide-treated rats.

Effect of vitamin B12-deficiency on the activity of hepatic cystathionine beta-synthase in rats.

The effect of vitamin B12(B12)-deficiency on the activities of hepatic methionine synthase, homocysteine methyltransferase, and cystathionine beta-synthase was investigated in rats. The rats bred from B12-deficient dams were fed the B12-deficient diets for 150 days after weaning. Growth retardation of the B12-deficient rats was already observed on day 30 and continued through 150 days. But dietary supplementation of 0.5% DL-methionine slightly improved the growth retardation. Urinary excretion of methylmalonic acid increased to about 15 mg/mg creatinine and hepatic B12 concentration declined to about 2 ng/g liver after a 150-day feeding of the B12-deficient diets. Hepatic methionine synthase activity in rats fed the B12-deficient diets supplemented with or without methionine decreased to about 5% of B12-supplemented controls. Hepatic betaine-homocysteine methyltransferase activity showed no significant change caused by B12-deficiency. Hepatic cystathionine beta-synthase activity in rats fed the B12-deficient diets supplemented with or without methionine decreased to about 61% and 27% of their B12-supplemented controls, respectively, but the decrease was partially improved by methionine supplementation. In conclusion, the rats bred from B12-deficient dams showed a severe B12-deficiency after a 150-day feeding of the B12-deficient diets. The decrease of hepatic cystathionine beta-synthase activity was supposed to be due to the adaptation by the defect of methionine resynthesis.

Effect of vitamin B6 on the synthesis and degradation of aspartate aminotransferase in chicken embryo fibroblasts.

The effect of pyridoxal depletion and supplementation on the intracellular level of mitochondrial and cytosolic aspartate aminotransferase in cultured chicken embryo fibroblasts was examined. No apoenzyme was detected in cells grown in the presence of pyridoxal, and the specific activity of total enzyme did not vary profoundly from primary to quaternary cultures. Under pyridoxal depletion, up to 40% apoenzyme was found in tertiary cultures which was entirely due to the mitochondrial isoenzyme. Cytosolic apoenzyme was never detected. Total aspartate aminotransferase relative to total protein was increased 2-fold in secondary cultures; only the mitochondrial isoenzyme contributed to the increased specific activity. The cytosolic isoenzyme decreased steadily and was below the limit of detection in quaternary cultures. The changes are attributed to an increased and decreased synthesis of mitochondrial and cytosolic isoenzyme, respectively. No induction of either isoenzyme was observed after incubating the cells with different hormones and substrates. In secondary cultures, no degradation of mitochondrial isoenzyme could be detected under pyridoxal deficiency or supplementation during 4.4 days, an interpassage duration. The cytosolic aspartate aminotransferase was degraded initially with an apparent half-life of approximately 0.9 day under both sets of conditions. The pronounced stability of mitochondrial aspartate aminotransferase, even though one-third of it was present as apoenzyme, excludes the formation of the apoform to be the rate-limiting step in its degradation. The present results show that pyridoxal affects the synthesis of mitochondrial and cytosolic aspartate aminotransferase, but differently.

Control of metF gene expression in maxicell preparations of Escherichia coli K-12: reversible action of the metJ protein and effect of vitamin B12

Expression of methionine regulon elements was controlled by the metJ protein gpMetJ. A maxicell system with cloned copies of the metF transcription unit allowed reversible action of gpMetJ. Expression of the metF transcription unit in maxicells was reduced by exogenous vitamin B12 at concentrations of 0.5 nM or greater.

Effects of vitamin B12 and B6 on 2,5-hexanedione-induced neuropathy.

The therapeutic effect of Vitamin B12 or Vitamin B6 on 2,5-hexanedione induced-neuropathy in animals was examined by using our electrodiagnostic technique in order to investigate the mechanism of the development of the neuropathy. Pyridoxal phosphate and two forms of Vitamin B12 were administered to rats intoxicated by the neurotoxin for a period of 18 weeks, and the sensory and motor fiber conduction velocity and the motor distal latency of the tail nerve were periodically determined. None of the groups treated with the therapeutic drugs exhibited a definite improvement in the nerve fiber conduction velocity and motor distal latency of the rat tail nerve, as compared with those of the 2,5-hexanedione-treated controls.

In vivo and in vitro inhibition of B16 melanoma growth by vitamin B6.

The effect of vitamin B6 on the growth of B16 melanoma cells in vivo and in vitro was studied. B16 melanoma cells grown for three days in medium supplemented with 5.0 mM pyridoxine or 0.5 mM pyridoxal showed an 80% reduction in cell proliferation compared with control culture. Cells cultured for six hours in medium supplemented with 0.5 mM pyridoxal took up and incorporated 13 and 32% less [3H]thymidine, respectively, than did control cultures. A 17% reduction in [3H]glucose uptake was observed at this time point. When the incubation time was decreased to three hours, an inhibition of cellular uptake of [3H]thymidine (22%), [3H]uridine (14%), and [3H]glucose (15%) was observed; however, little or no inhibition in incorporation was detected. In in vivo studies, mice pretreated with pyridoxal for two weeks and then injected with B16 melanoma cells had a 62% reduction in tumor weight compared with controls at the end of a three-week period. If tumors were first established in mice and then treated with pyridoxal for six days, a 39% reduction in tumor growth was observed. There were no differences observed in body weights or liver weights in any of the animal groups. These results indicate that supraphysiological doses of vitamin B6 can inhibit the growth of B16 melanoma cells both in vitro and in vivo. The exact mechanism by which pyridoxal exerts its inhibitory effect was not ascertained, but experiments suggest that the vitamer may be acting on the plasma membrane to reduce precursor transport into the cell.

Effect of vitamin B<sub>12</sub> on the complement system

Effect of vitamin B12 on the complement system was investigated in vitro and in vivo. Vitamin B12 was found to reduced both the classical and alternative pathway activity of the complement in vitro. And vitamin B12 was also found to increase serum complement level in guinea pig, measured by hemolytic assay using sensitized sheep erythrocytes (EA) for the classical pathway activity and unsensitized rabbit erythrocytes (RaE) for the alternative pathway activity. And assay of complement components revealed a significant increase in C3 and C4.These evidences suggested that vitamin B12 might potentiate immune response of the host by elevating serum complement level, in additino to activate the complement system.

The Effect of Vitamin B12 on the Tolerance of Chicks for High Levels of Dietary Fat and Carbohydrate

Three experiments were conducted with White Leghorn chicks hatched from hens fed diets varying in levels of protein, fat, and vitamin B12. Adding animal fat at a level of 10% in the chick diet caused growth depression of vitamin B12 deficient chicks, regardless of protein or energy level of hen or chick diet. Increasing the level of fat to 20% in the chick diet caused further growth depression and increased mortality. Feed efficiency of vitamin B12 deficient chicks was severely depressed by each additional increment in the fat level. Increasing protein content from 20 to 30% in the chick diet resulted in severe growth depression and poor feed efficiency. Although the added fat in the 30% protein chick diet depressed growth of chicks hatched from hens fed the 16 and 32% protein with added fat, it improved growth of those hatched from hens fed the similar diets with no added fat. Added fat in the 30% protein chick diet also improved feed efficiency of all chicks regardless of breeder diet treatments.Chicks hatched with an adequate carry-over of vitamin B12 from hens or chicks fed a diet with 10 μg of added vitamin B12/kg of feed did not show the growth depression caused by the high level of fat in the 20 and 30% protein chick diets. Feed efficiency was greatly improved by the addition of vitamin B12 to all chick diets.In a 22% protein vitamin B12 deficient diet, isocaloric substitution of glucose for fat depressed chick growth significantly and this growth depression was counteracted by supplementing the diet with 10 or 100 μg of vitamin B12/kg of feed. The vitamin B12 requirement was not increased by such substitution in the 22% protein diet. In contrast, isocaloric substitution of fat for glucose in the 32% protein chick diet increased the vitamin B12 need for optimum growth.

The effect of vitamin B12 on tetracycline-induced fatty liver.

The effect of vitamin B12 on the metabolic alterations due to tetracycline toxicity was studied experimentally on laboratory animals. Treatment of Sprague-Dawley rats with 120 or 250 mg tetracycline (i.p.) per kg per day for two or three days caused an accumulation of lipids, mainly triglycerides in the liver of 75% of animals studied, while phospholipid level tend to decrease. These doses are approximately twice and four times the recommended maximum dose for man. In the present work no direct relationship was observed between dose of tetracycline and hepatic accumulation of triglyceride, although livers of rats treated with 250 mg tetracycline/kg appeared uniformly pale yellow. Elevated serum triglyceride was found predominantly in rats treated with 120 mg/kg, while there was no obvious difference between serum triglyceride of rats treated with 250 mg tetracycline and control rats, indicating a block in the release of hepatic triglycerides. Where protection by vitamin B12 was studied, the vitamin was given i.m. (50 microgram/animal) 3 hours before the injection of 120 mg tetracycline per kg. There was a good evidence that lipid abnormalities caused by tetracycline improved by vitamin B12. Thus both hepatic and serum total lipid and triglycerides were significantly lower than those of rats treated with tetracycline, although hepatic total cholesterol was significantly increased as in case of tetracycline only.

Effect of vitamin B6 on the serum concentration of pituitary hormones in normal humans and under pathologic conditions.

The effect of the acute intravenous administration of B6(300 mg pyridoxine chloride and 10 mg pyridoxal 5 — phosphate) on the circulating levels of pituitary hormones was investigated in humans under normal and pathologic conditions. In normal subjects maximal changes expressed as per cent of the basal levels were as follows: 52% suppression of prolactin (PRL) at 90 minutes, 18% of TSH at 90 minutes and 315% stimulation of GH at 30 minutes. LH was also mildly suppressed (38%) at 60 minutes but there were no appreciable changes in serum FSH and Cortisol. The effect of Beon PRL and GH release was abolished after 3 day pretreatment with sulpiride; this finding suggests a dopaminergic mediation. In hypothalamo-pituitary diseases the response to Be was found altered: the inhibition of serum PRL was diminished in normo- or hyperprolactinemic women with galactorrhea and disturbed menses but without X-ray evidence of pituitary tumor. When PRL or GH secreting adenomas were present, the responses of PRL and GH to Be were absent or paradoxical. Our observations support the hypothesis that in normal subjects Be activates hypothalamic aromatic-L-aminoacid-decarboxylase with a consequent increase of dopamine concentration. The lack of response to Be observed in hypothalamo-pituitary disorders might be attributed either to an abnormal response of the pituitary to dopamine or to a reduced ability of the coenzyme to promote the synthesis of this neurotransmitter.

Necessity of vitamin B12 for growth of rats fed on an odd- or even-carbon-number fat.

1. The effect of vitamin B12 on growth was studied in young male and female rats fed on diets sufficient (+B12) or deficient (-B12) in vitamin B12 containing 30% of the dietary energy as fat, either maize oil (CO) or triundecanoin (TUD). 2. Vitamin B12 deficiency severely depressed growth. After 6 weeks the weight gain of CO(-B12) rats was only 72% of that of CO(+B12) rats and the gain of TUD(-B12) rats was only 47% of TUD(+B12) rats. 3. After fasting 24 or 96 h TUD-fed rats, both +B12 and -B12, had greater glycogen reserves and higher plasma glucose levels than CO-fed rats. 4. It is concluded that vitamin B12 is required for the metabolism and utilization of both an odd-carbon-number medium-chain fat, TUD, and an even-C-number long-chain fat, CO, during growth in rats.

Effect of vitamin B6 on L-glutamate dehydrogenase activity in mice brain.

Investigations were carried out to obtain information on the effect of vitamin B6 level on L-glutamate dehydrogenase activity in mice brain. Subcutaneous and intracerebral injection of pyridoxal phosphate or pyridoxamine resulted in a significant enhancement of the L-glutamate dehydrogenase activity. In the case of pyridoxine, much larger doses and more prolonged time were necessary to exhibit the effect. The above effect of vitamin B6 was much more evidently observed in vitamin B6-deficient animals.

Effect of Vitamin B12 and Folic Acid Deficiencies on Neutrophil Function

Morphological and quantitative neutrophil abnormalities are common in the megaloblastic anemias of vitamin B12 and folic acid deficiency. Little is known, however, about the role of these vitamins in normal leukocyte function. Seven patients with megaloblastic bone marrows, four with vitamin B12 deficiency and three with folic acid deficiency, were studied to determine the effect, if any, of these deficiencies on leukocyte function. Phagocytosis of staphylococci, hexose monophosphate shunt activation with phagocytosis, and microbicidal capacity against Staphylococcus aureus were determined prior to the institution of specific therapy. In two instances, these studies were repeated following treatment. There was no impairment of phagocytosis per se, and resting metabolism was not significantly decreased. With phagocytosis, however, metabolic activation was decreased to 35%-36% of control values in the leukocytes of patients with vitamin B12 deficiency but not in the leukocytes of patients with folic acid deficiency. Bacterial killing was slightly decreased in vitamin B12 but not in folic acid deficiency. These abnormalities of function were reversed after specific therapy. These findings suggested a specific role for vitamin B12 in the production of intermediates necessary for normal cell function.

Effect of vitamin B12 and folate on biosynthesis of methionine from homocysteine in the nematode Caenorhabditis briggsae.

(i) Omission of L-methionine from the medium resulted in an 80% population reduction. Substitution of D,L-homocysteine corrected methionine deficiency in C. briggsae in the presence of supraoptimal vitamin B12 and folic acid. (ii) An absolute vitamin B12 requirement in C. briggsae developed in the medium containing homocysteine at the second subculture. Concentration of 6 ng/ml of vitamin B12 (at 100 ng/ml of folic acid) was sufficient to support maximum growth of C. briggsae in the medium containing homocysteine. (iii) It was found that either supraoptimal folic acid (2000 ng/ml) or supraoptimal vitamin B12 (3750 ng/ml), with homocysteine, supported very little population growth of C. briggsae. However, supraoptimal folic acid and supraoptimal vitamin B12 together supported a maximum population growth. Therefore, it was concluded that both vitamin B12 and folic acid were required for the biosynthesis of methionine from homocysteine. Studies also showed that the two vitamins spared each other for population growth in the medium containing homocysteine.