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Results for “PYRIDOXINE DEFICIENCY”

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At least 19 recordsLinked to original sources
PubMed1988

Pineal indoleamine metabolism in pyridoxine-deficient rats.

Pyridoxine deficiency causes physiologically significant decrease in brain serotonin (5-HT) due to decreased decarboxylation of 5-hydroxytryptophan (5-HTP). We have examined the effect of pyridoxine deficiency on indoleamine metabolism in the pineal gland, a tissue with high indoleamine turnover. Adult male Sprague-Dawley rats were fed either a pyridoxine-supplemented or pyridoxine-deficient diet for 8 weeks. Pyridoxine deficiency did not alter the pattern of circadian rhythm of pineal 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), N-acetylserotonin (NAS), and melatonin. However the levels of these compounds were significantly lower in the pineal glands of pyridoxine-deficient animals. Pineal 5-HTP levels were consistently higher in the pyridoxine-deficient animals and a conspicuous increase was noticed at 22.00 h. Increase in pineal NAS and melatonin levels caused by isoproterenol (5 mg/kg at 17.00 h) were significantly lower (P less than 0.05) in the pyridoxine-deficient animals. Treatment of pyridoxine-deficient rats with pyridoxine restored the levels of pineal 5-HT, 5-HIAA, NAS, and melatonin to values seen in pyridoxine-supplemented control animals. These results suggest that 5-HT availability could be an important factor in the regulation of the synthesis of pineal NAS and melatonin.

Animals↗
PubMed1991

Increased calcium influx in caudal artery of rats made hypertensive with pyridoxine deficiency.

Moderate pyridoxine deficiency in rats has been shown to induce hypertension, which can be corrected by pyridoxine supplementation. In this study, calcium handling by isolated caudal arteries from pyridoxine-deficient and age-matched control rats was evaluated. We found 45Ca influx into the intracellular compartment to be significantly elevated in deficient rats. This increased influx could be attenuated with nifedipine, a calcium channel blocker, in a dose-dependent manner, suggesting alterations in the calcium channels that would make them leaky. The pyridoxine-deficient arterial segments maintained a higher resting tone; removal of extracellular calcium by EGTA or entry blockade by nifedipine decreased the tone significantly in the deficient arteries, compared with little or no effect in controls.

Animals↗
PubMed1986

Hypothyroidism of hypothalamic origin in pyridoxine-deficient rats.

Pyridoxine-deficient young rats (3 weeks old) had significantly reduced levels of pituitary TSH, serum thyroxine (T4) and tri-iodothyronine (T3) compared with pyridoxine-supplemented rats. The status of the pituitary-thyroid axis of normal, pyridoxine-supplemented and pyridoxine-deficient rats was evaluated by studying the binding parameters of [3H](3-methyl-histidine2)TRH in the pituitary of these rats. The effects of TRH and T4 injections on pituitary TSH and serum TSH, T4 and T3 of these two groups were also compared. The maximal binding of TRH receptors in the pituitary of pyridoxine-deficient rats was significantly higher than that of pyridoxine-supplemented control and normal rats, but there was no change in the binding affinity. Treatment with TRH stimulated TSH synthesis and release. It also increased serum T4 and T3 in both pyridoxine-supplemented and pyridoxine-deficient rats. Treatment with T4 decreased serum and pituitary TSH in both pyridoxine-supplemented and pyridoxine-deficient rats, compared with saline-treated rats. The increased pituitary TRH receptor content, response to TRH administration and the fact that regulation at the level of the pituitary is not affected in the pyridoxine-deficient rat indicates a hypothalamic origin for the hypothyroidism of the pyridoxine-deficient rat.

Animals↗
PubMed1975

Tryptophan metabolism in baboons: effect of riboflavin and pyridoxine deficiency.

Seven urinary metabolites of tryptophan-kynurenine pathway were measured in riboflavin-deficient, pyridoxine-deficient, pair-fed and natural diet baboons. The most significant changes in the pyridoxine-deficient baboons was a mean sevenfold increase in the excretion of xanthurenic acid and a threefold decrease in 3-hydroxy anthranilic acid. The riboflavin-deficient baboons showed a twelvefold increase in the excretion of anthranilic acid, and a tenfold decrease in 3-hydroxy kynurenine. Red blood-cell pyridine nucleotides decreased only in the pyridoxine-deficient baboons, while plasma 11-hydroxy corticosteroids increased only in the riboflavin-deficient baboons. These results are discussed in relation to enzymatic changes that may be expected during these deficiencies.

11-Hydroxycorticosteroids↗
PubMed1975

Brain lipids in pyridoxine-deficient young rats.

Pyridoxine deficiency produced in rats during the period of development of the central nervous system resulted in a decreased incorporation of (1-14C) acetate into total lipid extracts of brain. It also resulted in a uniform decrease in the incorporation of the labeled precursor into the cholesterol, glycolipid and phospholipid fractions of brain. The specific radioactivity of purified cerebrosides and sulfatides was decreased by 78% in pyridoxine-deficient rats with respect to controls. The decreased incorporation of labeled precursor in the deficient rats was not due to the labeled precursor, since the specific radioactivity of brain acetate and the brain concentrations of acetyl coenzyme A and acetate were similar in both deficient and control rats. The results indicate that in pyridoxine deficiency established in the young rat there is an impaired formation of myelin.

Acetates↗
PubMed1981

The endocrine pancreas in pyridoxine deficient rats.

Because the supplementation of pyridoxine (vitamin B6) improves the glucose tolerance in gestational diabetes and adult onset diabetes, pyridoxine deficiency has been considered to be one of the factors that cause diabetes mellitus. We produced pyridoxine deficient rats by giving pyridoxine-free food with deoxypyridoxine which competitively the activity of pyridoxal phosphate. In these pyridoxine deficient rats plasma insulin during the glucose tolerance test was significantly low as compared with controls. In vitro experiments of pancreas perfusion showed that secretion of insulin and glucagon was impaired in the pyridoxine deficiency. Since the restriction of diet-calorie caused a decrease in arginine-induced secretion of insulin and glucagon from the isolated pancreas, the impairment of the endocrine pancreas may depend on malnutrition. Pyridoxine deficiency is surely one of the factors that impair the endocrine pancreas by multifactorial derangement of metabolism besides the tryptophan-nicotinic acid pathway.

Animals↗
PubMed1993

Embryogenesis in Litomosoides carinii from pyridoxine deficient cotton rats.

Pyridoxine (vitamin B6) deficiency was induced in cotton rats which were then infected with the filarial parasite Litomosoides carinii. Embryogenesis was assessed microscopically in worms taken from pyridoxine deficient cotton rats and from various categories of control animals. Embryogenesis was retarded in worms from pyridoxine deficient hosts and more abnormal embryos were present in such worms than in those from control animals.

Animals↗
PubMed1982

Stimulation of cholesterol metabolism in pyridoxine-deficient rats.

The effect of pyridoxine deficiency on cholesterol catabolism was studied in rats. The concentrations of bile lipid components were higher in pyridoxine-deficient rats than in controls. A decreased ratio of taurine to glycine conjugates was observed in the deficient rats. No change in the neutral sterol content, but an increase in the bile acid content of the feces was observed in the deficient rats. Increased cholesterol catabolism in pyridoxine-deficient rats was also shown by the shorter half-life of the [14C] cholesterol injected into these animals.

Animals↗
PubMedDate not supplied

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.

Age Factors↗
PubMed1982

Role of glucose on fatty liver formation in pyridoxine-deficient rats.

Studies were made on whether glucose starvation causes fatty liver in pyridoxine-deficient male Wistar rats. Pyridoxine deficiency resulted in significantly lower levels of liver glucose than in pair-fed controls but no significant change in the serum glucose concentration. In non-starving animals, serum immuno-reactive insulin (IRI) was significantly lower in pyridoxine-deficient rats than in pair- or ad libitum-fed controls. Liver glucokinase activity in pyridoxine-deficient rats was also significantly lower than in ad libitum-fed controls. The extent of insulin deficiency was evaluated by examining the effect of administration of insulin on pyridoxine-deficient rats. Administration of insulin had no effect on the activity of liver glucokinase in pyridoxine-deficient rats, but induced the enzyme in ad libitum-fed controls. In response to a decrease in the activity of liver glucokinase or hexokinase in the deficient group, glycolytic activity, estimated as lactate production from glucose in the liver supernatant spun at 100,000 X g, was reduced to half the control level in pyridoxine-deficient rats. The effects of glucose administration on the liver lipid content, serum insulin and serum glucose were investigated. The serum glucose concentration was not significantly different in pyridoxine-deficient and control rats at any time after the glucose load. The level of serum IRI after the load was similar in the two groups after 30 min but then gradually decreased in the deficient group. The liver lipid content of the deficient rats tended to decrease whereas that of the controls remained unchanged throughout the experiment. Thus glucose starvation in pyridoxine-deficient rats is one factor responsible for fatty liver formation. Possible mechanisms of this phenomenon are discussed.

Animals↗
PubMed1994

Picrotoxin and pentylene tetrazole induced seizure activity in pyridoxine-deficient rats.

Computerized electroencephalography and thalamic ventro-posterior lateral (VPL) unit activities were recorded from pyridoxine-deficient and pair-fed pyridoxine-supplemented adult male rats. Pyridoxine-deficient animals exhibited slow electroencephalograms (EEG) represented by the dominance of delta activity and reduced seizure thresholds to local (VPL) application of either picrotoxin or pentylene tetrazole. Frequency and amplitude of thalamic VPL unit activity were significantly reduced in pyridoxine-deficient rats as compared to pyridoxine-supplemented controls. Pyridoxine-deficient rats exhibited irregular unit activity with frequent bursts and electrosilent periods in response to local (VPL) picrotoxin or pentylene tetrazole microinjections. They also exhibited severe seizure discharge activity of prolonged duration at any given dose of either picrotoxin or pentylene tetrazole. This was represented by significantly increased burst frequency, burst duration and reduced seizure latencies. Unit activity was transformed into burst discharge activity with intermittent electrosilent zones during picrotoxin or pentylene tetrazole epileptogenesis. Cerebral gamma aminobutyric acid (GABA) level was reduced and glutamate concentration increased in pyridoxine-deficient rats when compared with pyridoxine-supplemented controls. Local (VPL) microinjection of GABA or pyridoxine induced neuronal recovery in both convulsant-treated normal and pyridoxine-deficient rats. Neuronal recovery was however delayed in pyridoxine-deficient rats. Neuronal recovery was associated with a significant increase in EEG background frequency and reduction in delta frequencies in the EEG records of both normal and pyridoxine-deficient rats. Reduced seizure threshold and delayed neuronal recovery are related to the significantly reduced brain regional GABA and elevated glutamate levels in pyridoxine-deficient rats.

Animals↗
PubMed1985

Pyridoxine deficiency in children treated with isoniazid.

Isoniazid-induced deficiency of pyridoxine (vitamin B6) is reportedly not uncommon in adults but rare in children. In the present study, 38 children had serum levels of pyridoxine tested while receiving therapy with isoniazid. A biologic assay using the protozoan Tetrahymena thermophila determined pyridoxine status after 2 to 18 months of therapy with isoniazid. Five children (13 percent) were deficient. None had definitive clinical symptoms or signs consistent with pyridoxine deficiency. Three had normal nerve conduction velocity. Children receiving isoniazid in dosages greater than 10 mg/kg/day had a higher incidence of deficiency. Present recommendations for withholding pyridoxine prophylaxis from children receiving isoniazid therapy must be reconsidered in light of these findings, particularly in those children who are debilitated or have a poor nutritional history with a known pyridoxine deficit prior to therapy with isoniazid.

Child↗
PubMed1987

Pyridoxine deficiency and ethanol-induced liver injury.

It has been suggested that pyridoxine deficiency may potentiate ethanol-induced liver injury. Our purpose was to clarify the effect of pyridoxine deficiency on ethanol-associated liver injury by comparing liver histology, serum liver enzymes, and the viability of cultured hepatocytes from pyridoxine-deficient and pyridoxine-sufficient rats that had been chronically fed ethanol-enriched diets. Our data fail to substantiate that pyridoxine-deficient animals are more susceptible to the hepatotoxic effects of ethanol than pair-fed pyridoxine-sufficient controls. Furthermore, the addition of pyridoxine to hepatocyte cultures fails to prevent in vitro cytotoxicity of added ethanol. Pyridoxine deficiency may augment ethanol-induced enhancement of hepatic urea synthesis. These data suggest that pyridoxine deficiency may contribute to the abnormal plasma amino acid profiles and nitrogen balance of chronic alcoholics, but that it does not potentiate ethanol-induced liver injury.

Animals↗
PubMed1990

Tissue iron content in riboflavin and pyridoxine deficient rats.

The effect of riboflavin and (or) pyridoxine deficiency and repletion on tissue iron content was studied in rats. The iron content in liver, spleen, and kidney and plasma iron concentration of riboflavin deficient (RD) rats was lower, but hematocrit was not. In pyridoxine deficient (PD) rats versus control rats, the iron content in liver was significantly higher but not in spleen and kidney. In PD rats hematocrit was lower but plasma iron concentration was not. Although combined riboflavin and pyridoxine deficient (CD) rats had lower iron content in liver and spleen compared with control rats, these values were intermediate between those of RD rats and PD rats. After RD and PD rats were repleted, the iron content in liver, spleen, and kidney returned to that of control rats, and the hematological indices were improved significantly. These results suggest that riboflavin and pyridoxine deficiency may impair the absorption and utilization of iron and may result in altered tissue iron content.

Journal Article↗
PubMed2004

Effect of pyridoxine deficiency on the structural and functional development of hippocampus.

In this study it was attempted to understand the effect of pyridoxine deficiency on the structural and functional development of the hippocampus. Hippocampus has been closely associated with complex neuroendocrine control of physiological activities as well as behavioural responses including learning process and memory retention. Prenatal, preweanling and weanling deficiency of pyridoxine was induced in the experimental rats by feeding dams with diet deficient in pyridoxine during pregnancy and lactation. The general growth profile for pyridoxine deficient (PD) rats is compared with control ones. The structural changes in the hippocampus of pyridoxine deficient rats was investigated using the histological techniques. Hippocampal electrical activity was recorded from in vitro brain slice preparation. The study clearly showed the structural impairment in the hippocampus of PD rats. These anatomic anomalies might be related to poor neurointegrative development and neurophysiological deficits that occur in young one. The electrical activity recorded from hippocampal slices of PD rats showed significant variation when compared to controls. Pyridoxine deficiency is common in pregnant women who used anovulatory steroids before pregnancy. The pyridoxine deficiency of the mother may result in permanent behavioural abnormality and intellectual deficit in the progeny.

Animals↗
PubMedDate not supplied

Effect of riboflavin or pyridoxine deficiency on inflammatory response.

Inflammatory response has been assessed in riboflavin or pyridoxine deficient rats. Edema was increased by 54% in pyridoxine deficiency as compared to weight-matched control rats. Food restriction per se reduced the volume of edema by 63%. In pyridoxine deficiency, concentrations of thiobarbituric acid reactive substances (which indicate the extent of lipid peroxidation) increase by 30 and 43% respectively in the edematous tissues of the paw as well as in the wounded skin. Both these parameters were not affected by riboflavin deficiency. Activities of NADPH oxidase and superoxide dismutase in elicited leukocytes from peritoneal cavity were reduced by 54 and 52%, respectively, in riboflavin deficiency but were unaltered in pyridoxine deficiency. Superoxide level and acid phosphatase activity were not influenced by either of the deficiencies, whereas hydrogen peroxide level was increased by 48% in riboflavin deficiency. Food restriction did not affect leukocyte enzymes or the levels of reduced oxygen species. The data suggest that inflammation is enhanced in pyridoxine deficiency but not in riboflavin deficiency.

Animals↗