• The Korean Journal of Zoology
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• v.16 no.1
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• pp.13-23
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• 1973

The changes in the quantitative distribution and in cytoplasmic granules of tongue mast cells and duodenal enterochromaffin cells in male albino rats were observed following oral administration of 40mg/kg body wt. isonicotinic acid hydraside (INH) and 20mg/kg body wt. pyridoxine. The results obtained are summarized as follows: 1. INH administered-rat showed a marked decrease in the number of mast cells, caused by leakage of cytoplasmic granules, while pyridoxine-rat showed increased the number of mast cells. 2. Similarly, INH-rat showed a marked decrease in the number of enterochromaffin cells. In the case of pyridoxine-rat, however, the number of enterochromaffin cells increased compared with that of the controls. 3. In view of the fact that a large dose of INH was harmful to the formation of mast cells and enterochromaffin cells. And considering that a moderate dose of pyridoxine stimulated the formation of the two kinds of cells and the amounts of cytoplasmic granules, it was concluded that pyridoxine might be concerned with the metabolism of secretory products, 5-Hydroxytryptamine.

• Journal of Nutrition and Health
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• v.20 no.5
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• pp.318-329
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• 1987

Weanling female Sprague Dawley rate were fed 1.2mg pyridoxine' HCl/kg diet Cdepleted diet) and 2 22mg pyridoxine' HCI/kg dietCcontrol diet). The control and one depleted group were fed their diets throughout growth, gestation, and lactation. Other three depleted groups were fed the depleted diet throught growth and gestation, and then pyridoxine w was supplemented by feeding control diet at 5, 10, and 21 days postpartum. The brains were analyzed for proteolipid protein, cholesterol, and cerebrosi­d de. Percentage stimulation of erythrocyte alanine aminotransferase activity was also determined. Body and brain weight were significantly lower at all ages in depleted group than the control and depleted group showed inadequacy of B6 at all ages. PProteolipid protein and cholesterol were significa­n ntlylower in the depleted group at 10, 21, 35 and 5 50 days. The postnatal development of cerebroside in brain was delayed in depleted groups suppleme­I nted at 5, 10, and 21 days. When supplementation was initiateo at 5 days postparturn, contents of cho­lesterol proteolipid protein were reversed. But some differences in brain development of pups we­re evident when supplementation of dams was de­layed to 10 days or 21 days.

• The Journal of the Korean dental association
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• v.10 no.4
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• pp.209-212
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• 1972

The effect of pyridoxine on the incisors were histochemically studied for the purpose of identifying the phosphoric acid. The microscopic observations were carried out by means of phosphoric acid reaction(Serraet Queiroz-Lopes method), mucoprotein reaction (Clara method), periodic acid-Schiff reaction (McManus method), methylen blue stain and hematoxylin-eosin stain. In the experimental result, it was found that phosphoric acid reactions of ameloblast, Tomes' process and preenamel were remarkably increased after pyridoxine administration.

• BMB Reports
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• v.39 no.1
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• pp.76-83
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• 2006

Pyridoxine-5-P oxidase catalyses the terminal step in the biosynthesis of pyridoxal-S-P, the biologically active form of vitamin $B_6$ Which acts as an essential cofactor. Here, a human brain pyridoxine-5-P oxidase gene was fused with a gene fragment encoding the HIV-1 Tat protein transduction domain (RKKRRQRRR) in a bacterial expression vector to produce a genetic in-frame Tat-pyridoxine-5-P oxidase fusion protein. Expressed and purified Tat-pyridoxine-5-P oxidase fusion protein transduced efficiently into PC12 cells in a time- and dose-dependent manner when added exogenously to culture media. Once inside the cells, the transduced Tat-pyridoxine-5-P oxidase protein showed catalytic activity and was stable for 48 h. Moreover, the formation of pyridoxal-5-P was increased by adding exogenous Tat-pyridoxine-5-P oxidase to media pre-treated with the vitamin $B_6$ precursor pyridoxine. In addition, the intracellular concentration of pyridoxal-S-P was markedly increased when Tat-pyridoxal kinase was transduced together with Tat-pyridoxine-5-P oxidase into cells. These results suggest that the transduction of Tat-pyridoxine-5-P oxidase fusion protein presents a means of regulating the level of pyridoxal-5-P and of replenishing this enzyme in various neurological disorders related to vitamin $B_6$.

• Asian-Australasian Journal of Animal Sciences
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• v.27 no.12
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• pp.1744-1748
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• 2014

A dose-response experiment with seven supplemental pyridoxine levels (0, 0.66, 1.32, 1.98, 2.64, 3.30, and 3.96 mg/kg) was conducted to investigate the effects of pyridoxine on growth performance and plasma aminotransferases and homocysteine of White Pekin ducks and to estimate pyridoxine requirement for these birds. A total of 336 one-day-old male White Pekin ducks were divided to 7 experimental treatments and each treatment contained 8 replicate pens with 6 birds per pen. Ducks were reared in raised wire-floor pens from hatch to 28 d of age. At 28 d of age, the weight gain, feed intake, feed/gain, and the aspartate aminotransferase, alanine aminotransferase, and homocysteine in plasma of ducks from each pen were all measured. In our study, the pyridoxine deficiency of ducks was characterized by growth depression, decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine. The ducks fed vitamin $B_6$-deficient basal diets had the worst weight gain and feed/gain among all birds and this growth depression was alleviated (p<0.05) when pyridoxine was supplemented to basal diets. On the other hand, plasma aspartate aminotransferase and homocysteine may be the sensitive indicators for vitamin $B_6$ status of ducks. The ducks fed basal diets had much lower aspartate aminotransferase activity and higher homocysteine level in plasma compared with other birds fed pyridoxine-supplemented diets (p<0.05). According to quadratic regression, the supplemental pyridoxine requirements of Pekin ducks from hatch to 28 days of age was 2.44 mg/kg for feed/gain and 2.08 mg/kg for plasma aspartate aminotransferase and the corresponding total requirements of this vitamin for these two criteria were 4.37 and 4.01 mg/kg when the pyridoxine concentration of basal diets was included, respectively. All data suggested that pyridoxine deficiency could cause growth retardation in ducks and the deficiency of this vitamin could be indicated by decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine.

• Journal of Nutrition and Health
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• v.19 no.4
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• pp.246-254
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• 1986

Weanling female Sprague Dawley rats were fed d diets containing 22mg pyridoxine. BCI/kg diet (control diet) and l.2mg pyridoxine. BCI/kg diet (deficient diet). One control group and one defi­c dent group were fed their diet throughout growth, g gestation and lactation. After the pups were born and weaned, the deficient group was divided into two groups. One switched to control diet(supple­I mented group) and the other continued the same d deficient diet( deficient group) until 10 week -old. The liver mitochondrial and cytosolic asparate a aminotransferase activity and pyridoxal phosphate content were determined in offspring rats. The aspartate aminotransferase activities in both liver mito$\phi$ondrial and cytosolic fractions of den­d cient group were significantly lower than those of controls, but there were no significant differences between two groups after addition of 1O^{-4}M pyri­d do뼈I phosphate to the medium. By pyridoxine s supplementation after weaning, the reduced aspar­a tate aminotnmsferase activities were only partialy I restored to control levels. The pyridoxal phospha­t te content of deficient group in Iiver mitochondr­ial and cytosoIic fractions were alo significantly different from those of controls, but readily restored by dietary supplementation. These results suggest that there is a quantitative and a qualitative changes of aspartate amino trans­f ferase and pyridoxal phosphate in liver mitochon­d drial and cytosolic fraction by long-term pyrido­x xine deficiency and these reductions can partially recovered by dietary pyridoxine supplementation after weaning.

• Korean Journal of Food Science and Technology
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• v.9 no.3
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• pp.183-189
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• 1977

Studies were made of the continuous production of Pyridoxal 5'-phosphate (pyridoxal-p) on simultaneously immobilized cell column. Whole-cell of Pseudomonas polycolor having high activity of pyridoxine 5'-phosphate (pyridoxine-p) oxidase and Kloeckera sp. No. 2201 having high activity of catalase were used as the enzyme materials. The enzyme sources were entrapped in a polyacrylamide gel. Enzymatic properties of the simultaneously immobilized cells were investigated, comparing with those of the mixed whole-cells of the microorganisms. The simultaneously immobilized cells had higher enzyme activity than singly immobilized cells of Pseudomonas polycolor. From this result, the simultaneously immobilized pyridoxine-p oxidase-catalase system could be available to exert a protective effect upon the pyridoxine-p oxidase by destroying $H_2O_2$ which is a by-product of pyridoxine-p oxidation. The optimum pH was 9.0 for the immobilized cells and the whole-cells. The optimum temperature was $45^{\circ}C$ for the immobilized cells and $40^{\circ}C$ for the whole-cells. The pyridoxine-p oxidase of the immobilized cells were activated by $Hg^{++}$ and some SH-compounds.

• Journal of Medicine and Life Science
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• v.21 no.1
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• pp.11-14
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• 2024

Excess of pyridoxine, in contrast to other nutrients, may result in neuropathy. Case reports are sparse, and little is known about the clinical and electrophysiological findings. Eight patients with pyridoxine-induced neuropathy were investigated, and a review of the literature was undertaken. Nerve conduction studies showed axonal sensory or sensorimotor polyneuropathy. And the blood levels of vitamin B6 were markedly elevated. After discontinuation of vitamin supplements, all patients showed no significant improvement in clinical and electrophysiological findings. Supplementation with pyridoxine at doses greater than 50 mg/day for extended durations may be harmful and should be discouraged.

• Journal of Nutrition and Health
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• v.17 no.3
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• pp.199-209
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• 1984

Pregnant rats were fed a pyridoxine deficient diet during the gestation and lactation. DEF I group received the deficient diet from delivery ; DEF II group, from the 15 th day of gestation. Body and brain weights, brain protein, DNA, RNA, plasma GOT and GPT, and catecholamines were measured. Effect of MAO inhibiting drug, pargyline, was determined. Brain protein, DNA, and RNA of offsprings of deficient groups were significantly lower than the control group, but RNA/ DNA, brain weight/DNA, and protein/DNA show that cell number were more affected than cell size by the pyridoxine deficiency during the 3rd week of gestation and lactation. Plasma GOT activities were more significantly different than plasma GPT between the control and deficient group. Brain norepinephrine of offsprings of deficient group were significantly lower than the control, but brain dopamine content was not significantly different from the control. At 2nd and 3rd week, norepinephrine was significantly depressed in deficient groups. Pargyline treatment affected a 1.2 fold increase in catecholamines in 3hr while the control had a 1.5 fold increase. Thus norepinephrine and dopamine synthesis was depressed in the deficient groups. Dopaminergic neurons may be less dependent on pyridoxine level than neurons from norepinephrine. Pyridoxine deficiency in maternal diet is not so critical to brain catecholamines of offspring except to the neonatal rats.

• Proceedings of the Korea Society of Poultry Science Conference
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• 2004.11a
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• pp.93-94
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• 2004

The experiments was conducted to investigate the effects of dietary supplementation of feather meal and pyridoxine on the taurine content of egg yolk and performance of laying hens. Feeding trial was conducted with 900 31-wk-old Hy-Line Brown layers for 4wks. The experiment consisted of six dietary treatments: control(basal diet), feather meal(FM) 3 % diet(FM 3 %), FM 3 % + pyridoxine supplemented diet(FM 3 % + Pyridox), FM 6 % diet, FM 6 % + pyridoxine supplemented diet(FM 6% + Pyridox), Synthetic taurine 0.25 % supplemented diet(Taurine). Egg production of birds fed FM 3% was highest and those of the FM diets were also higher than those of Taurine and the control. Egg weight of Taurine was significantly lower than those of FM 3 %, FM 6 % and the control but were not significantly different from those of FM 3 % + Pyridox or FM 6 % + Pyridox. Feed intake of the control was greater than those of FM 6 %, FM 6% + Pyridox or Taurine treatment but was not significantly different from those of FM 3 % and FM 3 % + Pyridox. Feed conversion of the control was significantly higher than other treatments in which that of FM 6 % was lowest. Broken and soft egg production of Taurine was highest while that of the control was lowest among treatments. Taurine content of egg yolk significantly increased by supplementation of taurine(64.7 %). FM 6 % + pyridoxine(57 %), FM 3% + pyridoxine (32.1%) and FM 6% (16.6 %). Sensory evaluation data of Taurine has shown the highest score in most of sensory attributes. It is concluded that taurine can be enriched in egg yolk by supplementation of 6 % FM diet and pyridoxine as well as 0.25 % synthetic taurine.