Journal articles: 'Pyridosin'

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Sullivan, DW, RC Peterson, CV Mujer, and SC Gad. "A 7-day intravenous toxicity study and neurotoxicity assessment of pyridorin in Sprague-Dawley rats." Human & Experimental Toxicology 36, no. 7 (August 9, 2016): 718–26. http://dx.doi.org/10.1177/0960327116661023.

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Pyridorin®, a naturally occurring metabolite of vitamin B6 that inhibits and scavenges reactive oxygen species, is being developed as a potential therapeutic for acute kidney injury. An investigational new drug application (IND) was opened for Pyridorin in support of its ongoing oral drug clinical development program. Currently, a Pyridorin intravenous (IV) formulation is being developed for use in surgical patients. To support the IND for Pyridorin, a full battery of nonclinical Good Laboratory Practice compliant studies was performed with no neurological or behavioral signs of toxicity seen following oral or IV administration of pyridoxine dihydrochloride (the active ingredient in Pyridorin). However, excessive ingestion of vitamin B6 has been reported to cause neurotoxic syndrome in humans. Therefore, under Food and Drug Administration recommendation, a 7-day IV study in rats was conducted to further evaluate the drug’s potential to cause neurotoxicity. Blood plasma samples indicated that exposure to pyridoxamine dihydrochloride and its metabolites, pyridoxal, pyridoxine, and 4-pyridoxic acid was linearly dose proportional and independent of gender. At doses of up to 200 mg/kg/day pyridoxine dihydrochloride, no treatment-related effects were seen in rats, providing further evidence for the absence of pyridoxine dihydrochloride-related changes in the nervous system. A no observed adverse effect level of 200 mg/kg/day was identified for this study.

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Obeid, Rima, Juergen Geisel, and Wilfred A. Nix. "4-Pyridoxic Acid/Pyridoxine Ratio in Patients with Type 2 Diabetes is Related to Global Cardiovascular Risk Scores." Diagnostics 9, no. 1 (March 6, 2019): 28. http://dx.doi.org/10.3390/diagnostics9010028.

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Background: Vascular diseases are multifactorial and several risk factors may have synergetic effect on the global vascular risk. Among patients with diabetes, we investigated whether vitamin B6 species differ according to global cardiovascular risk. Methods: The present observational study included 122 patients with type 2 diabetes (mean (SD) age = 69.9 (9.1) years; 50% men). Concentrations of vitamin B6 vitamers were measured. Classical blood biomarkers and risk factors were used to compute a multivariate risk score. Results: Plasma concentrations of 4-pyridoxic acid were higher in patients with high risk versus those with low risk scores (48.2 (63.7) vs. 31.9 (15.0) nmol/L; p = 0.031). Plasma pyridoxine was significantly lowered in patients at high risk (2.8 (28.4) vs. 38.1 (127.8) nmol/L; p = 0.003). PAr index (4-pyridoxic acid/pyridoxal + pyridoxal 5′-phosphate) (1.05 (0.07) vs. 0.84 (0.06); p = 0.017) and the ratio of 4-pyridoxic acid/pyridoxine (7.0 (4.8) vs. 3.9 (3.2); p < 0.001) were higher in patients at high risk. After adjustment for cystatin C and C-reactive protein, only pyridoxine and 4-pyridoxic acid/pyridoxine ratio remained significantly different according to vascular risk scores. 4-Pyridoxic acid/pyridoxine ratio was the best marker to discriminate between patients according to their risk scores—area under the curve (AUC) (95% confidence intervals (CI)) = 0.72 (0.62–0.81). 4-Pyridoxic acid/pyridoxine ratio was directly related to plasma levels of soluble vascular cell adhesion molecule 1. Conclusion: Vitamin B6 metabolism was shifted in patients with multiple vascular risk factors. The catabolism to 4-pyridoxic acid was enhanced, whereas the catabolism to pyridoxine was lowered. High 4-Pyridoxic acid/pyridoxine ratio is independently associated with global cardiovascular risk.

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BEYNON, Robert J., Deborah M. LEYLAND, Richard P. EVERSHED, Richard H. T. EDWARDS, and Stephen P. COBURN. "Measurement of the turnover of glycogen phosphorylase by GC/MS using stable isotope derivatives of pyridoxine (vitamin B6)." Biochemical Journal 317, no. 2 (July 15, 1996): 613–19. http://dx.doi.org/10.1042/bj3170613.

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The majority of vitamin B6 in the body is in skeletal muscle, bound as the cofactor pyridoxal 5´-phosphate to one abundant protein, glycogen phosphorylase. Previous work has established that radiolabelled vitamin B6 can be used as a turnover label for glycogen phosphorylase. In this study, a stable isotope derivative of pyridoxine {dideuterated pyridoxine; 3-hydroxy-4-(hydroxymethyl)-5-[hydroxymethyl-2H2]-2-methylpyridine} ([2H2]PN) has been used as a metabolic tracer to study the kinetics of labelling of the body pools of vitamin B6 in mice. A non-invasive method was developed in which the isotope abundance of the urinary excretory product of vitamin B6 metabolism, 4-pyridoxic acid, was analysed by GC/MS. The change in isotope abundance of urinary 4-pyridoxic acid following administration of [2H2]PN reflects the kinetics of labelling of the body pools of vitamin B6, and yields, non-invasively, the rate of degradation of glycogen phosphorylase.

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Knights, T. E. N., R. R. Grandhi, and S. K. Baidoo. "Interactive effects of selection for lower backfat and dietary pyridoxine levels on reproduction, and nutrient metabolism during the gestation period in Yorkshire and Hampshire sows." Canadian Journal of Animal Science 78, no. 2 (June 1, 1998): 167–73. http://dx.doi.org/10.4141/a96-116.

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Two experiments were conducted to determine the interactive effects of selection for lower backfat over six generations, and two dietary supplemental pyridoxine levels (1.0 vs. 15.0 ppm) on sow reproductive performance and nutrient metabolism in second-parity Yorkshire and Hampshire sows. Feeding increased pyridoxine at 16.0 vs. 2.6 ppm from day of weaning through gestation did not improve (P > 0.05) the sow reproductive performance in experiment 1 (N = 32) or 2 (N = 66). In exp. 2, feeding increased pyridoxine reduced the weaning to estrus interval (4.6 vs. 5.7 d, P = 0.11). It also increased the average daily apparent retention of nitrogen during gestation in both experiments 1 (17.2 vs. 7.8 g, P = 0.11) and 2 (10.5 vs. 5.0 g, P = 0.10). Sows fed increased pyridoxine had higher (P < 0.01) plasma pyridoxal and pyridoxic acid levels throughout the gestation period. The overall results indicate that increased dietary pyridoxine tended to have a positive influence on sow weaning to estrus interval and nitrogen metabolism, and it also tended to have a positive influence on litter size only in Yorkshire select line of sows. Key words: Breed, line, sows, pyridoxine, reproduction, metabolism

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Edwards, P., P. K. Liu, and G. A. Rose. "A simple liquid-chromatographic method for measuring vitamin B6 compounds in plasma." Clinical Chemistry 35, no. 2 (February 1, 1989): 241–45. http://dx.doi.org/10.1093/clinchem/35.2.241.

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Abstract This relatively simple high-performance liquid chromatographic (HPLC) method for measuring all seven known forms of vitamin B6 in plasma from individuals supplemented with pyridoxine hydrochloride shows good analytical recovery (85-98%) and precision. Within-run and between-run CVs for plasmas supplemented with standards were 4% and 7%, respectively. The major forms of B6 found in unsupplemented plasma from normal subjects were pyridoxal phosphate and 4-pyridoxic acid, with pyridoxal just detectable. The HPLC procedure correlated well (r = 0.94) with a modification of an enzymatic method involving apotryptophanase (Anal Biochem 1972;45:567-76) for measuring plasma pyridoxal phosphate, and also (r = 0.94) with a routine method for determining 4-pyridoxic acid in urine (Clin Chem 1964;10:479-89). Elimination of pyridoxine from the plasma of both normal and hyperoxaluric individuals was shown to be very rapid, with half-lives (t1/2) of 45 and 40 min, respectively. Finally, we present evidence for the existence of two other forms of B6 and discuss the possibility of a new metabolic pathway in vitamin B6 metabolism.

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Clement, Boylan, Miller, Driskell, Giraud, and Subih. "Vitamin B-6 Vitamer Levels in Plasma and Related Symptoms in Hemodialysis Subjects Taking low- and High-Dose Renal Multivitamin Supplements." International Journal for Vitamin and Nutrition Research 82, no. 2 (April 1, 2012): 130–36. http://dx.doi.org/10.1024/0300-9831/a000102.

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Introduction: The purpose of this study was to evaluate the B-6 vitamers in plasma and related symptoms in hemodialysis subjects taking high- or low-dose vitamins. Methods: A total of 24 hemodialysis (HD) subjects were divided into two groups. Twelve subjects received a high-dose vitamin supplement [50 mg pyridoxine hydrochloride (PN-HCl) /tablet] and 12 received a low-dose vitamin supplements containing (10 mg PN-HCl/tablet) for 6+ months. Plasma B-6 vitamers were analyzed using HPLC. Other data were obtained from subjects medical records. Subjects were assessed for vitamin B-6 related symptoms. Cluster analysis was used to form symptom groups. Student t-tests and analysis of variance were used to determine differences (p < 0.05) in group means. Results: The mean ±SD plasma B-6 vitamer and 4-pyridoxic acid concentrations (nmol/L) were as follows in the 10-mg and 50-mg PN-HCl groups, respectively: pyridoxal- 5-phosphate (PLP) 10 ± 3 and 16 ± 8 (p = 0.04); pyridoxal (PL) 50 ± 96 and 68 ± 06; pyridoxine (PN) 26 ± 50 and 191 ± 107; and 4-pyridoxic acid (4-PA) 43 ± 64 and 99 ± 361. The cluster group with a significantly higher (p = 0.04) plasma 4-PA concentration of 167 ± 697 nmol/L reported more tingling hands, tachycardia, and diarrhea. Conclusion: Plasma PLP levels and symptoms related to B-6 in HD subjects are impacted by dose of PN-HCl.

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Coburn, Stephen, Joel Stauffer, Kimberley Grobien, Beomjin Kim, and Douglas Townsend. "A Physiologically Based Pharmacokinetic (PBPK) Model of Vitamin B-6 Metabolism in the Mouse Incorporated With Visualization of Complex Compartmental Models." Current Developments in Nutrition 5, Supplement_2 (June 2021): 1307. http://dx.doi.org/10.1093/cdn/nzab059_008.

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Abstract Objectives To develop a compartmental model which describes vitamin B-6 metabolism in the blood and tissues of the mouse under a variety of circumstances and to develop a computer application which can utilize the data to display the movement of tracer through the various compartments. Methods A circulation model was developed. Literature data from vitamin B-6 feeding studies and tracer experiments were used to develop an appropriate compartmental model using the SAAM II program (The Epsilon Group, Charlottesville, VA). A web-based application transforms the mass and flux data into intuitive and interactive graphical illustrations. Results Describing the interconversions between pyridoxine, pyridoxine 5’-phosphate, pyridoxal, pyridoxal 5’-phosphate, pyridoxamine, pyridoxamine 5’-phosphate and 4-pyridoxic acid in multiple tissues required 231 compartments. The largest amount of data deals with liver and brain. The model includes less detailed information on plasma, erythrocytes, gut, bone, muscle, heart, kidney, skin, adipose tissue and lung. The model includes adjustments to food intake, water intake, cardiac output, binding sites and Vmax values for enzymes based on the specified body weight of experimental animals. We did not include growth curves at this time. The model uses two parallel systems to monitor the steady state of endogenous metabolites as well as following tracer administration. Binding mechanisms are included to provide conservation of vitamin B-6 when intake is reduced. The model provides reasonable agreement with literature data on various vitamin B-6 intakes as well as oral and intravenous administration of tracer. It also reveals some areas which need clarification. For example, we have not found any detailed analysis of vitamin B-6 metabolites in mouse urine. There is little pyridoxic acid in plasma or urine suggesting that pyridoxic acid may not be the primary end product for vitamin B-6 in the mouse. The visualization application shows changes in the content of all 231 compartments over time illustrating the value of such computer applications in the interpretation of large, complex models. Conclusions This model facilitates the simulation of various dietary and physiological conditions on vitamin B-6 metabolism in mice. We hope to adapt it to rats, pigs and humans. Funding Sources Purdue University Fort Wayne.

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Tabarki, B., and F. Thabet. "Dépression électrocérébrale prolongée après administration orale de pyridoxine pour des convulsions pyridoxino-dépendantes." Archives de Pédiatrie 17, no. 2 (February 2010): 184–85. http://dx.doi.org/10.1016/j.arcped.2009.11.006.

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Sharma, Pankaja, Soo Min Han, Nicola Gillies, Eric B. Thorstensen, Michael Goy, Matthew P. G. Barnett, Nicole C. Roy, David Cameron-Smith, and Amber M. Milan. "Circulatory and Urinary B-Vitamin Responses to Multivitamin Supplement Ingestion Differ between Older and Younger Adults." Nutrients 12, no. 11 (November 17, 2020): 3529. http://dx.doi.org/10.3390/nu12113529.

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Multivitamin and mineral (MVM) supplements are frequently used amongst older populations to improve adequacy of micronutrients, including B-vitamins, but evidence for improved health outcomes are limited and deficiencies remain prevalent. Although this may indicate poor efficacy of supplements, this could also suggest the possibility for altered B-vitamin bioavailability and metabolism in older people. This open-label, single-arm acute parallel study, conducted at the Liggins Institute Clinical Research Unit in Auckland, compared circulatory and urinary B-vitamer responses to MVM supplementation in older (70.1 ± 2.7 y, n = 10 male, n = 10 female) compared to younger (24.2 ± 2.8 y, n = 10 male, n = 10 female) participants for 4 h after the ingestion of a single dose of a commercial MVM supplement and standardized breakfast. Older adults had a lower area under the curve (AUC) of postprandial plasma pyridoxine (p = 0.02) and pyridoxal-5′phosphate (p = 0.03) forms of vitamin B6 but greater 4-pyridoxic acid AUC (p = 0.009). Urinary pyridoxine and pyridoxal excretion were higher in younger females than in older females (time × age × sex interaction, p < 0.05). Older adults had a greater AUC increase in plasma thiamine (p = 0.01), riboflavin (p = 0.009), and pantothenic acid (p = 0.027). In older adults, there was decreased plasma responsiveness of the ingested (pyridoxine) and active (pyridoxal-5′phosphate) forms of vitamin B6, which indicated a previously undescribed alteration in either absorption or subsequent metabolic interconversion. While these findings cannot determine whether acute B6 responsiveness is adequate, this difference may have potential implications for B6 function in older adults. Although this may imply higher B vitamin substrate requirements for older people, further work is required to understand the implications of postprandial differences in availability.

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Thomson, Petra, and Kateřina Ládová. "Pyridoxine use in children with epilepsy: a pharmacist's point of view." Praktické lékárenství 12, no. 6 (December 1, 2016): 232–35. http://dx.doi.org/10.36290/lek.2016.056.

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Massé, Priscilla G., Jaclyn Boudreau, Carole C. Tranchant, Rodney Ouellette, and Karen L. Ericson. "Type 1 diabetes impairs vitamin B6 metabolism at an early stage of women’s adulthood." Applied Physiology, Nutrition, and Metabolism 37, no. 1 (February 2012): 167–75. http://dx.doi.org/10.1139/h11-146.

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Vitamin B6 (pyridoxine) metabolism in diabetes has never been investigated except for a few reports on plasma pyridoxal 5′-phosphate (PLP). These studies indicated that this most active (coenzyme) vitamer can be reduced. The present clinical investigation aimed to measure all vitamers in blood and urine by high performance liquid chromatography as well as important related factors, in women during active reproductive years. Thirty-two insulin-treated type 1 diabetic (T1D) patients, without renal complication, and 27 well-matched healthy controls, aged 30 to 40 years old, were recruited using rigorous criteria. Both groups had normal hemoglobin and serum albumin levels. Plasma PLP and pyridoxal (PL) did not differ significantly in the T1D group but alkaline phosphatase (ALP) activity was greater (p < 0.01). This produced a shift in plasma PLP-PL profile, as evidenced by a lower plasma PLP/PL ratio (p < 0.05). Enhanced ALP activity meant more PLP being dephosphorylated to PL (the membrane transfer form), with more ending up in erythrocytes to be rephosphorylated in its active form, as suggested by the significant positive correlation (p < 0.001) between plasma PL and erythrocyte PLP. More PL into blood circulation also means more oxidation of this vitamer to 4′-pyridoxic acid in kidneys, as confirmed by the positive correlation between plasma PL and urinary 4′-pyridoxic acid (p < 0.001). The positive correlation (p < 0.001) between ALP activity and glycosylated hemoglobin indicated a direct effect of the disease. The T1D-induced alteration in vitamin B6 metabolism, consecutive to enhanced ALP activity, may put patients at greater risk of vitamin B6 deficiency and diabetic complications.

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Midttun, Øivind, Steinar Hustad, Einar Solheim, Jørn Schneede, and Per M. Ueland. "Multianalyte Quantification of Vitamin B6 and B2 Species in the Nanomolar Range in Human Plasma by Liquid Chromatography–Tandem Mass Spectrometry." Clinical Chemistry 51, no. 7 (July 1, 2005): 1206–16. http://dx.doi.org/10.1373/clinchem.2005.051169.

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Abstract Background: Homocysteine, a risk factor of cardiovascular disease, cognitive disorders, and pregnancy complications, exists at a point of metabolic convergence of several B vitamins, including vitamins B6 and B2 (riboflavin). Measurement of the various forms of these vitamins may be useful for the study of hyperhomocysteinemia as well as for the assessment of vitamin status. Methods: Plasma (60 μL) was deproteinized by mixing with an equal volume of 50 g/L trichloroacetic acid that contained d2-pyridoxal 5′-phosphate, d3-pyridoxal, and d8-riboflavin as internal standards. Pyridoxal (PL), pyridoxal 5′-phosphate (PLP), pyridoxine (PN), pyridoxine 5′-phosphate, pyridoxamine (PM), pyridoxamine 5′-phosphate, 4-pyridoxic acid (PA), riboflavin, flavin mononucleotide (FMN), and FAD were separated on a C8 reversed-phase column, which was developed with an acetonitrile gradient in a buffer containing acetic acid and heptafluorobutyric acid. The analytes were detected by tandem mass spectrometry in the positive-ion mode. Results: The chromatographic run lasted 8 min. Within- and between-day CVs were 3%–20% and 6%–22%, respectively, and recoveries were 78%–163%. Limits of detection (signal-to-noise ratio = 5) were in the range 0.1–4.0 nmol/L, and the response was linear over several orders of magnitude. In samples from 94 healthy persons, we obtained median concentrations (nmol/L) of 35.4 for PLP, 16.9 for PL, 22.4 for PA, 10.3 for riboflavin, 7.5 for FMN, and 63.1 for FAD. PN and PM were also detected in some cardiovascular patients taking B6 supplements. Conclusions: This method based on liquid chromatography–tandem mass spectrometry measures all known plasma forms of vitamins B6 and B2, which span a wide range of polarity. The assay is characterized by simple sample processing with no derivatization, low sample volume requirement, and a short run time.

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Dakshinamurti, K., C. S. Paulose, and J. Vriend. "Hypothyroidism of hypothalamic origin in pyridoxine-deficient rats." Journal of Endocrinology 109, no. 3 (June 1986): 345–49. http://dx.doi.org/10.1677/joe.0.1090345.

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ABSTRACT 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. J. Endocr. (1986) 109, 345–349

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Lugli, Licia, Maria Carolina Bariola, Luca Ori, Laura Lucaccioni, Alberto Berardi, and Fabrizio Ferrari. "Further Delineation of Pyridoxine-Responsive Pyridoxine Phosphate Oxidase Deficiency Epilepsy: Report of a New Case and Review of the Literature With Genotype-Phenotype Correlation." Journal of Child Neurology 34, no. 14 (August 9, 2019): 937–43. http://dx.doi.org/10.1177/0883073819863992.

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In recent years, the clinical spectrum of pyridoxine phosphate oxidase (PNPO) deficiency has broadened. There are a growing number of patients with a transient or lasting response to pyridoxine in addition to cases that respond more traditionally to pyridoxal-phosphate. However, among pyridoxine-responsive patients with PNPO gene mutation, there are only a few reports on electroencephalogram (EEG) ictal/interictal patterns, and data regarding the outcomes are inconsistent. We describe a case of neonatal onset epilepsy with missense mutation c(674G>A) p(R225 H) in PNPO gene and pyridoxine responsiveness. Comparing this patient with 24 cases of previously described pyridoxine-responsive pyridoxine phosphate oxidase deficiency epilepsy, we found that patients carrying the missense mutation c(674G>A) p(R225 H) of the PNPO gene might have a more severe epileptic phenotype, possibly because of their lower residual PNPO activity. Indeed, pyridoxine-responsive pyridoxine phosphate oxidase deficiency epilepsy remains a challenge, with neurodevelopmental disabilities occurring in about half of the cases.

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Büyükokuroglu, Gepdiremen, Tastekin, and Örs. "Pyridoxine May Protect the Cerebellar Granular Cells Against Glutamate-Induced Toxicity." International Journal for Vitamin and Nutrition Research 77, no. 5 (September 1, 2007): 336–40. http://dx.doi.org/10.1024/0300-9831.77.5.336.

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In the present study, the possible protective effect of the pyridoxine against glutamate-induced neurotoxicity in cerebellar granular cell culture of rat pups is investigated for its therapeutic potential. Glutamate (10-7 M) was administered to cerebellar granular cell cultures that were prepared from one-day-old Sprague-Dawley rats. The neuroprotective effect of pyridoxine was examined. Pyridoxine at the doses of 10-8, 10-7, 10-6, and 10-5 M was introduced into the culture flasks before inclusion of glutamate. Pyridoxine at the doses of 10-8 M and 10-7 M significantly reduced glutamate cytotoxicity. A 10-7 M dose of pyridoxine proved to be more effective than a 10-8 M dose. The present study demonstrates that pyridoxine may protect glutamate-induced neurotoxicity. Neuroprotective effect of pyridoxine, at least in part, may result from its anti-glutamatergic activity. Pyridoxine merits further investigation as a therapeutic option in hypoxic-ischemic brain injury.

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Driskell, Judy, David Giraud, and Susan Mitmesser. "Vitamin B-6 Intakes and Plasma B-6 Vitamer Concentrations of Men and Women, 19–50 Years of Age." International Journal for Vitamin and Nutrition Research 70, no. 5 (September 1, 2000): 221–25. http://dx.doi.org/10.1024/0300-9831.70.5.221.

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The vitamin B-6 intakes and plasma B-6 vitamer levels of healthy nonsupplemented men and women, 19–24 and 25–50 years, were compared. The subjects did not take nutrient supplements or medications or use tobacco products. Subjects were grouped as follows: eight, 19–24 y men; nine, 25–50 y men; 11, 19–24 y women; and 13, 25–50 y women. The estimated vitamin B-6 intakes, obtained via 24-h recalls followed by 2-d food records, of the two groups of men were significantly higher (P < 0.05) than those of the two groups of women. Thirty-five percent of the women reported consuming less than the Estimated Average Requirement for vitamin B-6. The four gender: age groups had similar B-6 vitamer concentrations of plasma pyridoxal-5’-phosphate, 4-pyridoxic acid, pyridoxine, pyridoxamine, and pyridoxamine-5’-phosphate. Males 25–50 y had significantly higher (P < 0.05) plasma pyridoxal concentrations than the two groups of females. All subjects had pyridoxal-5’-phosphate concentrations indicative of vitamin B-6 adequacy. Generally the plasma B-6 vitamer concentrations of these men and women, 19–24 and 25–50 years of age, all having adequate vitamin B-6 status, were similar.

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Beg, M. A., J. L. Fistein, G. A. Ingram, and D. M. Storey. "Activities of glycogen phosphorylase, alanine aminotransferase and aspartate aminotransferase in adult worms of Litomosoides carinii recovered from pyridoxine deficient cotton rats (Sigmodon hispidus)." Parasitology 112, no. 2 (February 1996): 227–32. http://dx.doi.org/10.1017/s0031182000084808.

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SummaryThis paper demonstrates that the activities of glycogen phosphorylase (GP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are reduced in adult worms of the filarial nematode Litomosoides carinii recovered from pyri-doxine-deficient cotton rats when compared to worms recovered from pyridoxine-sufficient controls. GP, ALT and AST activities were determined in adult worms L. carinii recovered from cotton rat hosts over a 20-week experimental period. Activities of GP, ALT and AST in the parasite showed a direct correlation with the dietary pyridoxine intake of their host. Throughout the experiment, enzyme activities were significantly lower (P < 0·001) in worms from rats fed a pyridoxine-free diet ad libitum that in worms from rats fed either a stock colony diet, a pyridoxine-free diet ad libitum with daily supplementation of 100 μg pyridoxine or limited amounts of pyridoxine-free diet with daily supplementation of 100 μg pyridoxine. The lower than normal activity of GP, ALT, AST and other enzymes dependent on the biologically active derivative of pyridoxine, the coenzyme pyridoxal-5-phosphate (PLP), interferes with the protein, carbohydrate and lipid metabolism of L. carinii and may in part cause the reduced establishment, development and growth of the parasite in pyridoxine-deficient hosts.

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Van Arsdale, Summer, Sarah E. Yost, Chiu-Hsieh Hsu, Mary Meer, Shari Schoentag, and Shahid Habib. "Pyridoxine Deficiency After Solid Organ Transplant." Progress in Transplantation 27, no. 3 (July 4, 2017): 251–56. http://dx.doi.org/10.1177/1526924817715465.

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Objective: Pyridoxine is 1 of 8 B vitamins that assist in a variety of essential functions including immune functions. The purpose of this study was to assess the risk factors associated with low pyridoxine levels in solid organ transplantation recipients. Design: The study cohort was divided into 2 groups: (a) patients with normal pyridoxine levels or (b) patients with low pyridoxine levels. Dietary evaluation and clinical characteristics of all patients, rejection episodes, and immunosuppression were collected. Simple descriptive statistics were used to analyze the overall cohort. Results: Of the 48 patients, 29 (60%) in the study cohort were identified to have low pyridoxine levels. The mean interval between transplantation and pyridoxine level check was 910 days (standard deviation [SD] 456). The mean weight at the time of dietary consultation was 80 kg (SD 20.7). More patients in the deficient group received thymoglobulin for rejection treatment (56% vs 0%; P = .01) and were thymoglobulin recipients (78% vs 10%; odds ratio [OR] = 31.5; 95% confidence interval [CI], 2.35-422.30; P < .01). A strong correlation was identified between thymoglobulin treatment for induction and a low level of pyridoxine (correlation coefficient R = 0.6, P = .004) and between thymoglobulin treatment for rejection and a low pyridoxine level (correlation coefficient R = 0.5, P = .05). Based on multivariate logistic regression analysis, only thymoglobulin treatment (induction or rejection treatment) was significantly associated with low pyridoxine levels (OR = 19.5, 95% CI, 1.01-375.24; P < .05). Conclusions: Low levels of pyridoxine appear to be relatively common, and thymoglobulin treatments are associated with low pyridoxine levels. Prospective studies are needed to confirm and valuate the significance of these findings.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1202 (May 2008): 30. http://dx.doi.org/10.2165/00128415-200812020-00094.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1215 (August 2008): 36. http://dx.doi.org/10.2165/00128415-200812150-00112.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1279 (November 2009): 29. http://dx.doi.org/10.2165/00128415-200912790-00085.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 310 (July 1990): 10–11. http://dx.doi.org/10.2165/00128415-199003100-00054.

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&NA;. "Pyridoxine." Reactions Weekly 844, no. 844 (March 2001): 11. http://dx.doi.org/10.2165/00128415-200108440-00034.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 713 (August 1998): 10. http://dx.doi.org/10.2165/00128415-199807130-00028.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 719 (September 1998): 9–10. http://dx.doi.org/10.2165/00128415-199807190-00032.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1306 (June 2010): 32–33. http://dx.doi.org/10.2165/00128415-201013060-00113.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 724 (October 1998): 11–12. http://dx.doi.org/10.2165/00128415-199807240-00037.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 755 (June 1999): 11–12. http://dx.doi.org/10.2165/00128415-199907550-00033.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 616 (August 1996): 11. http://dx.doi.org/10.2165/00128415-199606160-00039.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1184 (January 2008): 30. http://dx.doi.org/10.2165/00128415-200811840-00093.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1131 (December 2006): 30. http://dx.doi.org/10.2165/00128415-200611310-00096.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1411 (July 2012): 37. http://dx.doi.org/10.2165/00128415-201214110-00134.

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&NA;. "Pyridoxine." Reactions Weekly &NA;, no. 1393 (March 2012): 35. http://dx.doi.org/10.2165/00128415-201213930-00124.

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Hardy, Ronald W., Edmundo Casillas, and Toshiro Masumoto. "Determination of Vitamin B6 Deficiency in Rainbow Trout (Salmo gairdneri) by Liver Enzyme Assay and HPLC Analysis." Canadian Journal of Fisheries and Aquatic Sciences 44, no. 1 (January 1, 1987): 219–22. http://dx.doi.org/10.1139/f87-030.

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Rainbow trout (Salmo gairdneri), initially averaging 125 g, were fed a complete or a pyridoxine-deficient diet for 14 wk. Vitamin B6 status was evaluated biweekly by direct measurement of liver pyridoxine and pyridoxal levels by HPLC and by determining pyridoxal-5′-phosphate-enhanced liver aspartate aminotransferase (ASAT) activity. By 14 wk, mortality had severely reduced the number of fish remaining in the pyridoxine-deficient group. At 14 wk, no significant differences in liver pyridoxine and pyridoxal levels were detected between the trout fed the complete or pyridoxine-deficient diet. Significant differences between dietary groups are found in ASAT activity in liver and percent stimulation of liver ASAT by the addition of pyridoxal-5′-phosphate after 8 wk. Clinical signs of vitamin B6 deficiency including anorexia, listlessness, frantic and erratic swimming, and ataxia were observed after 11 wk of feeding a pyridoxine-deficient diet. This study shows that vitamin B6 deficiency in rainbow trout can be readily determined weeks before signs of clinical deficiency are apparent by measuring pyridoxine-enhanced liver ASAT activity. However, liver levels of pyridoxine and pyridoxal are not sensitive indicators of vitamin B6 status.

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Baxter, Peter. "Pyridoxine-dependent and pyridoxine-responsive seizures." Developmental Medicine and Child Neurology 43, no. 06 (June 12, 2001): 416. http://dx.doi.org/10.1017/s0012162201000779.

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HINDLEY, D. "Pyridoxine dependent and pyridoxine responsive seizures." Archives of Disease in Childhood 84, no. 1 (January 1, 2001): 89g—89. http://dx.doi.org/10.1136/adc.84.1.89g.

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Baxter, Peter. "Pyridoxine-dependent and pyridoxine-responsive seizures." Developmental Medicine & Child Neurology 43, no. 6 (March 2, 2007): 416–20. http://dx.doi.org/10.1111/j.1469-8749.2001.tb00231.x.

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Kreuziger, Lisa M. Baumann, Alexandra Wolanskyj, and David P. Steensma. "Lack of Efficacy of Pyridoxine (Vitamin B6) Treatment In Acquired Idiopathic Sideroblastic Anemia, Including Refractory Anemia with Ring Sideroblasts." Blood 116, no. 21 (November 19, 2010): 2919. http://dx.doi.org/10.1182/blood.v116.21.2919.2919.

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Abstract Abstract 2919 Background: Sideroblastic anemias can be either hereditary due to congenital mutations in factors critical for iron processing or heme biosynthesis, or acquired; acquired sideroblastic anemias may be induced by alcohol or medications, but are usually idiopathic. Pyridoxine, a form of vitamin B6, plays a critical role in heme synthesis as a cofactor for δ-aminolevulinic acid synthetase (ALAS). Some subtypes of congenital sideroblastic anemia, such as those associated with mutations in the ALAS2 gene encoding the erythrocyte-expressed isoform of ALAS, may respond to pyridoxine therapy at doses ranging from 5–500 mg/day. Anecdotal reports of improvement with pyridoxine therapy in cases of acquired idiopathic sideroblastic anemia (AISA) have led to widespread clinical use of this agent in patients with refractory anemia with ring(ed) sideroblasts (RARS) and refractory cytopenia with multilineage dysplasia associated with ring sideroblasts (RCMD-RS). However, there are no systematic studies of the effectiveness of pyridoxine in AISA. Methods: We reviewed clinical and laboratory data from 231 adult patients with marrow aspirate-proven AISA (i.e., RARS or RCMD-RS, based on 2001 WHO criteria) evaluated at our institution between 1994 and 2007. Responses to pyridoxine were assessed using 2006 International Working Group (IWG) standardized criteria for MDS (erythroid response with hemoglobin increase by '1.5 mg/dl). The relationship between response to pyridoxine and disease subtype or International Prognostic Scoring System (IPSS) stratification was assessed using χ2 test, using a p-value limit of <0.05 for statistical significance. Results: 86 of the 231 patients (42%) were treated with pyridoxine for an average of 19 months (range 1–114 months) at a mean dose of 167 mg/day (range 50–600 mg/day). Sufficient follow-up data to allow response evaluation were available from 74 (86%) of the 86 patients who received pyridoxine. Only 5/86 patients (6.8%) receiving pyridoxine met IWG response criteria for hematological improvement, but 3 of these 5 patients also received erythropoetin and 1 also received prednisone concomitantly with pyridoxine therapy. Therefore, only 1/86 (1.4%) patient's improvement in hemoglobin could be attributed to pyridoxine monotherapy. ALAS2 genotype data were not available from these 5 patients. The dose of pyridoxine was not associated with response to therapy (187.5 mg daily in responders vs. 157 mg daily in non-responders (p=0.60). Patients with RCMD-RS were more likely to be treated with vitamin B6 compared to patients with RARS (p=<0.001), possibly because of more severe anemia, but response to pyridoxine did not differ significantly between subtypes (3/49 vs. 2/25, response in RARS vs. RCMD-RS; p=0.76). Among the 74 evaluable patients, 3/46 patients in the low IPSS risk group responded to pyridoxine, compared to 2/24 of patients in the Intermediate-1 risk group and 0/4 in the Intermediate-2 risk group (p=0.82). Adverse effects associated with pyridoxine included new onset of irreversible symptomatic peripheral neuropathy in 2/86 patients (2.3%). Conclusions: Pyridoxine is commonly prescribed to patients with AISA in clinical practice, and this agent is often continued for a long period of time despite lack of evidence of objective response. Pyridoxine is an ineffective therapy in AISA that induces symptomatic peripheral neuropathy in some patients. Therefore, pyridoxine therapy should be limited to patients with known or suspected congenital mutations that confer pyridoxine responsiveness, and therapeutic trials should be brief to avoid adverse effects. Disclosures: No relevant conflicts of interest to declare.

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Ehrenshaft, Marilyn, and Margaret E. Daub. "Isolation of PDX2, a Second Novel Gene in the Pyridoxine Biosynthesis Pathway of Eukaryotes, Archaebacteria, and a Subset of Eubacteria." Journal of Bacteriology 183, no. 11 (June 1, 2001): 3383–90. http://dx.doi.org/10.1128/jb.183.11.3383-3390.2001.

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ABSTRACT In this paper we describe the isolation of a second gene in the newly identified pyridoxine biosynthesis pathway of archaebacteria, some eubacteria, fungi, and plants. Although pyridoxine biosynthesis has been thoroughly examined in Escherichia coli, recent characterization of the Cercospora nicotianae biosynthesis gene PDX1 led to the discovery that most organisms contain a pyridoxine synthesis gene not found in E. coli. PDX2was isolated by a degenerate primer strategy based on conserved sequences of a gene specific to PDX1-containing organisms. The role of PDX2 in pyridoxine biosynthesis was confirmed by complementation of two C. nicotianae pyridoxine auxotrophs not mutant in PDX1. Also, targeted gene replacement of PDX2 in C. nicotianae results in pyridoxine auxotrophy. Comparable to PDX1, PDX2 homologues are not found in any of the organisms with homologues to theE. coli pyridoxine genes, but are found in the same archaebacteria, eubacteria, fungi, and plants that containPDX1 homologues. PDX2 proteins are less well conserved than their PDX1 counterparts but contain several protein motifs that are conserved throughout all PDX2 proteins.

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Park, Channy, Hyewon Lim, Sung K. Moon, and Raekil Park. "Pyridoxine Preferentially Induces Auditory Neuropathy Through Mitochondrial Dysfunction and Endoplasmic Reticulum Stress-Mediated Apoptosis." Annals of Otology, Rhinology & Laryngology 128, no. 6_suppl (May 15, 2019): 117S—124S. http://dx.doi.org/10.1177/0003489419836116.

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Objectives: Auditory neuropathy due to toxicity mechanism of pyridoxine has not yet been fully documented. Therefore, the present study explored a direct mechanism underlying the effects of pyridoxine on auditory neuropathy in organ of Corti (OC) explants ex vivo and cochlear neuroblast cell line, VOT-33 in vitro. Methods: Primary OC explants containing spiral ganglion neurons and cultured VOT-33 cells were treated with pyridoxine. Results: In nerve fiber of primary OC explants, pyridoxine decreased staining for NF200, a neuro-cytoskeletal protein. We also found that pyridoxine-induced VOT-33 apoptosis, as indicated by accumulation of the sub-G0/G1 fraction, caspase-3 activation, and PARP cleavage. In addition, pyridoxine induced reactive oxygen species (ROS) generation and alteration of mitochondrial membrane potential transition (MPT), including Bcl-2 family protein expression and consequently Ca2+ accumulation and changes of endoplasmic reticulum (ER) stress-related protein expression such as phospho-PERK, caspase-12, Grp78, and CHOP. Conclusion: Pyridoxine preferentially induced severe cell death on nerve fiber in primary OC explants and markedly increased apoptotic cell death via mitochondria-mediated ER stress in VOT-33 cells.

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Marino, Silvia, Giovanna Vitaliti, Simona Domenica Marino, Piero Pavone, Simona Provvidenti, Catia Romano, and Raffaele Falsaperla. "Pyridoxine Add-On Treatment for the Control of Behavioral Adverse Effects Induced by Levetiracetam in Children: A Case-Control Prospective Study." Annals of Pharmacotherapy 52, no. 7 (February 14, 2018): 645–49. http://dx.doi.org/10.1177/1060028018759637.

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Background: Few studies on adult and pediatric patients have shown pyridoxine efficacy as additional therapy for those receiving levetiracetam (LEV) to prevent and mitigate behavioral adverse effects (BAEs). Objective: The aim of our study was to analyze the safety and efficacy of pyridoxine supplementation in the prevention of LEV adverse effects, including suicidal ideation. Methods: This randomized, case-control trial included patients receiving LEV as monotherapy treatment. Patients were subdivided into 2 groups, according to whether they were treated with LEV only (group 1) or LEV with supplemental pyridoxine (group 2). Results: In both cohorts, the most frequent BAEs were irritability/aggression followed by depression and confusion. Those patients (92%) who initiated pyridoxine after 1 month of LEV treatment did not need to change or suspend LEV ( P < 0.001), and BAE improved after 9.06 ± 3.05 days of pyridoxine supplementation. None of the patients complained of symptoms of pyridoxine toxicity, and no new adverse effects of LEV off-label were reported. Conclusions: In our study, we found pyridoxine to be safe and effective in controlling LEV-induced BAEs in children.

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Khaziev, Rail, Nikita Shtyrlin, Roman Pavelyev, Raushan Nigmatullin, Raylya Gabbasova, Denis Grishaev, Anna Shtro, et al. "Synthesis and Antimicrobial Activity of Adamantyl Substituted Pyridoxine Derivatives." Letters in Drug Design & Discovery 16, no. 12 (November 8, 2019): 1360–69. http://dx.doi.org/10.2174/1570180816666190911150705.

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Background: Adamantane derivatives possess multiple pharmacological activities such as antiviral, anticancer, antimycobacterial, antidiabetic, antiparkinsonian and others. The interest of medicinal chemists in adamantane compounds is due to their unique spatial structure, high lipophilicity, and carbon cage rigidity. As a result, these molecules can easily penetrate biological lipid membranes and often have unique target-specific activity profile. Another pharmacophore studied in this work is pyridoxine (vitamin B6). Pyridoxine plays highly important roles in living cells as a key cofactor of many enzymes. On the other hand, its molecular scaffold is a valuable structural platform which has led to the development of several launched drugs (Pyritinol, Pirisudanol, Cycletanine, Mangafodipir) and a wide number of preclinical and clinical drug candidates. Objective: The objective of this study is a synthesis of pyridoxine-adamantane and pyridoxinecyclooctane dipharmacophore molecules. The underlying idea was to assess the antibacterial and antiviral potential of such dipharmacophores, based on multiple examples of promising antiinfective agents which have in their structures adamantane and pyridoxine moieties. Another specific reason was to explore the ability of pyridoxine pharmacophore to suppress the potential of microbial pathogens to develop resistance to drug molecules. Methods: In this study, a series of pyridoxine-adamantane and pyridoxine-cyclooctane dipharmacophore molecules were synthesized based on reactions of three different cycloalkyl amines with the corresponding electrophilic derivatives of pyridoxine aldehydes, chlorides and acetates. All synthesized compounds have been tested for their in vitro activity against M. tuberculosis H37Rv strain and H3N2 (A/Aichi/2/68) influenza virus. Results: Series of pyridoxine-adamantane and pyridoxine-cyclooctane dipharmacophore molecules were synthesized based on reactions of three different cycloalkylamines with the corresponding electrophilic derivatives of pyridoxine aldehydes, chlorides and acetates. Reaction of cycloalkylamines with pyridoxine derivatives, in which meta-hydroxyl and ortho-hydroxymethyl groups are protected by acetyl groups, represents a useful alternative to reductive amination of aldehydes and nucleophilic substitution of alkyl halides. According to a tentative mechanism, it proceeds via paraand ortho-pyridinone methides which readily react with nucleophiles. None of the synthesized dipharmacophore compounds showed activity against M. tuberculosis H37Rv strain. At the same time, three compounds demonstrated some antiviral activity against H3N2 (A/Aichi/2/68) influenza virus (EC50 52-88 µg/mL) that was comparable to the activity of Amantadine, though lower than the activity of Rimantadine. The results of this work can be useful in the design of physiologically active derivatives of pyridoxine and adamantane. Conclusion: The results of this work can be useful in the design of physiologically active derivatives of pyridoxine and adamantane.

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Nayak, Gopal, Mahendra Kumar Trivedi, Alice Branton, Dahryn Trivedi, and Snehasis Jana. "Consciousness Energy Healing Treatment: Impact on the Physicochemical and Thermal Properties of Pyridoxine HCl." International Journal of Nutrition 4, no. 2 (May 29, 2019): 26–37. http://dx.doi.org/10.14302/issn.2379-7835.ijn-19-2831.

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Pyridoxine HCl plays an important role in the human body as a coenzyme in the synthesis process of amino acids and neurotransmitters such as serotonin, norepinephrine, aminolevulinic acid, sphingolipids, etc. The objective of this study was to determine the effect of the Trivedi Effect®-Consciousness Energy Healing Treatment on the various physicochemical and thermal properties of pyridoxine HCl using various analytical techniques such. The study plan involved dividing the pyridoxine HCl sample into two parts, in which, the first part was not given any treatment (control sample), while the second part was provided the Consciousness Energy Healing Treatment by a renowned Biofield Energy Healer, Gopal Nayak and named as the Biofield Energy Treated pyridoxine. The particle size values of the treated pyridoxine was altered by -19.51% (d10), -11.92% (d50), 2.46% (d90), and -2.44% {D(4,3)}; whereas, the surface area was significantly increased by 18.92%, compared to the control sample. The powder X-ray diffraction data showed the remarkable increase in the peak intensities and crystallite sizes of the treated pyridoxine in the range from 8.81% to 21.57% and 9.64% to 17.85%, respectively compared to the control sample. Moreover, the treated pyridoxine also showed an increase in the average crystallite size by 13.69%, compared to the control sample. The total weight loss of the treated pyridoxine was significantly reduced by 13.35% during the thermal degradation; however, the residue weight was increased by 29.48% after degradation, in comparison to the control sample. The maximum thermal degradation temperature of the treated pyridoxine corresponding to 1st and 2nd peak was altered by 4.37% and 2.24%, respectively than the control sample. The latent heat of fusion of the treated pyridoxine was significantly increased by 5.89% compared to the control sample. Hence, it was assumed that the Trivedi Effect®-Consciousness Energy Healing Treatment might form a new polymorph of pyridoxine HCl that might be helpful in designing more efficacious pharmaceutical/nutraceutical product due to its better solubility, absorption, bioavailability, and thermal stability than the untreated sample.

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Velásquez, Margarita, Darío Méndez, and Carlos Moneriz. "Pyridoxine Decreases Oxidative Stress on Human Erythrocyte Membrane Protein in vitro." Open Biochemistry Journal 13, no. 1 (May 31, 2019): 37–44. http://dx.doi.org/10.2174/1874091x01913010037.

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Background: Pyridoxine has reduction and prevention against the levels of reactive oxygen species in in vitro studies. However, the biochemical mechanism that explains this behavior has not yet been fully clarified. Objective: To evaluate the effect of pyridoxine against oxidative damage on the membrane of human erythrocytes. Methods: Cumene hydroperoxide was used to induce oxidative stress in protein and lipid. Human erythrocytes were incubated with pyridoxine and cumene hydroperoxide, either alone or together for 8 h. Oxidative damage was determined by measuring lipid peroxidation and membrane protein carbonylation. Results: The results indicate that the malondialdehyde concentration decreased with increasing concentration of pyridoxine. The membrane protein content also decreased with increasing concentration of vitamin B6, which was confirmed by the decreased signal intensity in the western blot when compared to control without pyridoxine. Results demonstrate that pyridoxine can significantly decrease lipid peroxidation and protein carbonylation in red cell membrane exposed to high concentrations of oxidant agent. Conclusion: Pyridoxine showed a protective effect against the oxidative stress in human erythrocytes in vitro, inhibiting the carbonylation and the oxidative damage of erythrocyte membrane proteins. To date, such an effect has not yet been reported in terms of protein oxidation.

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Srinivasan, Padmanabhan, Vignesh Ramesh, Jie Wu, Christopher Heskett, Brian D. Chu, and Hamid M. Said. "Pyridoxine and pancreatic acinar cells: transport physiology and effect on gene expression profile." American Journal of Physiology-Cell Physiology 317, no. 6 (December 1, 2019): C1107—C1114. http://dx.doi.org/10.1152/ajpcell.00225.2019.

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Pyridoxine (vitamin B6), an essential micronutrient for normal cell physiology, plays an important role in the function of the exocrine pancreas. Pancreatic acinar cells (PACs) obtain vitamin B6 from circulation, but little is known about the mechanism involved in the uptake process; limited information also exists on the effect of pyridoxine availability on the gene expression profile in these cells. We addressed both these issues in the current investigation using mouse-derived pancreatic acinar 266-6 cells (PAC 266-6) and human primary PACs (hPACs; obtained from organ donors), together with appropriate physiological and molecular (RNA-Seq) approaches. The results showed [3H]pyridoxine uptake to be 1) pH and temperature (but not Na+) dependent, 2) saturable as a function of concentration, 3) cis-inhibited by unlabeled pyridoxine and its close structural analogs, 4) trans-stimulated by unlabeled pyridoxine, 5) regulated by an intracellular Ca2+/calmodulin-mediated pathway, 6) adaptively-regulated by extracellular substrate (pyridoxine) availability, and 7) negatively impacted by exposure to cigarette smoke extract. Vitamin B6 availability was found (by means of RNA-Seq) to significantly (FDR < 0.05) modulate the expression profile of many genes in PAC 266-6 cells (including those that are relevant to pancreatic health and development). These studies demonstrate, for the first time, the involvement of a regulatable and specific carrier-mediated mechanism for pyridoxine uptake by PACs; the results also show that pyridoxine availability exerts profound effects on the gene expression profile in mammalian PACs.

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Montpetit, V. J., S. Dancea, L. Tryphonas, and D. F. Clapin. "Membrane-associated microtubular areays induced in proximal myelinated processes of dorsal root ganglia by large doses of vitamin B6." Proceedings, annual meeting, Electron Microscopy Society of America 44 (August 1986): 368–69. http://dx.doi.org/10.1017/s0424820100143468.

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Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.

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Millichap, J. Gordon. "Low-Dose Pyridoxine Masks Pyridoxine-Dependent Seizures." Pediatric Neurology Briefs 15, no. 7 (July 1, 2001): 52. http://dx.doi.org/10.15844/pedneurbriefs-15-7-4.

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Stolz, Jürgen, Heike J. P. Wöhrmann, and Christian Vogl. "Amiloride Uptake and Toxicity in Fission Yeast Are Caused by the Pyridoxine Transporter Encoded by bsu1+ (car1+)." Eukaryotic Cell 4, no. 2 (February 2005): 319–26. http://dx.doi.org/10.1128/ec.4.2.319-326.2005.

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ABSTRACT Amiloride, a diuretic drug that acts by inhibition of various sodium transporters, is toxic to the fission yeast Schizosaccharomyces pombe. Previous work has established that amiloride sensitivity is caused by expression of car1 +, which encodes a protein with similarity to plasma membrane drug/proton antiporters from the multidrug resistance family. Here we isolated car1 + by complementation of Saccharomyces cerevisiae mutants that are deficient in pyridoxine biosynthesis and uptake. Our data show that Car1p represents a new high-affinity, plasma membrane-localized import carrier for pyridoxine, pyridoxal, and pyridoxamine. We therefore propose the gene name bsu1 + (for vitamin B6 uptake) to replace car1 +. Bsu1p displays an acidic pH optimum and is inhibited by various protonophores, demonstrating that the protein works as a proton symporter. The expression of bsu1 + is associated with amiloride sensitivity and pyridoxine uptake in both S. cerevisiae and S. pombe cells. Moreover, amiloride acts as a competitor of pyridoxine uptake, demonstrating that both compounds are substrates of Bsu1p. Taken together, our data show that S. pombe and S. cerevisiae possess unrelated plasma membrane pyridoxine transporters. The S. pombe protein may be structurally related to the unknown human pyridoxine transporter, which is also inhibited by amiloride.

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Zavariyan, Abolfazl Masoumi, Mojtaba Yousefi Rad, and Mohsen Asghari. "Effect of seed priming by pyridoxine on germination and biochemical indices in Silybum marianum L. under drought stress." International Journal of Life Sciences 9, no. 1 (February 7, 2015): 17–22. http://dx.doi.org/10.3126/ijls.v9i1.11921.

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In order to investigation of the effect of seed priming by pyridoxine on germination and biochemical indices of Silybum marianum L. under drought stress, factorial experiment based on completely randomized design with two factor includingdifferent concentrations of pyridoxine including 0, 0.02% and 0.04% and different levels of drought stress including 0, -6 and -12 bar at three replicates was performed. The results indicated that drought stress affected measured indices at P<0.01 and pyridoxine significantly affected germination percentage and rate, seed vigor, mean time germination, seedling length and dry weight at P<0.01 and peroxidase activity at P<0.05. Interaction between the drought stress and pyridoxine was significantly (P<0.05) affected of germination rate and seed vigor. The results showed that with increasing drought stress, germination indices were decreased and biochemical indices were increased. Seed priming with pyridoxine cause to improvement of germination indices and decreases biochemical indices. According to the results, seed priming with 0.04% pyridoxine cause to improvement of germination indices at drought stress conditions.DOI: http://dx.doi.org/10.3126/ijls.v9i1.11921 International Journal of Life Sciences Vol.9(1) 2015 17-22

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Usov, K. I., T. A. Guskova, and G. G. Yushkov. "ROLE OF PYRIDOXINE HYDROCHLORIDE IN THE DEVELOPMENT OF TOLERANCE TO THE TOXIC ACTION OF ISONIAZID IN ANIMALS." Tuberculosis and Lung Diseases 96, no. 6 (July 19, 2018): 51–57. http://dx.doi.org/10.21292/2075-1230-2018-96-6-51-57.

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The objective of the study:to assess the impact of continuous and course (intermittent) use of pyridoxine hydrochloride in combination with isoniazid on the rate of tolerance development in rats under conditions of a toxicological experiment.Subjects and methods. Isoniazid (tablets, 0.3 g.) and the substance of pyridoxine hydrochloride (powder, 50.0 g.) were used for the experiment. Male white rats were used as experimental biological models.Main results. The article presents data on experimental study of toxicologic tolerance of rats to the anti-tuberculosis drug of isoniazid with its administration simultaneously with pyridoxine hydrochloride. The obtained data provided the evidence about the impact of pyridoxine hydrochloride on the rate of how fast the host developed the tolerance to the toxic action of isoniazid. It has been proved that intermittent (by short courses) use of pyridoxine hydrochloride with isoniazid versus its continuous use resulted in a slower development of toxicological tolerance to isoniazid in rats.

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Journal articles on the topic 'Pyridosin'

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