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Bioscience, Biotechnology, and... Jan 2009Enzymatic syntheses of pyridoxine glycosides were carried out in di-isopropyl ether organic medium using beta-glucosidase isolated from sweet almond. Optimum conditions...
Enzymatic syntheses of pyridoxine glycosides were carried out in di-isopropyl ether organic medium using beta-glucosidase isolated from sweet almond. Optimum conditions determined for the reaction with D-glucose were 40% (w/w D-glucose) beta-glucosidase at 0.18 mM (1.8 ml) of pH 5 acetate buffer over a 72 h incubation period. Of 11 carbohydrates employed, beta-glucosidase gave 7-O-(alpha-D-glucopyranosyl)pyridoxine 5a, 7-O-(beta-D-glucopyranosyl)pyridoxine 5b, 6-O-(alpha-D-glucopyranosyl)pyridoxine 5c, 7-O-(alpha-D-galactopyranosyl)pyridoxine 6a, 7-O-(beta-D-galactopyranosyl)pyridoxine 6b, 6-O-(alpha-D-galactopyranosyl)pyridoxine 6c, 7-O-(alpha-D-mannopyranosyl)pyridoxine 7a, 7-O-(beta-D-mannopyranosyl)pyridoxine 7b, and 6-O-(alpha-D-mannopyranosyl)pyridoxine 7c in yields ranging from 23 to 40%.
Topics: Carbohydrates; Glycosides; Prunus; Pyridoxine; Solvents; beta-Glucosidase
PubMed: 19129657
DOI: 10.1271/bbb.80463 -
Pakistan Journal of Pharmaceutical... Sep 2013Vitamin B6 (pyridoxine) is closely associated with the functions of the nervous, immune and endocrine systems. It also participates in the metabolic processes of... (Review)
Review
Vitamin B6 (pyridoxine) is closely associated with the functions of the nervous, immune and endocrine systems. It also participates in the metabolic processes of proteins, lipids and carbohydrates. Pyridoxine deficiency may result in neurological disorders including convulsions and epileptic encephalopathy and may lead to infant abnormalities. The Intravenous administration of pyridoxine to patients results in a dramatic cessation of seizures. A number of analytical methods were developed for the determination of pyridoxine in different dosage forms, food materials and biological fluids. These include UV spectrometric, spectrofluorimetric, mass spectrometric, thin-layer and high-performance liquid chromatographic, electrophoretic, electrochemical and enzymatic methods. Most of these methods are capable of determining pyridoxine in the presence of other vitamins and complex systems in µg quantities. The development and applications of these methods in pharmaceutical and clinical analysis mostly during the last decade have been reviewed.
Topics: Animals; Biomarkers; Chemistry Techniques, Analytical; Humans; Pyridoxine; Vitamin B 6 Deficiency
PubMed: 24035968
DOI: No ID Found -
Medicinal Chemistry (Shariqah (United... 2015A series of 26 quaternary ammonium pyridoxine derivatives were synthesized and their cytotoxicity and antibacterial activities against clinically relevant bacterial...
A series of 26 quaternary ammonium pyridoxine derivatives were synthesized and their cytotoxicity and antibacterial activities against clinically relevant bacterial strains were tested in vitro. The antibacterial activity of mono-ammonium salts increased with the rise of the lipophilicity and compound 3,3,5-trimethyl-8,8-dioctyl-1,7,8,9-tetrahydro-[1,3]dioxino[5,4-d]pyrrolo[3,4-b]pyridin-8-ium chloride (2d) reaches a maximum among them. Bis-ammonium salt of pyridoxine 4 with two dimethyloctylamine groups also demonstrated high antibacterial activity despite lower lipophilicity. The results of MTT assay indicated that HEK 293 cells were more sensitive than HSF to quaternary ammonium pyridoxine derivatives. Compounds 2d and 4 did not induce the damage of the DNA and might be of interest in the development of new antimicrobials.
Topics: Anti-Bacterial Agents; Bacteria; Chemistry Techniques, Synthetic; Hydrophobic and Hydrophilic Interactions; Microbial Sensitivity Tests; Mutagenicity Tests; Pyridoxine; Quaternary Ammonium Compounds
PubMed: 25938426
DOI: 10.2174/1573406411666150504122930 -
Archives of Biochemistry and Biophysics Feb 1984Uptake of [3H]pyridoxine by isolated rat hepatocytes was detected at substrate concentrations as low as 0.5 microM. At this concentration, an initial uptake rate was...
Uptake of [3H]pyridoxine by isolated rat hepatocytes was detected at substrate concentrations as low as 0.5 microM. At this concentration, an initial uptake rate was 1.87 +/- 0.17 pmol/10(6) cells X min at 37 degrees C. Both the initial and a subsequent much slower pyridoxine accumulation were strongly inhibited by low temperature as well as by 10 mM ethionine, which competes for available ATP, or 1 microM carbonylcyanide-p-trifluoromethoxyphenylhydrazone, which inhibits oxidative phosphorylation and the supply of ATP. The uptake process is apparently insensitive to 1 mM ouabain and is Na+ independent. The initial uptake rate was saturable at higher concentrations of [3H]pyridoxine with an apparent Km of 28 +/- 8 microM and Vmax of 106 +/- 27 pmol/10(6) cells X min. The Km value corresponds to that reported for pyridoxine as a substrate of pyridoxal kinase. Moreover, the transport process was inhibited by structural analogs of [3H]pyridoxine even at concentrations equimolar to the normal substrate. The established order of inhibitory effectiveness, 4'-deoxypyridoxine greater than unlabeled pyridoxine greater than 5'-deoxypyridoxine, is in agreement with known properties of the kinase. It is concluded that pyridoxine uptake probably occurs by diffusion, simple or facilitated, followed by metabolic trapping due to pyridoxal kinase-catalyzed phosphorylation. Pyridoxine deficiency had no significant effect on uptake of this B6 vitamer by hepatocytes.
Topics: Adenosine Triphosphate; Animals; Biological Transport; Cold Temperature; Kinetics; Liver; Male; Pyridoxal Kinase; Pyridoxine; Rats
PubMed: 6703693
DOI: 10.1016/0003-9861(84)90143-7 -
Annals of the New York Academy of... 1990Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most... (Review)
Review
Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100-150 mg/day have shown minimal or no toxicity in five- to 10-year studies. Women self-medicating for PMS taking 500 to 5000 mg/day have shown peripheral neuropathy within one to three years. It would appear from this retrospective analysis that pyridoxine is safe at doses of 100 mg/day or less in adults. In children there is not enough data to make any sort of suggestion. Because the major neurologic complication is a peripheral neuropathy and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition.
Topics: Animals; Carpal Tunnel Syndrome; Chronic Disease; Depression; Headache; Humans; Movement Disorders; Nervous System Diseases; Pain; Peripheral Nervous System Diseases; Pyridoxine; Seizures
PubMed: 2162644
DOI: 10.1111/j.1749-6632.1990.tb28058.x -
Neurology Nov 1987We report two patients who developed an acute, profound, and permanent sensory deficit after treatment with massive doses of parenteral pyridoxine. Aside from rapid...
We report two patients who developed an acute, profound, and permanent sensory deficit after treatment with massive doses of parenteral pyridoxine. Aside from rapid onset, their clinical picture resembles that described in chronic pyridoxine neurotoxicity. It also is consonant with experimental models of acute pyridoxine intoxication and is probably secondary to a sensory ganglion neuronopathy. These patients also had transient autonomic dysfunction, mild weakness, nystagmus, lethargy, and respiratory depression. These previously undocumented features may be attributable to either the preservative used in the parenteral pyridoxine preparation or to the exceptionally high doses of pyridoxine these patients received.
Topics: Acute Disease; Adult; Female; Humans; Male; Mushroom Poisoning; Peripheral Nervous System Diseases; Pyridoxine; Time Factors
PubMed: 2823181
DOI: 10.1212/wnl.37.11.1729 -
Seizure May 2024The main objective of this study was to evaluate the neurological consequences of delayed pyridoxine administration in patients diagnosed with Pyridoxin Dependent... (Observational Study)
Observational Study
BACKGROUND
The main objective of this study was to evaluate the neurological consequences of delayed pyridoxine administration in patients diagnosed with Pyridoxin Dependent Epilepsies (PDE).
MATERIALS AND METHODS
We reviewed 29 articles, comprising 52 genetically diagnosed PDE cases, ensuring data homogeneity. Three additional cases were included from the General Pediatric Operative Unit of San Marco Hospital. Data collection considered factors like age at the first seizure's onset, EEG reports, genetic analyses, and more. Based on the response to first-line antiseizure medications, patients were categorized into four distinct groups. Follow-up evaluations employed various scales to ascertain neurological, cognitive, and psychomotor developments.
RESULTS
Our study includes 55 patients (28 males and 27 females), among whom 15 were excluded for the lack of follow-up data. 21 patients were categorized as "Responder with Relapse", 11 as "Resistant", 6 as "Pyridoxine First Approach", and 2 as "Responders". The neurological outcome revealed 37,5 % with no neurological effects, 37,5 % showed complications in two developmental areas, 15 % in one, and 10 % in all areas. The statistical analysis highlighted a positive correlation between the time elapsed from the administration of pyridoxine after the first seizure and worse neurological outcomes. On the other hand, a significant association was found between an extended latency period (that is, the time that elapsed between the onset of the first seizure and its recurrence) and worse neurological outcomes in patients who received an unfavorable score on the neurological evaluation noted in a subsequent follow-up.
CONCLUSIONS
The study highlights the importance of early recognition and intervention in PDE. Existing medical protocols frequently overlook the timely diagnosis of PDE. Immediate administration of pyridoxine, guided by a swift diagnosis in the presence of typical symptoms, might improve long-term neurological outcomes, and further studies should evaluate the outcome of PDE neonates promptly treated with Pyridoxine.
Topics: Humans; Pyridoxine; Epilepsy; Male; Female; Anticonvulsants; Infant, Newborn; Vitamin B Complex; Infant
PubMed: 38735085
DOI: 10.1016/j.seizure.2024.04.012 -
Lancet (London, England) Sep 1946
Topics: Epilepsy; Humans; Pyridoxine; Vitamin B 6
PubMed: 20997253
DOI: 10.1016/s0140-6736(46)90842-2 -
Georgian Medical News Dec 2007The purpose of the study was to investigate the role of vitamin B6 in the process of melatonin biosynthesis. 30 laboratory white rats were divided into two groups -...
The purpose of the study was to investigate the role of vitamin B6 in the process of melatonin biosynthesis. 30 laboratory white rats were divided into two groups - experimental and control groups. The animals in the first group were treated with vitamin B6 injection. Every other day at 22 00, melatonin concentration was defined by means of ELISA. The experiment has lasted for two months. At the end of the experiment, the plasma level of melatonin increased by 35,95% in the first group of animals in comparison with the second control group. It is found that, B6 vitamin injections strengthens melatonin biosynthesis; consequently strengthening of melatonin biosynthesis influences positive therapeutic effects,; one of the reasons for pathological processes, developed in organism on the background of B6 vitamin deficiency, is reduction of endogen melatonin production.
Topics: Animals; Injections; Male; Melatonin; Pyridoxine; Rats
PubMed: 18250494
DOI: No ID Found -
The Journal of Organic Chemistry Feb 2013Vitamin B6 is involved in a variety of enzymatic transformations. Some recent findings also indicate an antioxidant role of the vitamin in biological systems. We set out...
Vitamin B6 is involved in a variety of enzymatic transformations. Some recent findings also indicate an antioxidant role of the vitamin in biological systems. We set out to turn pyridoxine (1a) into a catalytic chain-breaking and hydroperoxide-decomposing antioxidant by replacing the 2-methyl substituent with an alkyltelluro group. Target molecules 12 and derivatives 14, 17, 18, and 20 thereof were accessed by subjecting suitably substituted 2-halopyridin-3-ols to aromatic substitution using sodium alkanetellurolates as nucleophiles and then LAH-reduction of ester groups. The novel pyridoxine compounds were found to inhibit azo-initiated peroxidation of linoleic acid an order of magnitude more efficiently than α-tocopherol in a water/chlorobenzene two-phase system containing N-acetylcysteine as a reducing agent in the aqueous phase. The most lipid-soluble pyridoxine derivative 20c was regenerable and could inhibit peroxidation for substantially longer time (>410 min) than α-tocopherol (87 min). The chalcogen-containing pyridoxines could also mimic the action of the glutathione peroxidase enzymes. Thus, compound 20a catalyzed reduction of hydrogen peroxide three times more efficiently than Ebselen in the presence of glutathione as a stoichiometric reducing agent.
Topics: Acetylcysteine; Antioxidants; Catalysis; Hydrogen Peroxide; Pyridoxine; Vitamin B 6
PubMed: 23316758
DOI: 10.1021/jo3024297