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| pyridoxine |
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| CHEBI:16709 |
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| A hydroxymethylpyridine with hydroxymethyl groups at positions 4 and 5, a hydroxy group at position 3 and a methyl group at position 2. The 4-methanol form of vitamin B6, it is converted intoto pyridoxal phosphate which is a coenzyme for synthesis of amino acids, neurotransmitters, sphingolipids and aminolevulinic acid. |
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This entity has been manually annotated by the ChEBI Team.
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CHEBI:8671, CHEBI:14981, CHEBI:26429
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| ChemicalBook:CB8197940, ChemicalBook:CB0197939, eMolecules:593675, ZINC000000049154 |
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Molfile
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SDF
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more structures >>
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| Pyridoxine (PN) is a form of vitamin B6 found commonly in food and used as a dietary supplement. As a supplement it is used to treat and prevent pyridoxine deficiency, sideroblastic anaemia, pyridoxine-dependent epilepsy, certain metabolic disorders, side effects or complications of isoniazid use, and certain types of mushroom poisoning. It is used by mouth or by injection.
It is usually well tolerated. Occasionally side effects include headache, numbness, and sleepiness. Normal doses are safe during pregnancy and breastfeeding. Pyridoxine is in the vitamin B family of vitamins. It is required by the body to metabolise amino acids, carbohydrates, and lipids. Sources in the diet include meat, fish, fruit, vegetables, and grain. |
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Read full article at Wikipedia
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| InChI=1S/C8H11NO3/c1-5-8(12)7(4-11)6(3-10)2-9-5/h2,10-12H,3-4H2,1H3 |
| LXNHXLLTXMVWPM-UHFFFAOYSA-N |
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Saccharomyces cerevisiae
(NCBI:txid4932)
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Source: yeast.sf.net
See:
PubMed
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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Homo sapiens
(NCBI:txid9606)
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Found in
blood
(UBERON:0000178).
See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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Found in
urine
(BTO:0001419).
See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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From MetaboLights
See:
MetaboLights Study
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Homo sapiens
(NCBI:txid9606)
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From MetaboLights
See:
MetaboLights Study
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Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
Saccharomyces cerevisiae metabolite
Any fungal metabolite produced during a metabolic reaction in Baker's yeast (Saccharomyces cerevisiae ).
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
cofactor
An organic molecule or ion (usually a metal ion) that is required by an enzyme for its activity. It may be attached either loosely (coenzyme) or tightly (prosthetic group).
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
water-soluble vitamin (role)
Any vitamin that dissolves in water and readily absorbed into tissues for immediate use. Unlike the fat-soluble vitamins, they are not stored in the body and need to be replenished regularly in the diet and will rarely accumulate to toxic levels since they are quickly excreted from the body via urine.
(via B vitamin )
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nutraceutical
A product in capsule, tablet or liquid form that provide essential nutrients, such as a vitamin, an essential mineral, a protein, an herb, or similar nutritional substance.
(via B vitamin )
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View more via ChEBI Ontology
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4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol
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pyridoxina
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WHO MedNet
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pyridoxine
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WHO MedNet
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pyridoxine
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WHO MedNet
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pyridoxinum
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WHO MedNet
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2-methyl-3-hydroxy-4,5-bis(hydroxymethyl)pyridine
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ChemIDplus
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2-methyl-3-hydroxy-4,5-di(hydroxymethyl)pyridine
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ChemIDplus
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2-Methyl-3-hydroxy-4,5-dihydroxymethyl-pyridin
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ChemIDplus
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2-methyl-3-hydroxy-4,5-dihydroxymethylpyridine
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NIST Chemistry WebBook
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2-methyl-4,5-bis(hydroxymethyl)-3-hydroxypyridine
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ChemIDplus
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2-methyl-4,5-dimethylol-pyridin-3-ol
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ChEBI
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3-hydroxy-2-picoline-4,5-dimethanol
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ChemIDplus
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3-hydroxy-4,5-bis(hydroxymethyl)-2-methylpyridine
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ChEBI
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3-hydroxy-4,5-dimethylol-α-picoline
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NIST Chemistry WebBook
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4,5-bis(hydroxymethyl)-2-methyl-pyridin-3-ol
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ChEBI
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5-hydroxy-6-methyl-3,4-pyridinedimethanol
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NIST Chemistry WebBook
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piridossina
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HMDB
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pyridoxine
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UniProt
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Pyridoxol
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KEGG COMPOUND
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pyridoxolum
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HMDB
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vitamin B6
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NIST Chemistry WebBook
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1025
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ChemSpider
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2836
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DrugCentral
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C00001551
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KNApSAcK
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C00314
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KEGG COMPOUND
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D08454
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KEGG DRUG
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DB00165
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DrugBank
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FDB000574
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FooDB
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HMDB0000239
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HMDB
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LSM-5324
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LINCS
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Pyridoxine
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Wikipedia
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PYRIDOXINE
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MetaCyc
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UEG
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PDBeChem
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| View more database links |
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139854
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Reaxys Registry Number
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Reaxys
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563676
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Gmelin Registry Number
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Gmelin
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65-23-6
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CAS Registry Number
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ChemIDplus
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65-23-6
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CAS Registry Number
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NIST Chemistry WebBook
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Richts B, Commichau FM (2021)
Underground metabolism facilitates the evolution of novel pathways for vitamin B6 biosynthesis.
Applied microbiology and biotechnology 105, 2297-2305 [PubMed:33665688]
[show Abstract]
The term vitamin B6 is a designation for the vitamers pyridoxal, pyridoxamine, pyridoxine and the respective phosphate esters pyridoxal-5'-phosphate (PLP), pyridoxamine-5'-phosphate and pyridoxine-5'-phosphate. Animals and humans are unable to synthesise vitamin B6. These organisms have to take up vitamin B6 with their diet. Therefore, vitamin B6 is of commercial interest as a food additive and for applications in the pharmaceutical industry. As yet, two naturally occurring routes for de novo synthesis of PLP are known. Both routes have been genetically engineered to obtain bacteria overproducing vitamin B6. Still, major genetic engineering efforts using the existing pathways are required for developing fermentation processes that could outcompete the chemical synthesis of vitamin B6. Recent suppressor screens using mutants of the Gram-negative and Gram-positive model bacteria Escherichia coli and Bacillus subtilis, respectively, carrying mutations in the native pathways or heterologous genes uncovered novel routes for PLP biosynthesis. These pathways consist of promiscuous enzymes and enzymes that are already involved in vitamin B6 biosynthesis. Thus, E. coli and B. subtilis contain multiple promiscuous enzymes causing a so-called underground metabolism allowing the bacteria to bypass disrupted vitamin B6 biosynthetic pathways. The suppressor screens also show the genomic plasticity of the bacteria to suppress a genetic lesion. We discuss the potential of the serendipitous pathways to serve as a starting point for the development of bacteria overproducing vitamin B6. KEY POINTS: • Known vitamin B6 routes have been genetically engineered. • Underground metabolism facilitates the emergence of novel vitamin B6 biosynthetic pathways. • These pathways may be suitable to engineer bacteria overproducing vitamin B6. | Lee ASD (2021)
The Role of Vitamin B6 in Women's Health.
The Nursing clinics of North America 56, 23-32 [PubMed:33549283]
[show Abstract]
Vitamin B6, a cofactor in many biochemical reactions in the cells of living organisms, is an essential coenzyme for various catabolic and anabolic processes. Although vitamin B6 deficiency in young healthy women with a balanced diet is thought to be unusual, it can be seen with certain medications, health conditions, and dietary deficits, as well as aging. Vitamin B6 deficiency is associated with a variety of ill health effects, and correction of deficiency is considered beneficial. Women particularly are affected by unique health issues that are part of the array of disorders potentially alleviated through vitamin B6 supplementation. | Are S, Gatreddi S, Jakkula P, Qureshi IA (2020)
Structural attributes and substrate specificity of pyridoxal kinase from Leishmania donovani.
International journal of biological macromolecules 152, 812-827 [PubMed:32105687]
[show Abstract]
The enzyme pyridoxal kinase (PdxK) catalyzes the conversion of pyridoxal to pyridoxal-5'-phosphate (PLP) using ATP as the co-factor. The product pyridoxal-5'-phosphate plays a key role in several biological processes such as transamination, decarboxylation and deamination. In the present study, full-length ORF of PdxK from Leishmania donovani (LdPdxK) was cloned and then purified using affinity chromatography. LdPdxK exists as a homo-dimer in solution and shows more activity at near to physiological pH. Biochemical analysis of LdPdxK with pyridoxal, pyridoxamine, pyridoxine and ginkgotoxin revealed its affinity preference towards different substrates. The secondary structure analysis using circular dichroism spectroscopy showed LdPdxK to be predominantly α-helical in organization which tends to decline at lower and higher pH. Simultaneously, LdPdxK was crystallized and its three-dimensional structure in complex with ADP and different substrates were determined. Crystal structure of LdPdxK delineated that it has a central core of β-sheets surrounded by α-helices with a conserved GTGD ribokinase motif. The structures of LdPdxK disclosed no major structural changes between ADP and ADP- substrate bound structures. In addition, comparative structural analysis highlighted the key differences between the active site pockets of leishmanial and human PdxK, rendering LdPdxK an attractive candidate for the designing of novel and specific inhibitors. | Çatak J, Çaman R (2020)
Pyridoxal, pyridoxamine, and pyridoxine cooking loss: Characterizing vitamin B6 profiles of chicken meats before and after cooking
Journal of food processing and preservation. 44, Not Available [Agricola:IND607198670]
[show Abstract]
In the literature, the level of vitamin B₆ in foods is given as sum of the pyridoxal (PL), pyridoxamine (PM), and pyridoxine (PN) forms. There is little information on vitamin B₆ profiles in raw and cooked chickens. Since the levels of PL, PM, and PN forms of vitamin B₆ are different in chickens, knowing the amount of these forms is essential after cooking. The PL, PM, PN, and total vitamin B₆ concentrations in chickens were determined by HPLC. The cooking loss of total vitamin B₆ was ranged between 55% and 89%, and the values were significantly higher than those reported previously. The PL and PM losses in chickens were ranged from 50% to 92% and from 70% to 96%, respectively. The PN was found to be negligible. This is the first report on the cooking loss of vitamin B₆ vitamers in chicken meats commonly consumed in Turkey. PRACTICAL APPLICATIONS: The present study aimed to reveal the potential vitamin B₆ losses in chickens due to the widely used cooking methods. As a useful practical application for the food industry, this obtained results can be successfully integrated on the packages' surface, which can be easily seen from the consumers. Thus, the consumers can cook the foods depending on this cooking conditions and methods, especially at home. The loss of pyridoxal, pyridoxamine, and pyridoxine can be effectively protected by these practices at home and in the industrial applications. | Kim HH, Kang YR, Choi HY, Lee JY, Oh JB, Kim JS, Kim YC, Lee KW, Kwon YI (2019)
Postprandial anti-hyperglycemic effect of vitamin B6 (pyridoxine) administration in healthy individuals.
Food science and biotechnology 28, 907-911 [PubMed:31093449]
[show Abstract]
Postprandial blood glucose lowering effect of vitamin B6 (pyridoxine) was evaluated in healthy individuals with normal blood glucose levels. Blood glucose levels were measured every 30 min for 2 h after oral sugar administration with or without 50 mg of pyridoxine. Pyridoxine significantly lowered the postprandial blood glucose levels at 30 min (from 165.95 ± 17.19 to 138.36 ± 20.43, p < 0.01) and 60 min (from 131.40 ± 17.20 to 118.50 ± 15.95) after administration. In addition, the area under the concentration-time curve (AUCt) was reduced by about 8.3% (from 257.08 ± 22.38 to 235.71 ± 12.33, p < 0.05) and the maximum concentration of blood glucose (Cmax) was reduced by about 13.8% (from 165.95 ± 17.19 to 143.07 ± 11.34, p < 0.01) when compared with those of the control group. Our findings suggest that pyridoxine supplementation may be beneficial for controlling postprandial hyperglycemia. | Xu M, Yang X, Yang XA, Zhou L, Liu TZ, Fan Z, Jiang T (2016)
Structural insights into the regulatory mechanism of the Pseudomonas aeruginosa YfiBNR system.
Protein & cell 7, 403-416 [PubMed:27113583]
[show Abstract]
YfiBNR is a recently identified bis-(3'-5')-cyclic dimeric GMP (c-di-GMP) signaling system in opportunistic pathogens. It is a key regulator of biofilm formation, which is correlated with prolonged persistence of infection and antibiotic drug resistance. In response to cell stress, YfiB in the outer membrane can sequester the periplasmic protein YfiR, releasing its inhibition of YfiN on the inner membrane and thus provoking the diguanylate cyclase activity of YfiN to induce c-di-GMP production. However, the detailed regulatory mechanism remains elusive. Here, we report the crystal structures of YfiB alone and of an active mutant YfiB(L43P) complexed with YfiR with 2:2 stoichiometry. Structural analyses revealed that in contrast to the compact conformation of the dimeric YfiB alone, YfiB(L43P) adopts a stretched conformation allowing activated YfiB to penetrate the peptidoglycan (PG) layer and access YfiR. YfiB(L43P) shows a more compact PG-binding pocket and much higher PG binding affinity than wild-type YfiB, suggesting a tight correlation between PG binding and YfiB activation. In addition, our crystallographic analyses revealed that YfiR binds Vitamin B6 (VB6) or L-Trp at a YfiB-binding site and that both VB6 and L-Trp are able to reduce YfiB(L43P)-induced biofilm formation. Based on the structural and biochemical data, we propose an updated regulatory model of the YfiBNR system. | Nodwell MB, Koch MF, Alte F, Schneider S, Sieber SA (2014)
A subfamily of bacterial ribokinases utilizes a hemithioacetal for pyridoxal phosphate salvage.
Journal of the American Chemical Society 136, 4992-4999 [PubMed:24601602]
[show Abstract]
Pyridoxal 5'-phosphate (PLP) is the active vitamer of vitamin B6 and acts as an essential cofactor in many aspects of amino acid and sugar metabolism. The virulence and survival of pathogenic bacteria such as Mycobacterium tuberculosis depend on PLP, and deficiencies in humans have also been associated with neurological disorders and inflammation. While PLP can be synthesized by a de novo pathway in bacteria and plants, most higher organisms rely on a salvage pathway that phosphorylates either pyridoxal (PL) or its related vitamers, pyridoxine (PN) and pyridoxamine (PM). PL kinases (PLKs) are essential for this phosphorylation step and are thus of major importance for cellular viability. We recently identified a pyridoxal kinase (SaPLK) as a target of the natural product antibiotic rugulactone (Ru) in Staphylococcus aureus. Surprisingly, Ru selectively modified SaPLK not at the active site cysteine, but on a remote cysteine residue. Based on structural and biochemical studies, we now provide insight into an unprecedented dual Cys charge relay network that is mandatory for PL phosphorylation. The key component is the reactive Cys 110 residue in the lid region that forms a hemithioactetal intermediate with the 4'-aldehyde of PL. This hemithioacetal, in concert with the catalytic Cys 214, increases the nucleophilicity of the PL 5'-OH group for the inline displacement reaction with the γ-phosphate of ATP. A closer inspection of related enzymes reveals that Cys 110 is conserved and thus serves as a characteristic mechanistic feature for a dual-function ribokinase subfamily herein termed CC-PLKs. | Ahmad I, Mirza T, Qadeer K, Nazim U, Vaid FH (2013)
Vitamin B6: deficiency diseases and methods of analysis.
Pakistan journal of pharmaceutical sciences 26, 1057-1069 [PubMed:24035968]
[show Abstract]
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. | Jacobs DM, Spiesser L, Garnier M, de Roo N, van Dorsten F, Hollebrands B, van Velzen E, Draijer R, van Duynhoven J (2012)
SPE-NMR metabolite sub-profiling of urine.
Analytical and bioanalytical chemistry 404, 2349-2361 [PubMed:22932811]
[show Abstract]
NMR-based metabolite profiling of urine is a fast and reproducible method for detection of numerous metabolites with diverse chemical properties. However, signal overlap in the (1)H NMR profiles of human urine may hamper quantification and identification of metabolites. Therefore, a new method has been developed using automated solid-phase extraction (SPE) combined with NMR metabolite profiling. SPE-NMR of urine resulted in three fractions with complementary and reproducible sub-profiles. The sub-profile from the wash fraction (100 % water) contained polar metabolites; that from the first eluted fraction (10 % methanol-90 % water) semi-polar metabolites; and that from the second eluted fraction (100 % methanol) aromatic metabolites. The method was validated by analysis of urine samples collected from a crossover human nutritional intervention trial in which healthy volunteers consumed capsules containing a polyphenol-rich mixture of red wine and grape juice extract (WGM), the same polyphenol mixture dissolved in a soy drink (WGM_Soy), or a placebo (PLA), over a period of five days. Consumption of WGM clearly increased urinary excretion of 4-hydroxyhippuric acid, hippuric acid, 3-hydroxyphenylacetic acid, homovanillic acid, and 3-(3-hydroxyphenyl)-3-hydroxypropionic acid. However, there was no difference between the excreted amounts of these metabolites after consumption of WGM or WGM_Soy, indicating that the soy drink is a suitable carrier for WGM polyphenols. Interestingly, WGM_Soy induced a significant increase in excretion of cis-aconitate compared with WGM and PLA, suggesting a higher demand on the tricarboxylic acid cycle. In conclusion, SPE-NMR metabolite sub-profiling is a reliable and improved method for quantification and identification of metabolites in urine to discover dietary effects and markers of phytochemical exposure. | Gori AM, Sofi F, Corsi AM, Gazzini A, Sestini I, Lauretani F, Bandinelli S, Gensini GF, Ferrucci L, Abbate R (2006)
Predictors of vitamin B6 and folate concentrations in older persons: the InCHIANTI study.
Clinical chemistry 52, 1318-1324 [PubMed:16690736]
[show Abstract]
BackgroundLow dietary intake and low serum concentrations of vitamin B6 and/or folate are associated with increased risk of vascular events, possibly because of their association with inflammation, which plays a crucial role in the pathogenesis of cardiovascular diseases.MethodsUsing data from 1320 participants in the population-based InCHIANTI study (586 men and 734 women; median age, 69 years; range, 21-102 years) for whom complete data on folate, vitamin B6, inflammatory markers, 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T sequence variant, and important covariates were available, we evaluated the association of inflammatory markers with circulating concentrations of vitamin B6 and folate, independently of dietary vitamin intake, circulating vitamin concentrations, and MTHFR C677T sequence variant.ResultsAccording to multiple linear regression analysis, C-reactive protein and interleukin-6 receptor were strongly and negatively associated with circulating vitamin B6 but not with folate concentrations, independent of age, sex, serum creatinine, serum albumin, total energy intake, smoking history, dietary nutrient intake, and circulating homocysteine and vitamin concentrations. Serum folate concentrations were related to MTHFR 677 TT genotype in persons with folate intake in the lowest tertile (< 221.2 microg/day). Vitamin C and retinol intakes were strongly and positively associated with serum folate concentrations independent of age, sex, serum creatinine, serum albumin, total energy intake, smoking history, homocysteine plasma concentrations, dietary nutrient intakes, serum vitamin B6 and vitamin B12 concentrations, and MTHFR C677T sequence variant.ConclusionsLow serum vitamin B6, but not serum folate, concentrations are independent correlates of the proinflammatory state, and both are influenced by antioxidant reserves. | Walter FG, Chase PB, Fernandez MC, Cameron D, Roe DJ, Wolfson M (2006)
Pyridoxine does not prevent hyperbaric oxygen-induced seizures in rats.
The Journal of emergency medicine 31, 135-138 [PubMed:17044573]
[show Abstract]
Normobaric supplemental oxygen can prolong seizures not caused by hyperbaric oxygen therapy. In addition, hyperbaric oxygen therapy can cause seizures. The mechanism of hyperbaric oxygen-induced seizures is unknown. We hypothesized that pretreatment with pyridoxine may delay the onset of hyperbaric oxygen-induced seizures, recognizing that pyridoxine is already an antidote for some epileptogenic poisons such as isoniazid and monomethylhydrazine. Therefore, rats were pretreated with intraperitoneal injections of pyridoxine at 48, 24, and 2 h before undergoing hyperbaric oxygen (HBO) treatment at 3 atmospheres absolute with 100% oxygen and were compared to a control group of HBO-treated rats for time to onset of seizures. There was no difference in onset of seizure time between the pyridoxine-treated group of rats and the control rats. Supplemental pyridoxine pretreatment did not alter the time to onset of seizures during HBO treatment in this study. | Chiang EP, Selhub J, Bagley PJ, Dallal G, Roubenoff R (2005)
Pyridoxine supplementation corrects vitamin B6 deficiency but does not improve inflammation in patients with rheumatoid arthritis.
Arthritis research & therapy 7, R1404-11 [PubMed:16277693]
[show Abstract]
Patients with rheumatoid arthritis have subnormal vitamin B6 status, both quantitatively and functionally. Abnormal vitamin B6 status in rheumatoid arthritis has been associated with spontaneous tumor necrosis factor (TNF)-alpha production and markers of inflammation, including C-reactive protein and erythrocyte sedimentation rate. Impaired vitamin B6 status could be a result of inflammation, and these patients may have higher demand for vitamin B6. The aim of this study was to determine if daily supplementation with 50 mg of pyridoxine for 30 days can correct the static and/or the functional abnormalities of vitamin B6 status seen in patients with rheumatoid arthritis, and further investigate if pyridoxine supplementation has any effects on the pro-inflammatory cytokine TNF-alpha or IL-6 production of arthritis. This was a double-blinded, placebo-controlled study involving patients with rheumatoid arthritis with plasma pyridoxal 5'-phosphate below the 25th percentile of the Framingham Heart Cohort Study. Vitamin B6 status was assessed via plasma and erythrocyte pyridoxal 5'-phosphate concentrations, the erythrocyte aspartate aminotransferase activity coefficient (alphaEAST), net homocysteine increase in response to a methionine load test (DeltatHcy), and 24 h urinary xanthurenic acid (XA) excretion in response to a tryptophan load test. Urinary 4-pyridoxic acid (4-PA) was measured to examine the impact of pyridoxine treatment on vitamin B6 excretion in these patients. Pro-inflammatory cytokine (TNF-alpha and IL-6) production, C-reactive protein levels and the erythrocyte sedimentation rate before and after supplementation were also examined. Pyridoxine supplementation significantly improved plasma and erythrocyte pyridoxal 5'-phosphate concentrations, erythrocyte alphaEAST, urinary 4-PA, and XA excretion. These improvements were apparent regardless of baseline B6 levels. Pyridoxine supplementation also showed a trend (p < 0.09) towards a reduction in post-methionine load DeltatHcy. Supplementation did not affect pro-inflammatory cytokine production. Although pyridoxine supplementation did not suppress pro-inflammatory cytokine production in patients with rheumatoid arthritis, the suboptimal vitamin B6 status seen in rheumatoid arthritis can be corrected by 50 mg pyridoxine supplementation for 30 days. Data from the present study suggest that patients with rheumatoid arthritis may have higher requirements for vitamin B6 than those in a normal healthy population. | Lheureux P, Penaloza A, Gris M (2005)
Pyridoxine in clinical toxicology: a review.
European journal of emergency medicine : official journal of the European Society for Emergency Medicine 12, 78-85 [PubMed:15756083]
[show Abstract]
Pyridoxine (vitamin B6) is a co-factor in many enzymatic pathways involved in amino acid metabolism: the main biologically active form is pyridoxal 5-phosphate. Pyridoxine has been used as an antidote in acute intoxications, including isoniazid overdose, Gyromitra mushroom or false morrel (monomethylhydrazine) poisoning and hydrazine exposure. It is also recommended as a co-factor to improve the conversion of glyoxylic acid into glycine in ethylene glycol poisoning. Other indications are recommended by some sources (for example crimidine poisoning, zipeprol and theophylline-induced seizures, adjunct to d-penicillamine chelation), without significant supporting data. The value of pyridoxine or its congener metadoxine as an agent for hastening ethanol metabolism or improving vigilance in acute alcohol intoxication is controversial. This paper reviews the various indications of pyridoxine in clinical toxicology and the supporting literature. The potential adverse effects of excessive pyridoxine dosage will also be summarized. | Chen H, Xiong L (2005)
Pyridoxine is required for post-embryonic root development and tolerance to osmotic and oxidative stresses.
The Plant journal : for cell and molecular biology 44, 396-408 [PubMed:16236150]
[show Abstract]
Pyridoxine (vitamin B6) is a cofactor required by numerous enzymes in all cellular organisms. Plants are the major source of vitamin B6 for animals, yet the biosynthesis pathway and the function of vitamin B6 in plants are not well elucidated. In this study, an Arabidopsis pyridoxine synthase gene PDX1 was characterized and its in vivo functions were investigated. The PDX1 gene was expressed in all plant parts examined and its expression level was not significantly regulated by abiotic stress or the phytohormone abscisic acid. In roots, PDX1 was highly expressed in a defined region behind the root tips that undergoes rapid cell division. The PDX1 protein was mainly associated with the plasma membrane and endomembranes, implying a potential involvement of vitamin B6 in membrane function. To reveal the in vivo role of PDX1, Arabidopsis insertional mutants were isolated. Strikingly, the pdx1 knockout mutants were impaired in root growth and early seedling development. The stunted roots resulted from both reduced cell division and elongation. Supplementation of the growth media with pyridoxine or reintroduction of the wild-type PDX1 gene into the mutants completely restored the mutant growth, demonstrating that PDX1 is required for pyridoxine biosynthesis in planta. In addition to the developmental defects, pdx1 mutants are hypersensitive to osmotic stress and oxidative stress. These mutant seedlings had increased peroxidation of membrane lipids following UV treatment. Our study establishes a critical role of vitamin B6 in plant development and stress tolerance and suggests that vitamin B6 may represent a new class of antioxidant in plants. | Esteve-Romero J, Capella-Peiró ME, Monferrer-Pons L, Gil-Agustí M (2004)
Micellar liquid chromatography in clinical chemistry: application to the monitorization of B6 vitamins.
Clinica chimica acta; international journal of clinical chemistry 348, 69-77 [PubMed:15369738]
[show Abstract]
BackgroundA micellar reversed-phase liquid chromatographic procedure was developed for the determination of B6 group vitamins, i.e. pyridoxine, pyridoxal and pyridoxamine, in human serum.MethodsChromatographic conditions used were a C18 column, isocratic mode, flow-rate of 1 ml/min and UV-detection at 290 nm. Optimization of the composition of the mobile phase was performed using an interpretative strategy.ResultsAfter modeling, the composition of the selected mobile phase was 150 mM sodium dodecyl sulphate (SDS)--2% (v/v) pentanol-dihydrogenphosphate buffer 10 mM at pH 3. In this mobile phase, serum samples were injected without pretreatment and analysis time was below 14 min. Calibrations for the three vitamins were linear, with coefficient regression better than 0.999, and intra- and inter-day precision, achieved according to ICH, offering values below 4.3% and 3.2%, respectively. The method was applied to the determination of the B6 vitamins in spiked serum samples, with recoveries around 100%, and in the pharmacokinetic determination of pyridoxine half-life in serum, which was found to be 47.5 +/- 3.2 min (n = 5). The procedure was also applied for the analysis of pyridoxine in human serum spiked with several pharmaceutical preparations that contain other drugs which do not produce any kind of interference. Finally, solutions of B6 vitamins kept at -201 degrees C are stable for up to 3 months.ConclusionsUsing the method proposed here, with an SDS-pentanol mobile phase, it is possible to carry out the fast sensitive determination of B6 vitamins in serum following direct injection, without sample pretreatment. | McCully KS (2004)
Homocysteine, vitamins, and prevention of vascular disease.
Military medicine 169, 325-329 [PubMed:15132238]
[show Abstract]
Within the past four decades, the efforts of investigators worldwide have established the amino acid homocysteine as an important factor in arteriosclerosis and diseases of aging. After its discovery in 1932, homocysteine was demonstrated to be an important intermediate in the metabolism of amino acids. However, little was known about the broader biomedical significance of homocysteine until 1962, when children with mental retardation, accelerated growth, dislocated ocular lenses, and frequent vascular thrombosis were found to excrete homocysteine in the urine. My study of two patients with homocystinuria caused by different inherited enzymatic disorders in 1968 disclosed advanced widespread arteriosclerotic plaques in both cases. This discovery led to the conclusion that homocysteine causes vascular disease by a direct effect on the cells and tissues of the arteries. This interpretation suggests that homocysteine is important in the pathogenesis of arteriosclerosis in persons with hereditary, dietary, environmental, hormonal, metabolic, and other factors predisposing them to hyperhomocysteinemia. Within the past decade, many major clinical and epidemiological studies have proven that hyperhomocysteinemia is a potent independent risk factor for vascular disease. According to the homocysteine theory of arteriosclerosis, insufficient dietary intake of the B vitamins, folic acid and pyridoxine, caused by losses of these nutrients during processing of foods, leads to elevation of blood homocysteine and vascular disease in the general population. The dramatic decline in cardiovascular mortality since the 1960s in the United States is attributed to fortification of the food supply by synthetic pyridoxine and folic acid. The recent Swiss Heart Study showed that B vitamins slowed restenosis in patients with coronary arteriosclerosis treated with angioplasty. Currently, more than 20 prospective, worldwide, interventional trials involving at least 100,000 participants are examining whether lowering plasma homocysteine levels with supplemental B vitamins will prevent mortality and morbidity from arteriosclerotic vascular disease. | Pirulli D, Marangella M, Amoroso A (2003)
Primary hyperoxaluria: genotype-phenotype correlation.
Journal of nephrology 16, 297-309 [PubMed:12768081]
[show Abstract]
Primary hyperoxaluria type 1 (PH1) is an autosomal recessive disorder caused by a deficiency of alanine-glyoxylate aminotransferase (AGT), which is encoded by a single copy gene (AGXT). Molecular diagnosis was used in conjunction with clinical, biochemical and enzymological data to evaluate genotype-phenotype correlation. Patients can present a severe form of PH1, an adult form and a mild to moderate decrease in renal function. Biochemical diagnosis is made by plasma, urine and dialyzate oxalate and glycolate assays, and by liver AGT activity and pyridoxine responsitivity. Molecular genetic diagnosis can be made using different techniques, for example, the single strand conformation polymorphism technique (SSCP), followed by the sequencing of the 11 AGXT exons. The disease is clinically and genetically classified as highly heterogeneous. Mutant alleles can be recognised in 80- 90% of chromosomes, depending on the techniques used. Mutations in exons 1, 2, 4 and 10 are more frequent in Italian patients. Normalized AGT activity seems to be lower in the severe form than in the adult form. Double heterozygous patients present a lower age at disease onset and they were more frequent in the more severe than in mild severe disease. The 444T>C mutation was more frequent in the severe form, while the opposite was observed for 630G>A. 630G>A mutation homozygotes had a higher AGT residual activity. The presence of allelic heterogeneity of the AGXT could be responsible, to some extent, for the phenotypic heterogeneity in PH1. Homozygous genotypes were more frequent than expected and were associated with a less severe form of the disease. | Wasilewska A, Narkiewicz M, Rutkowski B, Łysiak-Szydłowska W (2003)
Is there any relationship between lipids and vitamin B levels in persons with elevated risk of atherosclerosis?
Medical science monitor : international medical journal of experimental and clinical research 9, CR147-51 [PubMed:12640345]
[show Abstract]
BackgroundThere is increasing evidence that plasma homocysteine level is an independent risk factor for atherosclerosis. Low levels of serum folates, cobalamin and pyridoxine are associated with increased risk of cardiovascular disease. Most dietary products contain cholesterol as well as methionine, so hyperlipidemia could be associated with a higher level of homocysteine and inversely with lower levels of B vitamins. The aim of this study was to investigate the differences in levels of lipids and vitamins affecting homocysteine metabolism in different groups of patients.Material/methodsWe examined 38 healthy persons, 55 patients hospitalised for cardiac surgery, and 62 patients without clinical evidence of atherosclerosis but with one of the atherosclerosis risk factors (hypercholesterolemia, NIDDM or chronic renal insufficiency). The levels of total cholesterol, triglycerides, vitamin B12, folic acid and vitamin B6 index in serum were determined using routine laboratory methods.ResultsWe found no association between lipids and B vitamins in any examined group. There were significant differences between concentrations of analysed parameters in all groups of patients as compared to controls.ConclusionsThe lack of correlation between the levels of lipid parameters and B vitamins in serum indicates that these may be independent, additional risk factors for atherosclerosis. Higher vitamin B6 deficiency in dialysis patients is probably caused by low intake combined with the increased requirements of uremic patients. Permanent monitoring of B vitamins in serum is necessary in patients with elevated risk of atherosclerosis, as well as long-term education, careful diet planning and supplementation. | Amoroso A, Pirulli D, Florian F, Puzzer D, Boniotto M, Crovella S, Zezlina S, Spanò A, Mazzola G, Savoldi S, Ferrettini C, Berutti S, Petrarulo M, Marangella M (2001)
AGXT gene mutations and their influence on clinical heterogeneity of type 1 primary hyperoxaluria.
Journal of the American Society of Nephrology : JASN 12, 2072-2079 [PubMed:11562405]
[show Abstract]
Primary hyperoxaluria type 1 (PH1) is an autosomal recessive disorder that is caused by a deficiency of alanine: glyoxylate aminotransferase (AGT), which is encoded by a single copy gene (AGXT). Molecular diagnosis was used in conjunction with clinical, biochemical, and enzymological data to evaluate genotype-phenotype correlation. Twenty-three unrelated, Italian PH1 patients were studied, 20 of which were grouped according to severe form of PH1 (group A), adult form (group B), and mild to moderate decrease in renal function (group C). All 23 patients were analyzed by using the single-strand conformation polymorphism technique followed by the sequencing of the 11 AGXT exons. Relevant chemistries, including plasma, urine and dialyzate oxalate and glycolate assays, liver AGT activity, and pyridoxine responsiveness, were performed. Both mutant alleles were found in 21 out of 23 patients, and 13 different mutations were recognized in exons 1, 2, 4, and 10. Normalized AGT activity was lower in the severe form than in the adult form (P < 0.05). Double heterozygous patients presented a lower age at the onset of the disease (P = 0.025), and they were more frequent in group A (75%) than in the group B (14%; P = 0.0406). The T444C mutation was more frequent in the severe form (P < 0.05), and the opposite was observed for G630A (P < 0.05). G630A mutation homozygotes had a higher AGT residual activity (P = 0.00001). This study confirms the allelic heterogeneity of the AGXT, which could to some extent be responsible for the phenotypic heterogeneity in PH1. | Plecko B, Stöckler-Ipsiroglu S, Paschke E, Erwa W, Struys EA, Jakobs C (2000)
Pipecolic acid elevation in plasma and cerebrospinal fluid of two patients with pyridoxine-dependent epilepsy.
Annals of neurology 48, 121-125 [PubMed:10894227]
[show Abstract]
Diagnosis of pyridoxine-dependent epilepsy is based on the clinical response to high-dosage application of pyridoxine. Here, we report on 2 patients with pyridoxine-dependent epilepsy with significant elevation of pipecolic acid concentrations in plasma and cerebrospinal fluid (CSF) and further increase of pipecolic acid in CSF during a 72-hour pyridoxine withdrawal in 1 of them. Patients with non-pyridoxine-dependent epilepsy had normal pipecolic acid concentrations in plasma and significantly lower concentrations in CSF. High plasma and CSF pipecolic acid concentrations might provide a diagnostic marker in pyridoxine-dependent epilepsy. | Chen S, Ito M, Saijo T, Naito E, Kuroda Y (1999)
Molecular genetic analysis of pyridoxine-nonresponsive homocystinuric siblings with different blood methionine levels during the neonatal period.
The journal of medical investigation : JMI 46, 186-191 [PubMed:10687314]
[show Abstract]
Two mutations in the cystathionine beta-synthase (CBS) gene were found in two Japanese siblings with pyridoxine non-responsive homocystinuria who had different methionine levels in their blood during the neonatal period. Both patients were compound heterozygotes of two mutant alleles: one had an A-to-G transition at nucleotide 194 (A194 G) that caused a histidine-to-arginine substitution at position 65 of the protein (H65R), while the other had a G-to-A transition at nucleotide 346 (G346A) which resulted in a glycine-to-arginine substitution at position 116 of the protein (G116R). The two mutant proteins were separately expressed in Escherichia coli, and they completely lacked catalytic activity. Despite their identical genotypes and almost equal protein intake, these siblings showed different levels of blood methionine during the neonatal period, suggesting that the level of methionine in blood is determined not only by the defect in the CBS gene and protein intake, but also by the activity of other enzymes involved in methionine and homocysteine metabolism, especially during the neonatal period. Therefore, high-risk newborns who have siblings with homocystinuria, even if the level of methionine in their blood is normal in a neonatal mass screening, should be followed up and diagnosed by an assay of enzyme activity or a gene analysis so that treatment can be begun as soon as possible to prevent the development of clinical symptoms. In addition, a new, more sensitive method for the mass screening of CBS deficiency in neonates should be developed. | Baldewicz T, Goodkin K, Feaster DJ, Blaney NT, Kumar M, Kumar A, Shor-Posner G, Baum M (1998)
Plasma pyridoxine deficiency is related to increased psychological distress in recently bereaved homosexual men.
Psychosomatic medicine 60, 297-308 [PubMed:9625217]
[show Abstract]
ObjectivePrevious research has demonstrated that a theoretical model including measures of life stressors, social support, and coping style significantly predicts psychological distress. This study tested plasma pyridoxine (vitamin B6) deficiency status as a predictor of overall psychological distress and specific mood states in this model, controlling for HIV-1 serostatus.MethodSubjects included HIV-1+ (N = 76) and HIV-1- (N = 58) recently bereaved homosexual men. At baseline, subjects completed a battery of psychosocial questionnaires, together with a physical examination and venipuncture. The Profile of Mood States (POMS) provided measures of overall psychological distress as well as specific mood states. Pyridoxine deficiency status (a categorical measure of deficient vs. adequate status) was determined with a bioassay of erythrocyte aspartate aminotransferase activity.ResultsPyridoxine deficiency was a significant predictor of increased overall psychological distress in this model, controlling for life stressors, social support, coping style, and HIV-1 serostatus. In post hoc analyses of specific mood state effects, pyridoxine deficiency status was significantly associated with increases in depressed, fatigued, and confused mood levels, but not with those of anxiety, anger, or vigor.DiscussionThese findings suggest that adequate pyridoxine status may be necessary to avert psychological distress in the setting of bereavement. Inasmuch as pyridoxine is a cofactor for 5-hydroxytryptophan decarboxylase--an enzyme in the biosynthesis pathway of serotonin--serotonin level in the brain is implicated as the mediating factor. | Manyam BV, Ferraro TN, Hare TA (1987)
Isoniazid-induced alteration of CSF neurotransmitter amino acids in Huntington's disease.
Brain research 408, 125-130 [PubMed:2885064]
[show Abstract]
During a randomized, double-blind, crossover, placebo-controlled clinical trial of isoniazid (plus pyridoxine) in Huntington's disease (HD), amino acids and related amino compounds were measured in both cerebrospinal fluid (CSF) and plasma utilizing a newly developed high-performance liquid chromatography ion-exchange/fluorometric assay method. Results showed that isoniazid (plus pyridoxine) significantly elevated the mean (+/- S.E.M.) levels of gamma-aminobutyric acid, aspartate, asparagine, homocarnosine, ornithine, histidine, alpha-aminobutyric acid, isoleucine, leucine and alanine in CSF and the levels of beta-alanine in both CSF and plasma. These alterations can be traced to inhibition of decarboxylation and transamination reactions requiring the cofactor pyridoxal phosphate and may be related to the observed equivocal clinical response in the HD patients. The differential influence of isoniazid on plasma and CSF amino acid profiles suggests that alterations of CNS amino acid metabolism may be reflected in CSF, and that isoniazid-induced alterations of amino acid metabolism in the CNS differ from those in the periphery. | Henderson JM, Codner MA, Hollins B, Kutner MH, Merrill AH (1986)
The fasting B6 vitamer profile and response to a pyridoxine load in normal and cirrhotic subjects.
Hepatology (Baltimore, Md.) 6, 464-471 [PubMed:3710434]
[show Abstract]
This study established the fasting plasma and urine profiles of vitamin B6 in cirrhotics and assessed the response to an oral dose of pyridoxine. High-performance liquid chromatography was used to measure all vitameric coenzymatic and degradatory forms. In 31 patients with cirrhosis and 15 healthy controls, fasting plasma and 24-hr urine collection showed: plasma pyridoxal-5'-phosphate, the biologically active form, was significantly (p less than 0.001) reduced in cirrhotics (mean +/- S.D.: 5.7 +/- 3.2 ng per ml) compared to normals (14.2 +/- 7.5 ng per ml); plasma pyridoxal was detected in more cirrhotics (48%) than normals (28%); pyridoxic acid, the end catabolite, was significantly (p less than 0.05) lower in plasma of cirrhotics compared to normals, but 24-hr urine excretion was not different. Administration of 25 mg of pyridoxine to 7 cirrhotics and 5 normals showed the following plasma changes: pyridoxine rapidly peaked at 30 min and was totally cleared from plasma by 3 hr; plasma pyridoxal and pyridoxic acid increased in parallel up to 40-fold over baseline by 1 to 2 hr and rapidly fell toward baseline by 8 hr, and plasma pyridoxal-5'-phosphate, in contrast, increased significantly (p less than 0.05) from baseline by 60 min and was maintained above normal for 24 hr. The area under the plasma concentration vs. time curve (AUC) for pyridoxal-5'-phosphate was significantly (p less than 0.05) less for the cirrhotics than normals and showed a significant negative correlation to hepatocyte function and blood flow.(ABSTRACT TRUNCATED AT 250 WORDS) | Brandon DL, Corse JW, Windle JJ, Layton LL (1985)
Two homogeneous immunoassays for pyridoxamine.
Journal of immunological methods 78, 87-94 [PubMed:2580028]
[show Abstract]
Protein conjugates of pyridoxal have been used to elicit anti-vitamin B6 antibodies in rabbits. These antibodies have been incorporated into 2 homogeneous assays systems, a spin immunoassay, using a paramagnetic derivative of the vitamin as ligand, and a fluorescence enzyme immunoassay, using beta-galactosidase conjugated to vitamin B6 as the indicator molecule. These assay systems do not require fractionation steps, and could be the basis of analytical methodology for nutritional research or clinical diagnosis. | Temesvári P, Szilágyi I, Eck E, Boda D (1983)
Effects of an antenatal load of pyridoxine (vitamin B6) on the blood oxygen affinity and prolactin levels in newborn infants and their mothers.
Acta paediatrica Scandinavica 72, 525-529 [PubMed:6624427]
[show Abstract]
The effects of a loading dose of pyridoxine (100 mg) given intramuscularly or per os to 24 earlier non-supplemented pregnant women at term was investigated. The in vitro oxygen affinity (P50) and the prolactin level in both maternal and newborn blood was sampled. The blood P50 values were measured by a variant of "mixing method". Blood prolactin levels were determined by RIA. After pyridoxine administration, the maternal P50 values increased moderately and the newborns' cord blood P50 values increased significantly when compared with the control group's (number of cases 12) values. The decrease of blood oxygen affinity was most pronounced in the supplemented groups in newborns' capillary blood at the age of five days. The pyridoxine supplementation had no effect on the maternal and the newborns' cord blood prolactin level or on the daily amount of breast milk. Pyridoxine supplementation of the mother at labour may influence favourably the oxygen transport function of the newborn's blood and it may be especially advantageous in early postnatal adaptation disturbances of newborns. | Kidd GS, Dimond R, Kark JA, Whorton N, Vigersky RA (1982)
The effects of pyridoxine on pituitary hormone secretion in amenorrhea-galactorrhea syndromes.
The Journal of clinical endocrinology and metabolism 54, 872-875 [PubMed:6801073]
[show Abstract]
Six patients with amenorrhea, five of whom had galactorrhea and elevated PRL levels, were evaluated on a metabolic ward. All had normal sella tomograms, normal thyroid functions, and routine laboratory evaluations. None of the patients had taken any medication in the previous 6 months. On alternate days, five patients received 500 microgram of TRH iv with the measurement of PRL, TSH, FSh, LH, and hGH; 500 mg L-dopa orally with the measurement of PRL, FSH, and LH; a bolus infusion of 300 mg pyridoxine (B6) with measurement of PRL, hGH, TSH, FSH, and LH; and 25 mg chlorpromazine (CPZ) im with the measurement of PRL, LH, and FSH. The patients were then discharged on 600 mg oral pyridoxine/day and were readmitted for a repeat of the complete protocol 21 days later. The patients were continued on 600 mg oral pyridoxine for 3-4 months with monthly evaluations of serum PRL, LH, and FSH levels. These evaluations continued for 3 months after discontinuing pyridoxine. There was no demonstrable change in serum PRL after acute or chronic B6 therapy, mor was there a significant change in the response of PRL to CPZ, L-dopa, or TRH. The mean basal PRL was 97.5 +/- 9.7 ng/ml and after 3-4 months of oral pyridoxine was 97.1 +/- 14.8. In addition, there was no significant change in LH or FSH levels in response to acute or chronic B6, TRH, L-dopa, or CPZ. Neither acute B6 infusion nor chronic B6 therapy had any effect on TSH or the TSH response to TRH. Finally, acute B6 infusion had no effect on hGH levels and there were no paradoxical hGH responses to TRH. Two patients began having regular menses while on chronic pyridoxine. Their hormonal responses did not differ from those of the group, however. | Tolis G, Laliberté R, Guyda H, Naftolin F (1977)
Ineffectiveness of pyridoxine (B6) to alter secretion of growth hormone and prolactin and absence of therapeutic effects on galactorrhea-amenorrhea syndromes.
The Journal of clinical endocrinology and metabolism 44, 1197-1199 [PubMed:559690]
[show Abstract]
The acute effect of pyridoxine (B6) on serum GH and PRL levels and its chronic effects on galactorrhea in nine subjects (group I, n=4, idiopathic galactorrhea with normal PRL levels and normal menses; Group II, n=5, galactorrhea-amenorrhea with increased PRL levels) have been studied. Pyridoxine did not acutely alter GH or PRL levels. There was no decrease in galactorrhea, no resumption of menses and no decrease in PRL following tow months of B6 therapy. In contrast, bromocriptine was effective in suppressing galactorrhea and restoring normal menses in group II subjects and remains the therapy of choice for this purpose. | HOCH R, PRESTON J, KILLAM K (1953)
Pyridoxine, an important vitamin and coenzyme.
Modern hospital 80, 108-118 [PubMed:13046427] |
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