|
pyridoxamine |
|
CHEBI:16410 |
|
A monohydroxypyridine that is pyridine substituted by a hydroxy group at position 3, an aminomethyl group at position 4, a hydroxymethyl group at position 5 and a methyl group at position 2. The 4-aminomethyl form of vitamin B6, it is used (in the form of the hydrochloride salt) for treatment of diabetic nephropathy. |
|
 
This entity has been manually annotated by the ChEBI Team.
|
|
CHEBI:45228, CHEBI:8669, CHEBI:14978, CHEBI:26426
|
|
ChemicalBook:CB8895262, eMolecules:5748034, ZINC000034926229 |
|
Molfile
XML
SDF
|
|
more structures >>
|
|
call loadScript javascripts\jsmol\core\package.js call loadScript javascripts\jsmol\core\core.z.js -- required by ClazzNode call loadScript javascripts\jsmol\J\awtjs2d\WebOutputChannel.js Jmol JavaScript applet jmolApplet0_object__127645292530607__ initializing getValue debug = null getValue logLevel = null getValue allowjavascript = null AppletRegistry.checkIn(jmolApplet0_object__127645292530607__) call loadScript javascripts\jsmol\core\corestate.z.js viewerOptions: { "name":"jmolApplet0_object","applet":true,"documentBase":"https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:16410","platform":"J.awtjs2d.Platform","fullName":"jmolApplet0_object__127645292530607__","display":"jmolApplet0_canvas2d","signedApplet":"true","appletReadyCallback":"Jmol._readyCallback","statusListener":"[J.appletjs.Jmol.MyStatusListener object]","codeBase":"https://www.ebi.ac.uk/chebi/javascripts/jsmol/","syncId":"127645292530607","bgcolor":"#000" } (C) 2012 Jmol Development Jmol Version: 13.2.7 $Date: 2013-10-01 11:35:15 -0500 (Tue, 01 Oct 2013) $ java.vendor: j2s java.version: 0.0 os.name: j2s Access: ALL memory: 0.0/0.0 processors available: 1 useCommandThread: false appletId:jmolApplet0_object (signed) starting HoverWatcher_1 getValue emulate = null defaults = "Jmol" getValue boxbgcolor = null getValue bgcolor = #000 backgroundColor = "#000" getValue ANIMFRAMECallback = null getValue APPLETREADYCallback = Jmol._readyCallback APPLETREADYCallback = "Jmol._readyCallback" getValue ATOMMOVEDCallback = null getValue CLICKCallback = null getValue ECHOCallback = null getValue ERRORCallback = null getValue EVALCallback = null getValue HOVERCallback = null getValue LOADSTRUCTCallback = null getValue MEASURECallback = null getValue MESSAGECallback = null getValue MINIMIZATIONCallback = null getValue PICKCallback = null getValue RESIZECallback = null getValue SCRIPTCallback = null getValue SYNCCallback = null getValue STRUCTUREMODIFIEDCallback = null getValue doTranslate = null language=en_US getValue popupMenu = null getValue script = null Jmol applet jmolApplet0_object__127645292530607__ ready call loadScript javascripts\jsmol\core\corescript.z.js call loadScript javascripts\jsmol\J\script\FileLoadThread.js starting QueueThread0_2 script 1 started starting HoverWatcher_3 starting HoverWatcher_4 The Resolver thinks Mol Marvin 03220818363D starting HoverWatcher_5 Time for openFile( Marvin 03220818363D 24 24 0 0 0 0 999 V2000 1.2159 -0.4350 0.2262 C 0 0 0 0 0 0 0 0 0 5 0 0 -0.1586 -2.3016 -0.4051 N 0 0 0 0 0 0 0 0 0 1 0 0 1.0138 -1.8255 0.0730 C 0 0 0 0 0 0 0 0 0 6 0 0 0.1565 0.4432 -0.1476 C 0 0 0 0 0 0 0 0 0 4 0 0 -1.0536 -0.1102 -0.6481 C 0 0 0 0 0 0 0 0 0 3 0 0 -1.1993 -1.5117 -0.7682 C 0 0 0 0 0 0 0 0 0 2 0 0 2.5131 0.0393 0.7757 C 0 0 0 0 0 0 0 0 0 0 0 0 2.2816 0.7126 2.0097 O 0 0 0 0 0 0 0 0 0 0 0 0 -2.4353 -2.1450 -1.2695 C 0 0 0 0 0 0 0 0 0 0 0 0 -2.0137 0.6365 -0.9860 O 0 0 0 0 0 0 0 0 0 0 0 0 0.2489 1.9306 -0.0333 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.7449 2.4365 0.9199 N 0 0 0 0 0 0 0 0 0 0 0 0 1.7333 -2.5100 0.3180 H 0 0 0 0 0 0 0 0 0 0 0 0 2.9848 0.7153 0.0598 H 0 0 0 0 0 0 0 0 0 0 0 0 3.2332 -0.7571 0.9751 H 0 0 0 0 0 0 0 0 0 0 0 0 3.1249 1.1588 2.2314 H 0 0 0 0 0 0 0 0 0 0 0 0 -3.2734 -1.8742 -0.6242 H 0 0 0 0 0 0 0 0 0 0 0 0 -2.6431 -1.7926 -2.2816 H 0 0 0 0 0 0 0 0 0 0 0 0 -2.3692 -3.2340 -1.2974 H 0 0 0 0 0 0 0 0 0 0 0 0 -2.7724 0.3048 -1.2828 H 0 0 0 0 0 0 0 0 0 0 0 0 0.0802 2.3873 -1.0102 H 0 0 0 0 0 0 0 0 0 0 0 0 1.2107 2.3109 0.3053 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.5723 3.4361 1.0413 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.5611 1.9852 1.8186 H 0 0 0 0 0 0 0 0 0 0 0 0 3 2 4 0 0 0 0 1 3 4 0 0 0 0 4 1 4 0 0 0 0 5 4 4 0 0 0 0 6 5 4 0 0 0 0 6 2 4 0 0 0 0 7 1 1 0 0 0 0 8 7 1 0 0 0 0 9 6 1 0 0 0 0 10 5 1 0 0 0 0 11 4 1 0 0 0 0 12 11 1 0 0 0 0 3 13 1 0 0 0 0 7 14 1 0 0 0 0 7 15 1 0 0 0 0 8 16 1 0 0 0 0 9 17 1 0 0 0 0 9 18 1 0 0 0 0 9 19 1 0 0 0 0 10 20 1 0 0 0 0 11 21 1 0 0 0 0 11 22 1 0 0 0 0 12 23 1 0 0 0 0 12 24 1 0 0 0 0 M END): 16 ms reading 24 atoms ModelSet: haveSymmetry:false haveUnitcells:false haveFractionalCoord:false 1 model in this collection. Use getProperty "modelInfo" or getProperty "auxiliaryInfo" to inspect them. Default Van der Waals type for model set to Babel 24 atoms created ModelSet: not autobonding; use forceAutobond=true to force automatic bond creation Script completed Jmol script terminated
|
Pyridoxamine (PM) is one form of vitamin B6. Chemically it is based on a pyridine ring structure, with hydroxyl, methyl, aminomethyl, and hydroxymethyl substituents. It differs from pyridoxine by the substituent at the 4-position. The hydroxyl at position 3 and aminomethyl group at position 4 of its ring endow pyridoxamine with a variety of chemical properties, including the scavenging of free radical species and carbonyl species formed in sugar and lipid degradation and chelation of metal ions that catalyze Amadori reactions. |
Read full article at Wikipedia
|
InChI=1S/C8H12N2O2/c1-5-8(12)7(2-9)6(4-11)3-10-5/h3,11-12H,2,4,9H2,1H3 |
NHZMQXZHNVQTQA-UHFFFAOYSA-N |
|
Mus musculus
(NCBI:txid10090)
|
Source: BioModels - MODEL1507180067
See:
PubMed
|
Mus musculus
(NCBI:txid10090)
|
From MetaboLights
of strain
C57bl/6 mouse (NCIT:C14424)
See:
MetaboLights Study
|
Escherichia coli
(NCBI:txid562)
|
See:
PubMed
|
Trypanosoma brucei
(NCBI:txid5691)
|
From MetaboLights
See:
MetaboLights Study
|
Homo sapiens
(NCBI:txid9606)
|
Found in
blood
(UBERON:0000178).
See:
Geigy Scientific Tables, 8th Rev edition, pp. 165-177. Edited by C. Lentner, West Cadwell, N.J.: Medical education Div., Ciba-Geigy Corp., Basel, Switzerland c1981-1992.
|
Homo sapiens
(NCBI:txid9606)
|
From MetaboLights
See:
MetaboLights Study
|
iron chelator
|
|
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
plant metabolite
Any eukaryotic metabolite produced during a metabolic reaction in plants, the kingdom that include flowering plants, conifers and other gymnosperms.
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
Saccharomyces cerevisiae metabolite
Any fungal metabolite produced during a metabolic reaction in Baker's yeast (Saccharomyces cerevisiae ).
Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
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 )
|
|
nephroprotective agent
Any protective agent that is able to prevent damage to the kidney.
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 )
|
|
View more via ChEBI Ontology
4-(aminomethyl)-5-(hydroxymethyl)-2-methylpyridin-3-ol
|
4-(AMINOMETHYL)-5-(HYDROXYMETHYL)-2-METHYLPYRIDIN-3-OL
|
PDBeChem
|
PM
|
KEGG COMPOUND
|
Pyridoxamine
|
KEGG COMPOUND
|
6993
|
Reaxys Registry Number
|
Reaxys
|
774473
|
Gmelin Registry Number
|
Gmelin
|
85-87-0
|
CAS Registry Number
|
ChemIDplus
|
85-87-0
|
CAS Registry Number
|
NIST Chemistry WebBook
|
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. | Pereira ENGDS, Silvares RR, Rodrigues KL, Flores EEI, Daliry A (2021) Pyridoxamine and Caloric Restriction Improve Metabolic and Microcirculatory Abnormalities in Rats with Non-Alcoholic Fatty Liver Disease. Journal of vascular research1-10 [PubMed:33535220] [show Abstract]
IntroductionThis study aims to examine the effect of a diet intervention and pyridoxamine (PM) supplementation on hepatic microcirculatory and metabolic dysfunction in nonalcoholic fatty liver disease (NAFLD).MethodsNAFLD in Wistar rats was induced with a high-fat diet for 20 weeks (NAFLD 20 weeks), and control animals were fed with a standard diet. The NAFLD diet intervention group received the control diet between weeks 12 and 20 (NAFLD 12 weeks), while the NAFLD 12 weeks + PM group also received PM. Fasting blood glucose (FBG) levels, body weight (BW), visceral adipose tissue (VAT), and hepatic microvascular blood flow (HMBF) were evaluated at the end of the protocol.ResultsThe NAFLD group exhibited a significant increase in BW and VAT, which was prevented by the diet intervention, irrespective of PM treatment. The FBG was elevated in the NAFLD group, and caloric restriction improved this parameter, although additional improvement was achieved by PM. The NAFLD group displayed a 31% decrease in HMBF, which was partially prevented by caloric restriction and completely prevented when PM was added. HMBF was negatively correlated to BW, FBG, and VAT content.ConclusionPM supplementation in association with lifestyle modifications could be an effective intervention for metabolic and hepatic vascular complications. | Nagai R, Shirakawa J, Ohno R, Moroishi N, Nagai M (2014) Inhibition of AGEs formation by natural products. Amino acids 46, 261-266 [PubMed:23504149] [show Abstract] Since advanced glycation end-products (AGEs) inhibitors such as benfotiamine, pyridoxamine and aminoguanidine significantly inhibit the development of retinopathy and neuropathy in streptozotocin-induced diabetic rats, treatment with AGEs inhibitors is believed to be a potential strategy for preventing lifestyle-related diseases such as diabetic complications and atherosclerosis. Furthermore, preventive medicine is the most important approach to preventing lifestyle-related diseases, and improving daily nutritional intake is thought to prevent the pathogenesis of such diseases. Therefore, AGEs inhibitors that can be obtained from daily meals are preferred to prescribed drugs. In this article, we describe a strategy for developing new AGEs inhibitors from natural products. | Almeida F, Santos-Silva D, Rodrigues T, Matafome P, Crisóstomo J, Sena C, Gonçalves L, Seiça R (2013) Pyridoxamine reverts methylglyoxal-induced impairment of survival pathways during heart ischemia. Cardiovascular therapeutics 31, e79-85 [PubMed:23841818] [show Abstract]
Background and aimsIncreased levels of advanced glycation end-products (AGE) and their precursors, such as methylglyoxal (MG), in patients with diabetes may account for impaired response to heart ischemia. Pyridoxamine is a derivate of vitamin B6, which has been shown to reduce AGE formation. Our goal was to assess the role of pyridoxamine in protecting from MG-induced impaired heart response to ischemia.MethodsWistar rats were subjected to MG administration (WM), MG plus pyridoxamine (WMPyr), or no treatment (W). Half of the hearts from each group were submitted to ischemia and the other half were perfused as control. The levels of CEL, Bcl-2, Bax, and total and phosphorylated forms of JNK and Akt were determined.ResultsMethylglyoxal led to higher levels of AGE and AGE receptor (RAGE) than in the W group. During ischemia, MG caused an impairment of survival pathways and Bcl-2/Bax ratio, a marker of apoptosis. Pyridoxamine treatment decreased glycation and restored the activation of JNK and Akt during ischemia. These events were followed by levels of Bcl-2/Bax ratio similar to W group.ConclusionMethylglyoxal-induced AGE accumulation impairs the activation of cell survival pathways during ischemia. Pyridoxamine-induced decrease of glycation inhibited the effects of MG accumulation in the heart, suggesting that it can be of added value to usual diabetic therapy. | Huang S, Zhang J, Wu M, Wu Q, Huang L (2013) Enzymatic transamination of pyridoxamine in tobacco plants. Plant science : an international journal of experimental plant biology 212, 55-59 [PubMed:24094054] [show Abstract] Vitamin B6 (VB6) comprises a group of pyridine compounds that are involved in a surprisingly high diversity of biochemical reactions. Humans and animals depend largely on plants for their VB6 nutrition. Many studies have focused on biosynthesis of VB6 and comparatively little is known about VB6 metabolic conversion in plants. Recently, we have found that an efficient conversion pathway between pyridoxal (PL) and pyridoxamine (PM) is present in tobacco, but the catalytic enzyme remains an unsolved mystery. In this study, enzymes catalyzing the transamination of PM were purified from tobacco leaves and characterized. Our results suggest that a specific PM-pyruvate aminotranferase dominates the reversible transamination of PM in tobacco, and also show that the apo form of glutamic-oxaloacetic aminotranferase from tobacco, but not the holoenzyme, is able to catalyze the analogous transamination reaction between PM and either oxaloacetate or α-ketoglutarate. PM-pyruvate aminotranferase is involved in a degradation pathway for VB6 compounds in bacteria. Therefore, our study raises questions about whether the degradation pathway of VB6 exists in plants. | Sreekumar A, Poisson LM, Rajendiran TM, Khan AP, Cao Q, Yu J, Laxman B, Mehra R, Lonigro RJ, Li Y, Nyati MK, Ahsan A, Kalyana-Sundaram S, Han B, Cao X, Byun J, Omenn GS, Ghosh D, Pennathur S, Alexander DC, Berger A, Shuster JR, Wei JT, Varambally S, Beecher C, Chinnaiyan AM (2009) Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression. Nature 457, 910-914 [PubMed:19212411] [show Abstract] Multiple, complex molecular events characterize cancer development and progression. Deciphering the molecular networks that distinguish organ-confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer (42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity. | Adrover M, Vilanova B, Frau J, Muñoz F, Donoso J (2008) The pyridoxamine action on Amadori compounds: A reexamination of its scavenging capacity and chelating effect. Bioorganic & medicinal chemistry 16, 5557-5569 [PubMed:18434162] [show Abstract] Amadori compounds act as precursors in the formation of advanced glycation end products (AGEs) by non-enzymatic protein glycation, which are involved in ensuing protein damage. Pyridoxamine is a potent drug against protein glycation, and can act on several pathways in the glycation process. Nevertheless, the pyridoxamine inhibition action on Amadori compounds oxidation is still unclear. In this work, we have studied the Schiff base formation between pyridoxamine and various Amadori models at pH 7.4 at 37 degrees C in the presence of NaCNBH(3). We detected an adduct formation, which suggests that pyridoxamine reacts with the carbonyl group in Amadori compounds. The significance of this mechanism is tested by comparison of the obtained kinetics rate constants with that obtained for 4-(aminomethyl)-pyridine, a structural analogue of pyridoxamine without post-Amadori action. We also study the chelating effect of pyridoxamine on metal ions. We have determined the complexation equilibrium constants between pyridoxamine, N-(1-deoxy-d-fructos-1-yl)-l-tryptophan, aminoguanidine, and ascorbic acid in the presence of Zn(2+). The results show that the strong stability of pyridoxamine complexes is the key in its post-Amadori inhibition action. On the other hand results explain the lack of inhibition of aminoguanidine (a glycation inhibitor) in the post-Amadori reactions. | 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. | Berzas Nevado JJ, Murillo Pulgarín JA, Gómez Laguna MA (1995) Determination of pyridoxamine in urine by matrix isopotential synchronous fluorescence spectrometry. The Analyst 120, 171-174 [PubMed:7710125] [show Abstract] A spectrofluorimetric technique was applied to the determination of compounds in samples with unknown background fluorescence, consisting of performing synchronous scans through a trajectory joining points of equal intensity of a fluorescence matrix three-dimensional spectrum, which is called 'matrix isopotential synchronous fluorescence'. This technique can be improved by application of derivatives. The determination of pyridoxamine in urine was performed using this technique and the validity, applicability and simplicity of the method were demonstrated. With first-derivative matrix isopotential synchronous fluorescence the maximum sensitivity was 12.5 mg l-1 for pyridoxamine in real urine samples. The measurements were performed in aqueous medium at pH 7.0, adjusted by adding 0.05 mol l-1 phosphate buffer, and without any previous derivatization reactions. A complete statistical analysis of the experimental data was performed. Pyridoxamine in urine was determined by this method with good results and without the need for tedious prior separation. | Rokitzki L, Sagredos AN, Reuss F, Büchner M, Keul J (1994) Acute changes in vitamin B6 status in endurance athletes before and after a marathon. International journal of sport nutrition 4, 154-165 [PubMed:8054960] [show Abstract] The vitamin B6 status of 13 endurance athletes was determined by whole blood B6 (microbiological) and urine 4-pyridoxic acid (4-PA) (HPLC), serum vitamin B6 (pyridoxal, pyridoxol, pyridoxamine) (HPLC), and erythrocyte alpha-EGOT measurements with the aid of 7-day records. In addition, blood and serum samples and urine were collected before (Time A), directly after (Time B), and 2 hr after a marathon race (Time C). The total energy intake was 12,303 +/- 3,464 kJ/day (34% fat, 48% carbohydrates, 14% protein). The vitamin B6 intake, serum concentrations, alpha-EGOT value, and 4-PA excretion were higher than the reference values at Time A. Only the vitamin B6 whole blood levels were below the normal level at Time A. The vitamin B6 status of the athletes corresponded essentially to reference values obtained for untrained individuals. There was a mean loss of about 1 mg vitamin B6 as a result of the marathon race. Vitamin B6 supplementation does not appear necessary if a balanced diet is consumed. | Sharma SK, Dakshinamurti K (1992) Determination of vitamin B6 vitamers and pyridoxic acid in biological samples. Journal of chromatography 578, 45-51 [PubMed:1400785] [show Abstract] For the determination of vitamin B6 vitamers (pyridoxal phosphate, pyridoxamine phosphate, pyridoxal, pyridoxine, pyridoxamine) and 4-pyridoxic acid in biological samples such as plasma, cerebrospinal fluid and rat brain regions, a sensitive micromethod using high-performance liquid chromatography (HPLC) with fluorescence detection in combination with post-column derivatization is described. Metaphosphoric acid tissue extracts with deoxypyridoxine as an internal standard were injected into the HPLC system with a binary gradient elution at a flow-rate of 1.2 ml/min. The excitation wavelength of the fluorescence detector was set at 328 nm and the emission wavelength at 393 nm with a 15-nm slit width for the photocell. This method allows the assay of vitamin B6 vitamers within 30 min in one chromatographic run. The present method has been applied extensively for the measurement of vitamin B6 vitamer levels in discrete brain regions of small animals, cells in culture and biopsy samples. | 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. |
|