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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__852246805462669__ initializing getValue debug = null getValue logLevel = null getValue allowjavascript = null AppletRegistry.checkIn(jmolApplet0_object__852246805462669__) 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:28747","platform":"J.awtjs2d.Platform","fullName":"jmolApplet0_object__852246805462669__","display":"jmolApplet0_canvas2d","signedApplet":"true","appletReadyCallback":"Jmol._readyCallback","statusListener":"[J.appletjs.Jmol.MyStatusListener object]","codeBase":"https://www.ebi.ac.uk/chebi/javascripts/jsmol/","syncId":"852246805462669","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__852246805462669__ 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 04091312233D starting HoverWatcher_5 Time for openFile( Marvin 04091312233D 14 14 0 0 0 0 999 V2000 -0.6596 0.9116 0.0000 N 0 0 0 0 0 0 0 0 0 0 0 0 -1.8440 0.2484 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 0.5643 0.3098 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 0.5938 -1.1062 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 -1.8440 -1.1573 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.6110 -1.8337 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 2.8354 0.5984 0.0000 O 0 0 0 0 0 0 0 0 0 0 0 0 1.7126 1.0844 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 1.6693 2.3097 0.0000 O 0 0 0 0 0 0 0 0 0 0 0 0 -2.7222 0.7707 0.0000 H 0 0 0 0 0 0 0 0 0 0 0 0 1.4765 -1.6213 0.0000 H 0 0 0 0 0 0 0 0 0 0 0 0 -2.7219 -1.6799 0.0000 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.5867 -2.8547 0.0000 H 0 0 0 0 0 0 0 0 0 0 0 0 2.4111 2.7850 0.0000 H 0 0 0 0 0 0 0 0 0 0 0 0 2 1 4 0 0 0 0 1 3 4 0 0 0 0 3 8 1 0 0 0 0 3 4 4 0 0 0 0 5 2 4 0 0 0 0 6 5 4 0 0 0 0 6 4 4 0 0 0 0 8 7 2 0 0 0 0 9 8 1 0 0 0 0 2 10 1 0 0 0 0 4 11 1 0 0 0 0 5 12 1 0 0 0 0 6 13 1 0 0 0 0 9 14 1 0 0 0 0 M END): 17 ms reading 14 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 14 atoms created ModelSet: not autobonding; use forceAutobond=true to force automatic bond creation Script completed Jmol script terminated
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| Picolinic acid is an organic compound with the formula NC5H4CO2H. It is a derivative of pyridine with a carboxylic acid (COOH) substituent at the 2-position. It is an isomer of nicotinic acid and isonicotinic acid, which have the carboxyl side chain at the 3- and 4-positions, respectively. It is a white solid although impure samples can appear tan. The compound is soluble in water. |
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Read full article at Wikipedia
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| InChI=1S/C6H5NO2/c8-6(9)5-3-1-2-4-7-5/h1-4H,(H,8,9) |
| SIOXPEMLGUPBBT-UHFFFAOYSA-N |
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via oxoacid )
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human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
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MALDI matrix material
A compound used to form the matrix for MALDI (matrix-assisted laser desorption/ionization) mass spectrometry. MALDI matrix materials are crystalline compounds with a fairly low molecular weight, so as to allow facile vaporization, have strong absorption at UV or IR wavelengths (to rapidly and efficiently absorb laser irradiation), generally contain polar groups (enabling them to be used in aqueous solutions) and are frequently acidic (so assisting ionisation of the compound being studied, which is contained within the matrix material).
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View more via ChEBI Ontology
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pyridine-2-carboxylic acid
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2-carboxypyridine
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NIST Chemistry WebBook
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2-Picolinic acid
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HMDB
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2-Pyridinecarboxylic acid
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KEGG COMPOUND
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α-picolinic acid
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ChEBI
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α-pyridinecarboxylic acid
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NIST Chemistry WebBook
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o-pyridinecarboxylic acid
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NIST Chemistry WebBook
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Picolinic acid
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KEGG COMPOUND
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PYRIDINE-2-CARBOXYLIC ACID
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PDBeChem
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109595
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Reaxys Registry Number
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Reaxys
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3318
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Gmelin Registry Number
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Gmelin
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98-98-6
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CAS Registry Number
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KEGG COMPOUND
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98-98-6
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CAS Registry Number
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ChemIDplus
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98-98-6
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CAS Registry Number
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NIST Chemistry WebBook
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Wang X, Davis I, Liu A, Miller A, Shamsi SA (2013)
Improved separation and detection of picolinic acid and quinolinic acid by capillary electrophoresis-mass spectrometry: application to analysis of human cerebrospinal fluid.
Journal of chromatography. A 1316, 147-153 [PubMed:24119749]
[show Abstract]
"Quinolinic acid (QA)", a metabolite of the kynurenine pathway (KP), is implicated as a major neurological biomarker, which causes inflammatory disorders, whereas there is an increase evidence of the role of picolinic acid (PA) in neuroinflammation. Therefore, there is an urgent need to develop new clinical test for early diagnosis of neuroinflammatory disorders. A comparison is made between three different platforms such as high performance liquid chromatography-electrospray mass spectrometry (HPLC-ESI-MS/MS), nano LC-Chip/ESI-MS/MS, as well as the use of cationic (quaternary ammonium) and anionic (sulfonated) coated capillaries in capillary electrophoresis (CE)-ESI-MS/MS. The comparison revealed that CE-ESI-MS/MS method using a quaternary ammonium coated capillary is the best method for analysis of PA and QA. A simple stacking procedure by the inclusion of acetonitrile in the artificial cerebrospinal fluid (CSF) sample was employed to improve the peak shape and sensitivity of KP metabolites in CE-ESI-MS/MS. The developed CE-ESI-MS/MS assay provided high resolution, high specificity and high sensitivity with a total analysis time including sample preparation of nearly 12 min. In addition, excellent intra-day and inter-day repeatability of migration times and peak areas of the metabolites were observed with respective relative standard deviation (RSD) of less than 2.0% and 2.5%. Somewhat broader variations in repeatability for a 3 independently prepared coated capillary (total 35 runs each) with % RSD up to 3.8% and 5.8% was observed for migration time and peak areas, respectively. Artificial CSF was used as a surrogate matrix to simultaneously generate calibration curves over a concentration range of 0.02-10 μM for PA and 0.4-40 μM for QA. The method was then successfully applied to analyze PA and QA in human CSF, demonstrating the potential of this CE-ESI-MS/MS method to accurately quantitate with high specificity and sensitivity. | Wu W, Nicolazzo JA, Wen L, Chung R, Stankovic R, Bao SS, Lim CK, Brew BJ, Cullen KM, Guillemin GJ (2013)
Expression of tryptophan 2,3-dioxygenase and production of kynurenine pathway metabolites in triple transgenic mice and human Alzheimer's disease brain.
PloS one 8, e59749 [PubMed:23630570]
[show Abstract]
To assess the role of the kynurenine pathway in the pathology of Alzheimer's disease (AD), the expression and localization of key components of the kynurenine pathway including the key regulatory enzyme tryptophan 2,3 dioxygenase (TDO), and the metabolites tryptophan, kynurenine, kynurenic acid, quinolinic acid and picolinic acid were assessed in different brain regions of triple transgenic AD mice. The expression and cell distribution of TDO and quinolinic acid, and their co-localization with neurofibrillary tangles and senile β amyloid deposition were also determined in hippocampal sections from human AD brains. The expression of TDO mRNA was significantly increased in the cerebellum of AD mouse brain. Immunohistochemistry demonstrated that the density of TDO immuno-positive cells was significantly higher in the AD mice. The production of the excitotoxin quinolinic acid strongly increased in the hippocampus in a progressive and age-dependent manner in AD mice. Significantly higher TDO and indoleamine 2,3 dioxygenase 1 immunoreactivity was observed in the hippocampus of AD patients. Furthermore, TDO co-localizes with quinolinic acid, neurofibrillary tangles-tau and amyloid deposits in the hippocampus of AD. These results show that the kynurenine pathway is over-activated in AD mice. This is the first report demonstrating that TDO is highly expressed in the brains of AD mice and in AD patients, suggesting that TDO-mediated activation of the kynurenine pathway could be involved in neurofibrillary tangles formation and associated with senile plaque. Our study adds to the evidence that the kynurenine pathway may play important roles in the neurodegenerative processes of AD. | Cai S, Sato K, Shimizu T, Yamabe S, Hiraki M, Sano C, Tomioka H (2006)
Antimicrobial activity of picolinic acid against extracellular and intracellular Mycobacterium avium complex and its combined activity with clarithromycin, rifampicin and fluoroquinolones.
The Journal of antimicrobial chemotherapy 57, 85-93 [PubMed:16303883]
[show Abstract]
ObjectivesA natural metal ion chelator, picolinic acid (PA), is known to potentiate macrophage antimycobacterial activity. Here, we studied the antimicrobial activity of PA against extracellular and intramacrophage Mycobacterium avium complex (MAC) organisms.MethodsMAC organisms, MAC-infected macrophages or MAC-infected type II pneumocytes were cultured in the presence or absence of PA with or without antimycobacterial drugs, and residual bacterial cfu of extracellular or intracellular MAC were counted on 7H11 agar plates.ResultsFirst, PA exhibited antimicrobial activity against extracellular and intramacrophage MAC. The effect of PA was mimicked by other metal ion-chelating agents, such as ethylenediamine tetraacetic acid and O,O'-bis (2-aminophenyl) ethyleneglycol-N,N,N',N'-tetraacetic acid. Second, PA potentiated antimicrobial effects of a two-drug combination of clarithromycin/rifampicin and some fluoroquinolones (levofloxacin, sitafloxacin and gatifloxacin) against extracellular and intramacrophage MAC. Similar combined effects of PA with clarithromycin/rifampicin were also seen in the case of MAC residing within type II alveolar epithelial cells.ConclusionsPA exerted an appreciable anti-MAC activity, when used singly or in combination with some antimycobacterial drugs (clarithromycin/rifampicin and fluoroquinolones), suggesting the usefulness of PA as an adjunct for clinical antimicrobial chemotherapy of MAC infections. | Abe S, Hu W, Ishibashi H, Hasumi K, Yamaguchi H (2004)
Augmented inhibition of Candida albicans growth by murine neutrophils in the presence of a tryptophan metabolite, picolinic acid.
Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy 10, 181-184 [PubMed:15290459]
[show Abstract]
The effects of picolinic acid (PLA), a product of tryptophan catabolism, on anti- Candida activity of neutrophils were studied. Casein-induced peritoneal neutrophils of C3H/He mice partially inhibited mycelial growth of Candida albicans when cultured with C. albicans for 16 h in vitro. The growth inhibition of Candida was augmented by a combination of neutrophils and more than 4 mM picolinic acid. Especially in the presence of 200 U/ml murine interferon-gamma (IFN-gamma), 2 mM picolinic acid augmented the anti- Candida activity of neutrophils. The physiological significance of the augmenting effects of picolinic acid is discussed. | Bosco MC, Rapisarda A, Reffo G, Massazza S, Pastorino S, Varesio L (2003)
Macrophage activating properties of the tryptophan catabolite picolinic acid.
Advances in experimental medicine and biology 527, 55-65 [PubMed:15206716]
[show Abstract]
Recent studies have suggested a role for aminoacid catabolites as important regulators of macrophage (Mphi) activities. We reported previously that picolinic acid (PA), a tryptophan catabolite produced under inflammatory conditions and a costimulus with IFNgamma of Mphi effector functions, is a selective inducer of the Mphi inflammatory protein-1alpha (MIP-1alpha) and -1beta (MIPs), two CC-chemokines involved in the elicitation of the inflammatory reactions and in the development of the Th1 responses. In this study, we have investigated the effects of IFNgamma on PA-induced MIPs expression and secretion by mouse Mphi as well as the regulation of MIP-1alpha/beta receptor, CCR5, by both stimuli alone or in combination. We demonstrated that IFNgamma inhibited MIPs mRNA stimulation by PA in a dose-and time-dependent fashion, despite its ability to induce other CC- or CXC chemokines. MIPs mRNA down-regulation was associated with decreased intracellular chemokine expression and secretion and was dependent on both mRNA destabilization and gene transcription inhibition. Moreover, IFNgamma inhibitory effects were stimulus-specific because MIPs induction by PA was either unaffected or increased by the anti-inflammatory cytokines, IL-10 and IL-4, or the pro-inflammatory stimulus, LPS, respectively. In contrast, we found that IFNgamma increased CCR5 basal expression, whereas PA down-regulated both constitutive and IFNgamma-induced CCR5 mRNA and protein levels. These results demonstrate that IFNgamma and PA have reciprocal effects on the production of MIPs chemokines and the expression of their receptor. The concerted action of IFNgamma and PA on MIP-1alpha/beta chemokine/receptor system is likely to be of pathophysiological significance and to represent an important regulatory mechanism for leukocyte recruitment and distribution into damaged tissues during inflammatory responses. | Smythe GA, Poljak A, Bustamante S, Braga O, Maxwell A, Grant R, Sachdev P (2003)
ECNI GC-MS analysis of picolinic and quinolinic acids and their amides in human plasma, CSF, and brain tissue.
Advances in experimental medicine and biology 527, 705-712 [PubMed:15206793]
[show Abstract]
To study the complex inter-relationships between inflammatory and apoptotic responses and the kynurenine pathway, we have utilized electron-capture negative ion mass spectrometry to develop trace analyses to concurrently quantify nicotinic acid (NIC), picolinic acid (PIC) and quinolinic acid (QUIN) in biological samples. We have shown that NIC and its amide nicotinamide (NAM) can be separately quantified by analyzing samples pre- and post-acid hydrolysis. We have now examined human plasma, CSF and brain tissue samples for the presence of putative picolinamide (PAM) and quinolinamide (QAM) by comparing PIC and QUIN concentrations pre- and post- gas phase hydrolysis. We report for the first time that, with respect to the free acids, relatively high concentrations of the amides (or, at least, hydrolysable precursors of the acids) are present in plasma and brain with marked relative increases in CSF. In normal control subjects (n=22) pre-hydrolysis plasma levels (+/- sem) of PIC and QUIN were 0.299 +/- 0.034 and 0.47 +/- 0.047 micromol/L respectively. Following hydrolysis the concentrations rose more than 4-fold to 1.33 +/- 0.115 and 2.2 +/- 0.27 micromol/L respectively. In CSF samples from patients with no sign of brain injury or pathology (n=10) pre-hydrolysis concentrations of PIC and QUIN were 0.017 +/- 0.005 and 0.018 +/- 0.006 micromol/L, respectively, which rose to 0.30 +/- 0.06 and 0.06 +/- 0.008 micromol/L respectively, after hydrolysis. In CSF samples from patients with a range of brain oedema or injury (eg subdural haemorrage, motor vehicle accident) (n=6) pre-hydrolysis concentrations of PIC and QUIN were 0.053 +/- 0.03 and 0.29 +/- 0.12 micromol/L, respectively. Following hydrolysis the concentrations were markedly increased to 6.06 +/- 1.5 and 0.94 +/- 0.63 micromol/L, respectively. The present investigation has shown for the first time that PAM and QAM are present endogenously with PAM being relatively higher than QAM, especially in CSF samples from patients with presumed brain inflammation. The site and mechanism of amidation of PIC and QUIN needs investigation. | Beninger RJ, Colton AM, Ingles JL, Jhamandas K, Boegman RJ (1994)
Picolinic acid blocks the neurotoxic but not the neuroexcitant properties of quinolinic acid in the rat brain: evidence from turning behaviour and tyrosine hydroxylase immunohistochemistry.
Neuroscience 61, 603-612 [PubMed:7969932]
[show Abstract]
Previous results suggest that the tryptophan metabolite, picolinic acid may have the unusual properties of antagonizing the neurotoxic but not the neuroexcitant effects of another tryptophan metabolite, quinolinic acid in the central nervous system. The present experiments tested this possibility utilizing behavioural and tyrosine hydroxylase immunohistochemical techniques. In the first series of experiments, rats received injections of relatively high concentrations of 6-hydroxydopamine (12 micrograms in 1 or 2 microliters), quinolinic acid (120 nmol in 0.5 microliters), picolinic acid (480 nmol in 0.5 microliters) or co-treatments (0.5 microliters) with quinolinic (120 nmol) plus picolinic acid (480 nmol) into the region of the substantia nigra. Results revealed that 6-hydroxydopamine and quinolinic acid alone produced a large loss of tyrosine hydroxylase-positive cells in the pars compacta of the substantia nigra. Behavioural results for all 6-hydroxydopamine (n = 10) and for some quinolinate-treated rats (n = 5) revealed ipsi- and contraversive circling following amphetamine (1 mg/kg, i.p.) and apomorphine (0.5 mg/kg, s.c.), respectively, consistent with unilateral loss of dopamine cells in the substantia nigra. The remaining quinolinate-treated rats (n = 9) circled ipsiversively following either stimulant suggesting damage to the pars reticulata. Groups treated with picolinic acid alone (n = 6) or co-injected (n = 6) showed no loss of tyrosine hydroxylase-positive cells in the substantia nigra and no circling response to the stimulants. In the second series of experiments, low concentrations of quinolinic acid (2.5, 5.0, 7.5 nmol), picolinic acid (10, 20, 30 nmol), or the two together (7.5 plus 30 nmol, respectively) were microinjected (0.5 microliter) into the dorsal striatum and circling behaviour evaluated. These results revealed dose-dependent contralateral circling with either quinolinate or picolinate; co-injection of the two tryptophan metabolites also produced contralateral circling. It was concluded that picolinic acid blocks the neurotoxic but not the neuroexcitant effects of quinolinic acid. | Rebello T, Lönnerdal B, Hurley LS (1982)
Picolinic acid in milk, pancreatic juice, and intestine: inadequate for role in zinc absorption.
The American journal of clinical nutrition 35, 1-5 [PubMed:7064867]
[show Abstract]
Picolinic acid (PA) was measured by high pressure liquid chromatography in human milk and other fluids and tissues. Skimmed human milk, intestinal homogenates from human infants and rats, and human and rat pancreatic juice were ultrafiltered and analyzed by high pressure liquid chromatography using an anion-exchange column. Identity of sample components was verified by comparing retention times with those of pure nicotinic acid and PA. The detection limit for PA was 2.5 microM. Human milk contained less than 3.7 microM PA. PA was undetectable in human infant or rat intestine or in human or rat pancreatic juice. The extremely low concentration of PA in milk and its apparent absence in pancreatic juice and intestine provide additional evidence that PA is not the low molecular weight zinc binding ligand of human milk and that it does not have an important physiological role in intestinal zinc absorption. |
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