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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__249666162914086__ initializing getValue debug = null getValue logLevel = null getValue allowjavascript = null AppletRegistry.checkIn(jmolApplet0_object__249666162914086__) 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:41941","platform":"J.awtjs2d.Platform","fullName":"jmolApplet0_object__249666162914086__","display":"jmolApplet0_canvas2d","signedApplet":"true","appletReadyCallback":"Jmol._readyCallback","statusListener":"[J.appletjs.Jmol.MyStatusListener object]","codeBase":"https://www.ebi.ac.uk/chebi/javascripts/jsmol/","syncId":"249666162914086","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__249666162914086__ 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 02010809073D starting HoverWatcher_5 Time for openFile( Marvin 02010809073D 20 20 0 0 0 0 999 V2000 0.8904 -0.2008 0.5427 C 0 0 0 0 0 0 0 0 0 0 0 0 1.7147 0.6284 -0.2428 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.5164 -0.0626 0.5227 C 0 0 0 0 0 0 0 0 0 0 0 0 -1.0860 0.9302 -0.3065 C 0 0 0 0 0 0 0 0 0 0 0 0 -0.2711 1.7656 -1.0901 C 0 0 0 0 0 0 0 0 0 0 0 0 1.1299 1.6187 -1.0605 C 0 0 0 0 0 0 0 0 0 0 0 0 -1.7146 -2.1536 0.5551 C 0 0 0 0 0 0 0 0 0 0 0 0 -2.8753 -2.4285 0.2909 O 0 0 0 0 0 0 0 0 0 0 0 0 -0.8520 -2.9187 0.1352 O 0 0 0 0 0 0 0 0 0 0 0 0 -1.3742 -0.9731 1.3215 C 0 0 0 0 0 0 0 0 0 0 0 0 1.8392 2.3759 -1.7692 O 0 0 0 0 0 0 0 0 0 0 0 0 2.9609 0.4643 -0.2022 O 0 0 0 0 0 0 0 0 0 0 0 0 1.3235 -0.9216 1.1280 H 0 0 0 0 0 0 0 0 0 0 0 0 -2.1011 1.0503 -0.3534 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.7074 2.4767 -1.6826 H 0 0 0 0 0 0 0 0 0 0 0 0 0.0015 -2.7532 0.2793 H 0 0 0 0 0 0 0 0 0 0 0 0 -2.2716 -0.4446 1.6580 H 0 0 0 0 0 0 0 0 0 0 0 0 -0.8673 -1.2841 2.2392 H 0 0 0 0 0 0 0 0 0 0 0 0 1.4649 2.9925 -2.2746 H 0 0 0 0 0 0 0 0 0 0 0 0 3.3122 -0.1619 0.3093 H 0 0 0 0 0 0 0 0 0 0 0 0 2 1 4 0 0 0 0 2 12 1 0 0 0 0 1 3 4 0 0 0 0 3 10 1 0 0 0 0 4 3 4 0 0 0 0 5 4 4 0 0 0 0 6 2 4 0 0 0 0 6 5 4 0 0 0 0 11 6 1 0 0 0 0 8 7 2 0 0 0 0 9 7 1 0 0 0 0 10 7 1 0 0 0 0 1 13 1 0 0 0 0 4 14 1 0 0 0 0 5 15 1 0 0 0 0 9 16 1 0 0 0 0 10 17 1 0 0 0 0 10 18 1 0 0 0 0 11 19 1 0 0 0 0 12 20 1 0 0 0 0 M END): 19 ms reading 20 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 20 atoms created ModelSet: not autobonding; use forceAutobond=true to force automatic bond creation Script completed Jmol script terminated
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| 3,4-Dihydroxyphenylacetic acid (DOPAC) is a metabolite of the neurotransmitter dopamine. Dopamine can be metabolized into one of three substances. One such substance is DOPAC. Another is 3-methoxytyramine (3-MT). Both of these substances are degraded to form homovanillic acid (HVA). Both degradations involve the enzymes monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT), albeit in reverse order: MAO catalyzes dopamine to DOPAC, and COMT catalyzes DOPAC to HVA; whereas COMT catalyzes dopamine to 3-MT and MAO catalyzes 3-MT to HVA. The third metabolic end-product of dopamine is norepinephrine (noradrenaline).
It can also be found in the bark of Eucalyptus globulus.
This product has been synthesized (52% yield) from 4-hydroxyphenylacetic acid via aerobic biotransformation using whole cell cultures of Arthrobacter protophormiae. |
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Read full article at Wikipedia
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| InChI=1S/C8H8O4/c9-6-2-1-5(3-7(6)10)4-8(11)12/h1-3,9-10H,4H2,(H,11,12) |
| CFFZDZCDUFSOFZ-UHFFFAOYSA-N |
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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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View more via ChEBI Ontology
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Outgoing
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(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
has functional parent
phenylacetic acid
(CHEBI:30745)
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
has role
human metabolite
(CHEBI:77746)
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
is a
catechols
(CHEBI:33566)
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
is a
dihydroxyphenylacetic acid
(CHEBI:61409)
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
is conjugate acid of
(3,4-dihydroxyphenyl)acetate
(CHEBI:17612)
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Incoming
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homovanillic acid
(CHEBI:545959)
has functional parent
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
isohomovanillic acid
(CHEBI:70818)
has functional parent
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
(3,4-dihydroxyphenyl)acetate
(CHEBI:17612)
is conjugate base of
(3,4-dihydroxyphenyl)acetic acid
(CHEBI:41941)
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(3,4-dihydroxyphenyl)acetic acid
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2-(3,4-DIHYDROXYPHENYL)ACETIC ACID
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PDBeChem
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3,4-Dihydroxyphenyl acetic acid
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KEGG COMPOUND
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3,4-Dihydroxyphenylacetic acid
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KEGG COMPOUND
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dopacetic acid
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NIST Chemistry WebBook
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homoprotocatechuic acid
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NIST Chemistry WebBook
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102-32-9
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CAS Registry Number
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NIST Chemistry WebBook
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102-32-9
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CAS Registry Number
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ChemIDplus
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2211017
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Beilstein Registry Number
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Beilstein
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2211017
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Reaxys Registry Number
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Reaxys
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874810
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Gmelin Registry Number
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Gmelin
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Roux A, Xu Y, Heilier JF, Olivier MF, Ezan E, Tabet JC, Junot C (2012)
Annotation of the human adult urinary metabolome and metabolite identification using ultra high performance liquid chromatography coupled to a linear quadrupole ion trap-Orbitrap mass spectrometer.
Analytical chemistry 84, 6429-6437 [PubMed:22770225]
[show Abstract]
Metabolic profiles of biofluids obtained by atmospheric pressure ionization mass spectrometry-based technologies contain hundreds to thousands of features, most of them remaining unknown or at least not characterized in analytical systems. We report here on the annotation of the human adult urinary metabolome and metabolite identification from electrospray ionization mass spectrometry (ESI-MS)-based metabolomics data sets. Features of biological interest were first of all annotated using the ESI-MS database of the laboratory. They were also grouped, thanks to software tools, and annotated using public databases. Metabolite identification was achieved using two complementary approaches: (i) formal identification by matching chromatographic retention times, mass spectra, and also product ion spectra (if required) of metabolites to be characterized in biological data sets to those of reference compounds and (ii) putative identification from biological data thanks to MS/MS experiments for metabolites not available in our chemical library. By these means, 384 metabolites corresponding to 1484 annotated features (659 in negative ion mode and 825 in positive ion mode) were characterized in human urine samples. Of these metabolites, 192 and 66 were formally and putatively identified, respectively, and 54 are reported in human urine for the first time. These lists of features could be used by other laboratories to annotate their ESI-MS metabolomics data sets. | Appeldoorn MM, Vincken JP, Aura AM, Hollman PC, Gruppen H (2009)
Procyanidin dimers are metabolized by human microbiota with 2-(3,4-dihydroxyphenyl)acetic acid and 5-(3,4-dihydroxyphenyl)-gamma-valerolactone as the major metabolites.
Journal of agricultural and food chemistry 57, 1084-1092 [PubMed:19191673]
[show Abstract]
Procyanidins (PCs) are highly abundant phenolic compounds in the human diet and might be responsible for the health effects of chocolate and wine. Due to low absorption of intact PCs, microbial metabolism might play an important role. So far, only a few studies, with crude extracts rich in PCs but also containing a multitude of other phenolic compounds, have been performed to reveal human microbial PC metabolites. Therefore, the origin of the metabolites remains questionable. This study included in vitro fermentation of purified PC dimers with human microbiota. The main metabolites identified were 2-(3,4-dihydroxyphenyl)acetic acid and 5-(3,4-dihydroxyphenyl)-gamma-valerolactone. Other metabolites detected were 3-hydroxyphenylacetic acid, 4-hydroxyphenylacetic acid, 3-hydroxyphenylpropionic acid, phenylvaleric acids, monohydroxylated phenylvalerolactone, and 1-(3',4'-dihydroxyphenyl)-3-(2'',4'',6''-trihydroxyphenyl)propan-2-ol. Metabolites that could be quantified accounted for at least 12 mol % of the dimers, assuming 1 mol of dimers is converted into 2 mol of metabolite. A degradation pathway, partly different from that of monomeric flavan-3-ols, is proposed. | Nunes C, Almeida L, Laranjinha J (2008)
3,4-Dihydroxyphenylacetic acid (DOPAC) modulates the toxicity induced by nitric oxide in PC-12 cells via mitochondrial dysfunctioning.
Neurotoxicology 29, 998-1007 [PubMed:18706927]
[show Abstract]
It has been postulated that dihydroxyphenylacetic acid (DOPAC), a major dopamine metabolite, and nitric oxide (NO) induce mitochondrial dysfunction in a synergistic manner. We examined the combined effects of NO and DOPAC on PC-12 cells in terms of cell viability, nuclear morphology, mitochondrial parameters and cell death mechanisms. The apoptotic cell death induced by the NO-donor, S-nitroso-N-acetylpenicillamine (SNAP), was differently modulated by DOPAC as a function of DOPAC/cell ratios. Whereas below 200nmol/10(6) cells, DOPAC inhibited a typical apoptotic pathway induced by exposure the cells to the NO donor, above 200nmol DOPAC/10(6) cells, the cell death was not only enhanced but encompassed a distinct mechanism. Loading the cells with dopamine mimicked the effects of DOPAC. Specifically, the combination of DOPAC and NO induced an early mitochondrial membrane potential dissipation and ATP depletion followed by loss of cellular membrane integrity. Mitochondrial dysfunction was accompanied by the release of cytochrome c in both cases, NO individually and in combination with DOPAC, but caspase-3 and caspase-9 activation were only observed in the absence of DOPAC. DOPAC alone was ineffective. Thus, our results suggest a role for DOPAC as a modulator of cell fate and point to a pathway of cell death involving DOPAC and NO, via mechanisms that include mitochondrial dysfunction but do not involve the activation of the typical apoptotic caspase cascade. The significance of these results is discussed in connection with the mechanisms of cell death underlying Parkinson's disease. | Kurling S, Kankaanpää A, Ellermaa S, Karila T, Seppälä T (2005)
The effect of sub-chronic nandrolone decanoate treatment on dopaminergic and serotonergic neuronal systems in the brains of rats.
Brain research 1044, 67-75 [PubMed:15862791]
[show Abstract]
Anabolic-androgenic steroids (AASs) are widely abused by adolescents, although persistent AAS use can cause several adverse physical and mental effects, including drug dependence. The first aim of the present study was to study the action of nandrolone decanoate on dopaminergic and serotonergic activities in the brains of rats. In order to evaluate the anabolic or toxic effects of the dosing regimens used, selected peripheral effects were monitored as well. Male Wistar rats were treated for 2 weeks. Injections containing nandrolone (5 and 20 mg/kg, i.m.) or vehicle were given once daily, 5 days a week. The levels of dopamine (DA), 5-hydroxytryptamine (5-HT) and their metabolites were assayed from dissected brain regions 3 days after the last injection. Blood was collected for chemical assays before, after 1 week treatment and at decapitation. Both doses of nandrolone significantly increased the levels of 3,4-dihydroxyphenylacetic acid (DOPAC), a metabolite of DA in the cerebral cortex, and the higher dose of nandrolone increased the concentrations of 5-HT in the cerebral cortex compared with the vehicle. In addition, after nandrolone treatment, the levels of hemoglobin and erythrocytes increased, and reticulocyte levels decreased. The results suggest that nandrolone at supraphysiological doses, high enough to induce erythropoiesis, induces changes in the dopaminergic and serotonergic neuronal system in the brains of rats. These phenomena may account to some of the observed central stimulatory properties that have been reported following AAS abuse. | Janhunen S, Ahtee L (2004)
Comparison of the effects of nicotine and epibatidine on the striatal extracellular dopamine.
European journal of pharmacology 494, 167-177 [PubMed:15212971]
[show Abstract]
We compared the effects of nicotine and epibatidine on striatal extracellular dopamine and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), by microdialysis in freely moving rats. Nicotine (0.5 mg/kg) elevated dopamine in the caudate-putamen and somewhat more in the nucleus accumbens. Epibatidine at 0.3 microg/kg reduced, and at 0.6 and 1.0 microg/kg increased, dopamine in the caudate-putamen; 2.0 and 3.0 microg/kg had no effect. Accumbal dopamine epibatidine elevated only at 3.0 microg/kg. Thus, in contrast to nicotine, epibatidine increased dopamine output in the caudate-putamen at smaller doses than in the accumbens. Both epibatidine and nicotine enhanced accumbal dopamine metabolism clearly more than that in the caudate-putamen. Also epibatidine was found to elevate 5-hydroxyindoleacetic acid (5-HIAA) in the nucleus accumbens at smaller doses than in the caudate-putamen. Similarly to what has been reported concerning nicotine, the dose-response curve of epibatidine to increase the dopamine output in the caudate-putamen was bell-shaped and clearly differed from that in the accumbens. These findings indicate that the nicotinic mechanisms controlling dopamine release and metabolism in the nigrostriatal and mesolimbic dopaminergic pathways differ fundamentally. | Ferreira A, Bettencourt P, Pimenta J, Friões F, Pestana M, Soares-da-Silva P, Cerqueira-Gomes M (2002)
The renal dopaminergic system, neurohumoral activation, and sodium handling in heart failure.
American heart journal 143, 391-397 [PubMed:11868042]
[show Abstract]
BackgroundDopamine of renal origin exerts natriuretic and diuretic actions by activating specific receptors located in the renal proximal tubular epithelial cells. Heart failure (HF) is accompanied by activation of several neurohumoral systems. The interaction of these systems with the renal dopaminergic system and its effect on sodium handling in HF are not clarified.Methods and resultsWe studied 13 patients with decompensated New York Heart Association class III/IV HF and 17 sex- and age-matched patients with mild to moderate stable class I/II HF. We measured plasma catecholamines, aldosterone, type B natriuretic peptide (BNP), sodium, creatinine (UCr), and 24-hour urinary excretion of sodium, UCr, levo-3,4-dihydroxyphenylalanine (L-DOPA), 3-o -methyldopa, dopamine and its metabolites, 3,4-dihydroxyphenylacetic acid and homovallinic acid, and norepinephrine. All patients had HF of ischemic etiology. No statistically significant differences were found between the groups with respect to urine volume (1.79 +/- 0.23 L x d(-1) vs 2.20 +/- 0.18 L x d(-1), P =.18) and urinary sodium (161.3 +/- 27.5 mmol x d(-1) vs 232.9 +/- 28.8 mmol x d(-1), P =.12). Urinary L-DOPA was significantly lower in patients with decompensated class III/IV HF than in the other group (79.0 +/- 13.8 nmol x g UCr(-1) vs 108.4 +/- 10.3 nmol x g UCr(-1), P =.04). Urinary dopamine showed a nonstatistically significant trend to be slightly higher (1294.3 +/- 188.5 nmol x g UCr(-1) vs 953.2 +/- 107.4 nmol x g UCr(-1), P =.14). Consequently, urinary dopamine/L-DOPA ratios were markedly higher in patients with decompensated class III/IV HF than in the other patients (20.6 +/- 3.4 vs 9.0 +/- 0.9, P <.001). Plasma L-DOPA (38.1 +/- 4.4 pmol x mL(-1) vs 40.0 +/- 3.0 pmol x mL(-1), P =.48), dopamine (37.0 +/- 6.3 pmol x mL(-1) vs 41.1 +/- 2.6 pmol x mL(-1), P =.53), 3,4-dihydroxyphenylacetic acid (51.7 +/- 11.7 pmol x mL(-1) vs 56.5 +/- 5.4 pmol x mL(-1), P =.09), and norepinephrine (9.5 +/- 2.4 pmol x mL(-1) vs 5.6 +/- 1.0 pmol x mL(-1), P =.12) did not differ between groups. Plasma aldosterone (180.2 +/- 28.0 pg x mL(-1) vs 69.9 +/- 13.3 pg x mL(-1), P <.001) and BNP (677.5 +/- 133.9 pg x mL(-1) vs 389.4 +/- 88.4 pg x mL(-1), P <.04) levels were higher in the decompensated class III/IV HF group than in the other group, whereas serum sodium was lower (137.3 +/- 1.2 mmol x L(-1) vs 143.2 +/- 1.0 mmol x L(-1), P =.001).ConclusionsThese results suggest that, in patients with HF, the increased renal utilization of L-DOPA may constitute a compensatory mechanism, activated in response to stimuli leading to sodium reabsorption. | Lee JJ, Chang CK, Liu IM, Chi TC, Yu HJ, Cheng JT (2001)
Changes in endogenous monoamines in aged rats.
Clinical and experimental pharmacology & physiology 28, 285-289 [PubMed:11251641]
[show Abstract]
1. It has been documented that ageing may alter endogenous neurotransmitters. However, these results are controversial. Thus, in the present study, cerebral cortex and plasma from male Wistar rats aged 8 weeks and 6, 12 or 24 months were used to investigate the changes in monoamines using electrochemical detection. 2. A marked decrease in L-dihydroxyphenylalanine (L-DOPA) was observed in aged rats. Like the decrease in dopamine (DA), levels of 5-hydroxytryptamine (5-HT) and 5-hydroxyindolacetic acid (5-HIAA), the major metabolite of 5-HT, in aged rats were decreased in the cerebral cortex and plasma. Plasma levels of noradrenaline and levels of adrenaline in the cerebral cortex were also decreased in aged rats. Moreover, levels of 3,4-dihydroxyphenylacetic acid (DOPAC), a metabolite of DA, in the cerebral cortex and plasma were reduced by ageing. The level of homovanillic acid (HVA) in all samples was markedly increased with ageing. 3. The ratio of DOPAC/DA and 5-HIAA/5-HT, being closely linked with the activity of monoamine oxidase, was increased in the cerebral cortex and plasma with ageing. The ratio of HVA/DOPAC, an index of the activity of catechol-O-methyltransferase, was also higher in the cerebral cortex and plasma of aged rats. 4. These data suggest that ageing may alter endogenous monoamines in both the brain and peripheral tissues. | Eldrup E, Clausen N, Scherling B, Schmiegelow K (2001)
Evaluation of plasma 3,4-dihydroxyphenylacetic acid (DOPAC) and plasma 3,4-dihydroxyphenylalanine (DOPA) as tumor markers in children with neuroblastoma.
Scandinavian journal of clinical and laboratory investigation 61, 479-490 [PubMed:11681538]
[show Abstract]
Catecholamines and their metabolites are important in the diagnosis of neuroblastoma (NB). Plasma (p-) levels of 3,4-dihydroxyphenylalanine (DOPA) are increased in most NB, probably reflecting decreased DOPA decarboxylase activity. Urine (u-) homovanillic acid (HVA), a DOPA and dopamine (DA) metabolite. is also increased in most NB. DOPAC (3,4-dihydroxyphenylacetic acid) is an important metabolite of DA in tissues with monoamine oxidase (MAO) activity. Because MAO is expressed in NB tumor cells, we studied the importance of measuring p-DOPAC and p-DOPA as compared to u-HVA and u-vanillylmandelic acid (VMA) in the diagnosis and follow-up of NB. DOPAC, DOPA, dopamine, noradrenaline, adrenaline, VMA and HVA were measured by reverse-phase HPLC with electrochemical detection in 106 children (28 with NB (13 newly diagnosed), 25 with other solid tumors, 28 hospitalized for nonneoplastic diseases, and 25 healthy children). P-DOPAC or p-DOPA concentrations were above the upper normal range in 92% of untreated NB patients, as were u-HVA or u-VMA levels. None of these tumor markers was correlated to tumor stage or survival. P-DOPA but not p-DOPAC was correlated to age in NB children. Increased values of p-DOPAC and p-DOPA were found in one patient surviving NB for 10 years. Plasma DOPAC concentrations were decreased in children hospitalized for non-NB diseases, probably reflecting reduced food intake. Plasma analyses of DOPA and DOPAC seem to be useful alternatives in the diagnosis and follow-up of NB if urine sampling is to be avoided. Plasma DOPAC may be an index of nutritional status in various diseases. | Sparnins VL, Chapman PJ, Dagley S (1974)
Bacterial degradation of 4-hydroxyphenylacetic acid and homoprotocatechuic acid.
Journal of bacteriology 120, 159-167 [PubMed:4420192]
[show Abstract]
A species of Acinetobacter and two strains of Pseudomonas putida when grown with 4-hydroxyphenylacetic acid gave cell extracts that converted 3,4-dihydroxyphenylacetic acid (homoprotocatechuic acid) into carbon dioxide, pyruvate, and succinate. The sequence of enzyme-catalyzed steps was as follows: ring-fission by a 2,3-dioxygenase, nicotinamide adenine dinucleotide-dependent dehydrogenation, decarboxylation, hydration, aldol fission, and oxidation of succinic semialdehyde. Two new metabolites, 5-carboxymethyl-2-hydroxymuconic acid and 2-hydroxyhepta-2,4-diene-1,7-dioic acid, were isolated from reaction mixtures and a third, 4-hydroxy-2-ketopimelic acid, was shown to be cleaved by extracts to give pyruvate and succinic semialdehyde. Enzymes of this metabolic pathway were present in Acinetobacter grown with 4-hydroxyphenylacetic acid but were effectively absent when 3-hydroxyphenylacetic acid or phenylacetic acid served as sources of carbon. |
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