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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__1414244864076415__ initializing getValue debug = null getValue logLevel = null getValue allowjavascript = null AppletRegistry.checkIn(jmolApplet0_object__1414244864076415__) 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:566274","platform":"J.awtjs2d.Platform","fullName":"jmolApplet0_object__1414244864076415__","display":"jmolApplet0_canvas2d","signedApplet":"true","appletReadyCallback":"Jmol._readyCallback","statusListener":"[J.appletjs.Jmol.MyStatusListener object]","codeBase":"https://www.ebi.ac.uk/chebi/javascripts/jsmol/","syncId":"1414244864076415","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__1414244864076415__ 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 Mrv0541 02021514262D starting HoverWatcher_5 Time for openFile( Mrv0541 02021514262D 5 4 0 0 0 0 999 V2000 5.1417 -4.5875 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 5.8561 -4.1750 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 4.4272 -4.1750 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 3.7119 -4.5880 0.0000 O 0 0 0 0 0 0 0 0 0 0 0 0 6.5739 -4.5867 0.0000 O 0 0 0 0 0 0 0 0 0 0 0 0 1 3 1 0 0 0 0 1 2 1 0 0 0 0 3 4 2 0 0 0 0 2 5 2 0 0 0 0 M END): 14 ms reading 5 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 5 atoms created ModelSet: not autobonding; use forceAutobond=true to force automatic bond creation Script completed Jmol script terminated
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InChI=1S/C3H4O2/c4-2-1-3-5/h2-3H,1H2 |
WSMYVTOQOOLQHP-UHFFFAOYSA-N |
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biomarker
A substance used as an indicator of a biological state.
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View more via ChEBI Ontology
1,3-Propanedial
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ChemIDplus
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1,3-Propanedialdehyde
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ChemIDplus
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1,3-Propanedione
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ChemIDplus
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malonaldehyde
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UniProt
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Malondialdehyde
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KEGG COMPOUND
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Malondialdehyde
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ChemIDplus
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Malonic aldehyde
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ChemIDplus
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Malonic dialdehyde
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ChemIDplus
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Malonodialdehyde
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ChemIDplus
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Malonyldialdehyde
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ChemIDplus
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MDA
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ChEBI
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MDD
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ChEBI
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1209262
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Reaxys Registry Number
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Reaxys
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362229
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Gmelin Registry Number
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Gmelin
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542-78-9
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CAS Registry Number
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ChemIDplus
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542-78-9
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CAS Registry Number
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NIST Chemistry WebBook
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Jouyban A, Khoubnasabjafari M (2018) Comments on "Malondialdehyde: A novel predictive biomarker for post-stroke depression". Journal of affective disorders 225, 52-53 [PubMed:28783520] [show Abstract] In a recent work by Liu et al. (2017) appeared in this journal, malondialdehyde levels proposed as a novel biomarker. Despite of wide usage of malondialdehyde as a biomarker, there are some points from analytical viewpoint which should be considered in future works. This work aimed to discuss the points briefly. | Senders ML, Que X, Cho YS, Yeang C, Groenen H, Fay F, Calcagno C, Meerwaldt AE, Green S, Miu P, Lobatto ME, Reiner T, Fayad ZA, Witztum JL, Mulder WJM, Pérez-Medina C, Tsimikas S (2018) PET/MR Imaging of Malondialdehyde-Acetaldehyde Epitopes With a Human Antibody Detects Clinically Relevant Atherothrombosis. Journal of the American College of Cardiology 71, 321-335 [PubMed:29348025] [show Abstract]
BackgroundOxidation-specific epitopes (OSEs) are proinflammatory, and elevated levels in plasma predict cardiovascular events.ObjectivesThe purpose of this study was to develop novel positron emission tomography (PET) probes to noninvasively image OSE-rich lesions.MethodsAn antigen-binding fragment (Fab) antibody library was constructed from human fetal cord blood. After multiple rounds of screening against malondialdehyde-acetaldehyde (MAA) epitopes, the Fab LA25 containing minimal nontemplated insertions in the CDR3 region was identified and characterized. In mice, pharmacokinetics, biodistribution, and plaque specificity studies were performed with Zirconium-89 (89Zr)-labeled LA25. In rabbits, 89Zr-LA25 was used in combination with an integrated clinical PET/magnetic resonance (MR) system. 18F-fluorodeoxyglucose PET and dynamic contrast-enhanced MR imaging were used to evaluate vessel wall inflammation and plaque neovascularization, respectively. Extensive ex vivo validation was carried out through a combination of gamma counting, near infrared fluorescence, autoradiography, immunohistochemistry, and immunofluorescence.ResultsLA25 bound specifically to MAA epitopes in advanced and ruptured human atherosclerotic plaques with accompanying thrombi and in debris from distal protection devices. PET/MR imaging 24 h after injection of 89Zr-LA25 showed increased uptake in the abdominal aorta of atherosclerotic rabbits compared with nonatherosclerotic control rabbits, confirmed by ex vivo gamma counting and autoradiography. 18F-fluorodeoxyglucose PET, dynamic contrast-enhanced MR imaging, and near-infrared fluorescence signals were also significantly higher in atherosclerotic rabbit aortas compared with control aortas. Enhanced liver uptake was also noted in atherosclerotic animals, confirmed by the presence of MAA epitopes by immunostaining.Conclusions89Zr-LA25 is a novel PET radiotracer that may allow noninvasive phenotyping of high-risk OSE-rich lesions. | Liu Z, Zhu Z, Zhao J, Ren W, Cai Y, Wang Q, Luan X, Zhao K, He J (2017) Malondialdehyde: A novel predictive biomarker for post-stroke depression. Journal of affective disorders 220, 95-101 [PubMed:28600933] [show Abstract]
BackgroundThere is evidence that stroke is accompanied by oxidative stress. However, the links between oxidative stress and depression in stroke patients are poorly understood. This study examines whether post-stroke depression (PSD) is associated with oxidative stress.MethodsOverall, 216 acute stroke patients were consecutively recruited and followed up for 1 month. Blood specimens were collected within 24h after admission and measured for the following oxidative stress biomarkers: malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). All enrolled patients were divided into the PSD group or the non-PSD group according to an assessment of clinical depression. One hundred normal control subjects were also recruited.ResultsThere was a positive correlation between serum MDA levels and HAMD scores in stroke patients (r=0.536, p<0.001). Based on the Receiver-operating characteristic (ROC) curve, the optimal cutoff value of serum MDA levels as an indicator for an auxiliary diagnosis of PSD was projected to be 2.898 nmol/ml, which yielded a sensitivity of 77.9% and a specificity of 81.1%, with an area under the curve of 0.883 (95% CI, 0.836-0.929). Elevated MDA (≥2.898 nmol/ml) was an independent predictive marker of PSD (odds ratio OR=24.295; 95% CI, 9.461-62.388; p<0.001, adjusted for relevant confounders).LimitationsWe excluded patients with severe aphasia or with serious conditions. In addition, the information for dietary intake was not recorded, which may influence oxidative stress levels.ConclusionOur study demonstrated that an elevated serum MDA level at admission was positively associated with an increased risk of developing depression after acute stroke, especially minor stroke. | Roomruangwong C, Kanchanatawan B, Sirivichayakul S, Anderson G, Carvalho AF, Duleu S, Geffard M, Maes M (2017) IgM-mediated autoimmune responses to oxidative specific epitopes, but not nitrosylated adducts, are significantly decreased in pregnancy: association with bacterial translocation, perinatal and lifetime major depression and the tryptophan catabolite (TRYCAT) pathway. Metabolic brain disease 32, 1571-1583 [PubMed:28600633] [show Abstract] Immunoglubulin (Ig)M responses directed to oxidative specific epitopes (OSEs) and nitric oxide (NO)-adducts are significantly associated with major depression and physio-somatic symptoms. End of term serum IgM responses to OSEs and NO-adducts were assayed in pregnant women with (n = 24) and without prenatal depression (n = 25) as well as in 24 non-pregnant women. Associations of IgM/IgA responses to Gram-negative gut commensal bacteria (leaky gut index) and IgA/IgM responses to tryptophan catabolites (TRYCATs) were analyzed. IgM responses to OSEs, but not NO-adducts, were significantly reduced at the end of term. There were no significant associations between IgM responses to OSEs and perinatal depression, whilst IgM responses to NO-adducts, especially NO-cysteinyl, were significantly associated with a lifetime major depression. IgM responses to OSEs and NO-cysteinyl were significantly associated with IgA/IgM responses to Gram-negative bacteria, especially Morganella morganii, Klebsiella pneumoniae and Citrobacter koseri. IgM responses to NO-adducts and OSEs, especially malondialdehyde and myristic acid, and C-reactive protein (CRP) were inversely associated with TRYCAT pathway activity, whilst a lifetime depression and Pseudomonas putida were positively associated. The attenuation of natural IgM-mediated responses to OSEs at the end of term may indicate lowered activity of this part of the compensatory (anti-)inflammatory reflex system and may be partly explained by lowered bacterial translocation. Increased IgM responses to NO-cysteinyl is a biomarker of lifetime depression and may be induced by bacterial translocation. Natural IgM-mediated autoimmune responses, increased nitrosylation and higher CRP levels may have negative regulatory effects on the TRYCAT pathway. | Kummu O, Turunen SP, Prus P, Lehtimäki J, Veneskoski M, Wang C, Hörkkö S (2014) Human monoclonal Fab and human plasma antibodies to carbamyl-epitopes cross-react with malondialdehyde-adducts. Immunology 141, 416-430 [PubMed:24168430] [show Abstract] Oxidized low-density lipoprotein (OxLDL) plays a crucial role in the development of atherosclerosis. Carbamylated LDL has been suggested to promote atherogenesis in patients with chronic kidney disease. Here we observed that plasma IgG and IgM antibodies to carbamylated epitopes were associated with IgG and IgM antibodies to oxidation-specific epitopes (ρ = 0·65-0·86, P < 0·001) in healthy adults, suggesting a cross-reaction between antibodies recognizing carbamyl-epitopes and malondialdehyde (MDA)/malondialdehyde acetaldehyde (MAA) -adducts. We used a phage display technique to clone a human Fab antibody that bound to carbamylated LDL and other carbamylated proteins. Anti-carbamyl-Fab (Fab106) cross-reacted with oxidation-specific epitopes, especially with MDA-LDL and MAA-LDL. We showed that Fab106 bound to apoptotic Jurkat cells known to contain these oxidation-specific epitopes, and the binding was competed with soluble carbamylated and MDA-/MAA-modified LDL and BSA. In addition, Fab106 was able to block the uptake of carbamyl-LDL and MDA-LDL by macrophages and stained mouse atherosclerotic lesions. The observed cross-reaction between carbamylated and MDA-/MAA-modified LDL and its contribution to enhanced atherogenesis in uraemic patients require further investigation. | Wang C, Turunen SP, Kummu O, Veneskoski M, Lehtimäki J, Nissinen AE, Hörkkö S (2013) Natural antibodies of newborns recognize oxidative stress-related malondialdehyde acetaldehyde adducts on apoptotic cells and atherosclerotic plaques. International immunology 25, 575-587 [PubMed:23900424] [show Abstract] Malondialdehyde acetaldehyde (MAA) adducts are generated under oxidative stress and shown to be highly immunogenic. Our aim was to investigate the recognition of MAA adducts by human natural antibodies in newborns before or at the time of full-term pregnancy. Plasma samples of pre-term (n = 11) and full-term (n = 36) newborns were enriched in specific IgM binding to MAA adducts compared with the maternal plasma IgM levels. Umbilical cord blood lymphocyte phage display library was generated to clone Fabs that specifically recognized MAA adducts without cross-reactivity to malondialdehyde. Fab clones from the antibody libraries of the pre-term and full-term newborns showed high sequence homology to the germline genes encoding the variable regions of antibodies, confirming that these Fabs represented the natural antibody repertoire of human fetuses. The MAA-specific umbilical cord blood Fabs bound to apoptotic human endothelial cells and the binding was efficiently competed with MAA adducts. The MAA-specific Fabs also recognized epitopes on advanced atherosclerotic lesions, and the uptake of infrared (IR)-labeled MAA-low-density lipoprotein by mouse J774A.1 macrophages was significantly reduced in the presence of these Fabs. In conclusion, MAA adducts were identified as one of the major antigenic targets for human natural antibodies already before the time of birth. MAA-specific natural antibodies are suggested to regulate apoptotic cell clearance starting from fetal development and to participate in the immunomodulation of atherosclerosis development during adulthood. | Bellia F, Amorini AM, La Mendola D, Vecchio G, Tavazzi B, Giardina B, Di Pietro V, Lazzarino G, Rizzarelli E (2008) New glycosidic derivatives of histidine-containing dipeptides with antioxidant properties and resistant to carnosinase activity. European journal of medicinal chemistry 43, 373-380 (Source: ChEMBL) [PubMed:17548130] [show Abstract] Synthesis, antioxidant properties and resistance to carnosinase hydrolysis of histidine-containing dipeptides are reported in this study. Carnosine (beta-alanyl-l-histidine), homocarnosine (gamma-aminobutyryl-l-histidine) and anserine (beta-alanyl-3-methyl-l-histidine) were covalently derivatized with beta-cyclodextrin to form different OH- or NH-bound conjugates. Mass spectroscopic and (1)H NMR data were used to determine the structure and the purity of the various beta-cyclodextrin derivatives. The inhibitory effect towards oxidation of human LDL induced by Cu(2+) ions, was estimated by measuring malondialdehyde formation as a function of increasing concentrations of these newly synthesized compounds (the beta-cyclodextrin-anserine conjugated in 3 had the highest antioxidant effect). All derivatives had higher antioxidant effects than those of the corresponding free histidine-containing dipeptides. Resistance to rat brain carnosinase hydrolysis of the most active derivatives indicated that these compounds are good candidates for further studies in more complex cellular and animal models. Their possible applications for remedies in neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases, are discussed. | Lykkesfeldt J (2007) Malondialdehyde as biomarker of oxidative damage to lipids caused by smoking. Clinica chimica acta; international journal of clinical chemistry 380, 50-58 [PubMed:17336279] [show Abstract] Thiobarbituric acid reactive substances (TBARS) and malondialdehyde (MDA) have been used as biomarkers of lipid oxidation for more than thirty years. The validity of these biomarkers has been rightfully criticized for a lack of specificity and problems with post sampling formation. Numerous assays have been published for their analysis giving rise to reference intervals for healthy non-smoking humans varying more than to orders of magnitude. In spite of these problems, these biomarkers remain among the most commonly reported indices of oxidative damage and the present review focuses on the problems associated with MDA/TBARS analysis, their potential as biomarkers of oxidative stress and the effect of smoking on MDA status. | Shukla R, Rajani M, Srivastava N, Barthwal MK, Dikshit M (2006) Nitrite and malondialdehyde content in cerebrospinal fluid of patients with Parkinson's disease. The International journal of neuroscience 116, 1391-1402 [PubMed:17145675] [show Abstract] Evidence from clinical and experimental studies supports the hypothesis of free radical-mediated damage of dopaminergic neurons in the pathology of Parkin's disease (PD). The present study was undertaken to evaluate the role of nitric oxide and oxidative stress in PD. Estimation of the stable metabolites of nitric oxide (NO, nitrite, nitrate) and malondialdehyde (MDA), an acceptable marker of lipid peroxidation, can provide indirect evidence of involvement of free radicals. Nitrite and malondialdehyde (MDA) levels were estimated in the lumbar cerebrospinal fluid (CSF) of 20 controls and 21 patients with PD. Nitrite and MDA content was not significantly altered in the CSF of PD patients as compared to the controls. Nitrite and MDA levels in CSF of PD patients exhibited no correlation with age, duration of disease, and severity of illness (measured by the Unified Parkinson's Disease Rating Score). There was no correlation between the CSF nitrite and MDA level. Findings of the present study do not provide evidence for the involvement of nitric oxide and oxidative stress in PD. | Chang MK, Binder CJ, Miller YI, Subbanagounder G, Silverman GJ, Berliner JA, Witztum JL (2004) Apoptotic cells with oxidation-specific epitopes are immunogenic and proinflammatory. The Journal of experimental medicine 200, 1359-1370 [PubMed:15583011] [show Abstract] Oxidation of low density lipoprotein (LDL) generates a variety of oxidatively modified lipids and lipid-protein adducts that are immunogenic and proinflammatory, which in turn contribute to atherogenesis. Cells undergoing apoptosis also display oxidized moieties on their surface membranes, as determined by binding of oxidation-specific monoclonal antibodies. In the present paper, we demonstrated by mass spectrometry that in comparison with viable cells, membranes of cells undergoing apoptosis contain increased levels of biologically active oxidized phospholipids (OxPLs). Indeed, immunization of mice with syngeneic apoptotic cells induced high autoantibody titers to various oxidation-specific epitopes of oxidized LDL, including OxPLs containing phosphorylcholine, whereas immunization with viable thymocytes, primary necrotic thymocytes, or phosphate-buffered saline did not. Reciprocally, these antisera specifically bound to apoptotic cells through the recognition of oxidation-specific epitopes. Moreover, splenocyte cultures from mice immunized with apoptotic cells spontaneously released significant levels of T helper cell (Th) 1 and Th2 cytokines, whereas splenocytes from controls yielded only low levels. Finally, we demonstrated that the OxPLs of apoptotic cells activated endothelial cells to induce monocyte adhesion, a proinflammatory response that was abrogated by an antibody specific to oxidized phosphatidylcholine. These results suggest that apoptotic cell death generates oxidatively modified moieties, which can induce autoimmune responses and a local inflammatory response by recruiting monocytes via monocyte-endothelial cell interaction. | Agarwal R, Chase SD (2002) Rapid, fluorimetric-liquid chromatographic determination of malondialdehyde in biological samples. Journal of chromatography. B, Analytical technologies in the biomedical and life sciences 775, 121-126 [PubMed:12101069] [show Abstract] Current chromatographic methods of estimation of malondialdehyde, a marker of oxidative lipid injury, often require extensive extraction procedures, column cleaning or specialized equipment. A rapid and sensitive HPLC method is described for the determination of MDA in plasma and urine. The mobile phase consisted of 40:60 ratio (v/v) of methanol to 50 mM potassium monobasic phosphate at pH 6.8, pumped at a rate of 1.0 ml/min on a Hewlett-Packard Hypersil 5 micro ODS 100 x 4.6 mm placed in a column warmer set to 37 degrees C. Samples of plasma and urine were treated with the antioxidant, butylated hydroxytoluene and heat derivatized at 100 degrees C for 1 h with thiobarbituric acid at an acid pH. Samples were extracted with n-butanol and 10 microl of the extract was injected at 1 min intervals using an autosampler. The Hewlett-Packard model 1046A programmable fluorescence detector was set at excitation of 515 nm and emission of 553 nm. Retention time was 1.87 min, however absence of interfering peaks, allowed analysis to be carried out in increments of 1 min per sample. Within day variability in estimation was between 8.6% and 10.3%. Between days variability was 3.6-7.9%. Recovery was between 88 and 101%. Samples of urine and plasma from ten normotensive volunteers were 1.94 +/- 0.79 micromol/g creatinine and 0.69 +/- 0.13 micromol/l respectively and were similar to those reported in the literature. MDA degrades at room temperature at a rate of 10% per hour. It is therefore, suggested that the total assay time be limited to 1 h beginning with sample preparation. |
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