Stable-Isotope Dilution Liquid Chromatography–Electrospray Injection Tandem Mass Spectrometry Method for Fast, Selective Measurement of S-Adenosylmethionine and S-Adenosylhomocysteine in Plasma

Gellekink, Henkjan; Oppenraaij-Emmerzaal, Dinny; Rooij, Arno van; Struys, Eduard A.; Heijer, Martin den; Blom, Henk J.

doi:10.1373/clinchem.2004.046995

Cited by 104 publications

(79 citation statements)

References 16 publications

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“…Ion suppression effects were calculated from the peak areas of the internal standard added to the calibrator solutions and compared with the peak areas of the internal standard that was added to each urinary sample. The relative change in peak area of the internal standard was attributed to matrix effects (26 ). In this correlation between urinary 8-oxodGuo and cotinine in smokers…”

Section: Limits Of Quantification (Loq) and Detection (Lod)mentioning

confidence: 77%

Clinical-Scale High-Throughput Analysis of Urinary 8-Oxo-7,8-Dihydro-2′-Deoxyguanosine by Isotope-Dilution Liquid Chromatography–Tandem Mass Spectrometry with On-Line Solid-Phase Extraction

Wang

Chang

et al. 2006

Clinical Chemistry

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Background: Quantification of 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxodGuo) in urine or blood is used to assess and monitor oxidative stress in patients. We describe the use of on-line solid-phase extraction (SPE) and isotope-dilution liquid chromatography-tandem mass spectrometry (LC-MS/MS) for automated measurement of urinary 8-oxodGuo. Methods: Automated purification of urine was accomplished with a switching valve and an Inertsil ODS-3 column. After the addition of 15 N 5 -labeled 8-oxodGuo as an internal standard, urine samples were analyzed within 10 min without sample purification. This method was applied to measure urinary 8-oxodGuo in a group of healthy persons (32 regular smokers and 35 nonsmokers). Urinary cotinine was also assayed by an isotopedilution LC-MS/MS method. Results: The lower limit of detection was 5.7 ng/L on column (2.0 fmol). Inter-and intraday imprecision (CV) was <5.0%. Mean recovery of 8-oxodGuo in urine was 99%-102%. Mean (SD) urinary concentrations of 8-oxodGuo in smokers [7.26 (3.14) g/g creatinine] were significantly higher than those in nonsmokers [4.69 (1.70) g/g creatinine; P <0.005]. Urinary concentrations of 8-oxodGuo were significantly correlated with concentrations of cotinine in smokers (P <0.05).

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Section: Limits Of Quantification (Loq) and Detection (Lod)mentioning

confidence: 77%

Clinical-Scale High-Throughput Analysis of Urinary 8-Oxo-7,8-Dihydro-2′-Deoxyguanosine by Isotope-Dilution Liquid Chromatography–Tandem Mass Spectrometry with On-Line Solid-Phase Extraction

Wang

Chang

et al. 2006

Clinical Chemistry

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“…Measurements of AdoMet and AdoHcy in plasma and CSF and of adenosine in dried blood spots AdoMet and AdoHcy were measured in plasma and CSF via a stable-isotope dilution liquid chromatography-electrospray tandem mass spectrometry method, as published before (Gellekink et al 2005). Likewise, adenosine concentration in dried blood spots were measured via a stable-isotope dilution liquid chromatography-electrospray tandem mass spectrometry method, see reference (Azzari et al 2011) for details.…”

Section: Liver Histopathologymentioning

confidence: 99%

Adenosine kinase deficiency: expanding the clinical spectrum and evaluating therapeutic options

Staufner

Dionisi‐Vici

Freisinger

et al. 2015

J of Inher Metab Disea

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Background Adenosine kinase deficiency is a recently described defect affecting methionine metabolism with a severe clinical phenotype comprising mainly neurological and hepatic impairment and dysmorphism. Methods Clinical data of 11 additional patients from eight families with adenosine kinase deficiency were gathered through a retrospective questionnaire. Two liver biopsies of one patient were systematically evaluated. Results The main clinical symptoms are mild to severe liver dysfunction with neonatal onset, muscular hypotonia, global developmental retardation and dysmorphism (especially frontal bossing). Hepatic involvement is not a constant finding. Most patients have epilepsy and recurrent hypoglycemia due to hyperinsulinism. Major biochemical findings are intermittent hypermethioninemia, increased S-adenosylmethionine and Sadenosylhomocysteine in plasma and increased adenosine in urine. S-adenosylmethionine and S-adenosylhomocysteine are the most reliable biochemical markers. The major histological finding was pronounced microvesicular hepatic steatosis. Therapeutic trials with a methionine restricted diet indicate a potential beneficial effect on biochemical and clinical parameters in four patients and hyperinsulinism was responsive to diazoxide in two patients. Conclusion Adenosine kinase deficiency is a severe inborn error at the cross-road of methionine and adenosine metabolism that mainly causes dysmorphism, brain and liver symptoms, but also recurrent hypoglycemia.

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“…Plasma AdoMet and AdoHcy concentrations were determined using stable isotope dilution tandem mass spectrometry. 9 Guanidinoacetate and creatine were measured in plasma and urine using stable isotope dilution gas chromatography-mass spectrometry as previously reported. 10,11 Statistical analyses.…”

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confidence: 99%

Reduced brain choline in homocystinuria due to remethylation defects

Debray¹,

Boulanger²,

Khiat³

et al. 2008

Neurology

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Reduced brain choline in homocystinuria due to remethylation defects This information is current as of January 30, 2009http://www.neurology.org/cgi/content/full/71/1/44 located on the World Wide Web at:The online version of this article, along with updated information and services, is Objective:To investigate whether secondary impairment of the transmethylation pathway is a mechanism underlying the neurologic involvement in homocystinuria due to remethylation defects.Methods: Twelve patients with neurologic disease due to remethylation defects were examined by brain magnetic resonance spectroscopic imaging ( 1 H MRSI). Brain N-acetylaspartate, cholinecontaining compounds (Cho), and creatine (Cr) were quantified and compared to with controls. Metabolites of remethylation cycle and creatine biosynthesis pathway were measured in plasma and urine.Results: MRSI revealed isolated Cho deficiency in all regions examined (mean concentration units Ϯ SD, patients vs controls): frontal white matter (0.051 Ϯ 0.010 vs 0.064 Ϯ 0.010; p ϭ 0.001), lenticular nucleus (0.056 Ϯ 0.011 vs 0.069 Ϯ 0.009; p Ͻ 0.001), and thalamus (0.063 Ϯ 0.010 vs 0.071 Ϯ 0.007; p ϭ 0.006). In contrast to controls, the Cho/Cr ratio decreased with age in patients in the three brain regions examined. Low creatine urinary excretion (p Ͻ 0.005), normal urine and plasma guanidinoacetate, and a paradoxical increase in plasma S-adenosylmethionine (p Ͻ 0.005) concentrations were observed. Conclusion:Patients with homocystinuria due to remethylation defects have an isolated brain choline deficiency, probably secondary to depletion of labile methyl groups produced by the transmethylation pathway. Although biochemical studies suggest mild peripheral creatine deficiency, brain creatine is in the reference range, indicating a possible compartmentation phenomenon. Paradoxical increase of S-adenosylmethionine suggests that secondary inhibition of methylases contributes to the transmethylation defect in these conditions. Neurology GLOSSARYCblC ϭ combined homocystinuria-methylmalonic aciduria; CblG ϭ methionine synthase deficiency; CBS ϭ cystathionine ␤-synthase; Cho ϭ water-soluble choline-containing compounds; Cr ϭ creatine; DQ ϭ developmental quotient; Met ϭ plasma methionine; MR ϭ magnetic resonance; MSRI ϭ magnetic resonance spectroscopic imaging; MTHFR ϭ methylene tetrahydrofolate reductase; NA ϭ not available; NAA ϭ N-acetylaspartate; NN ϭ neonatal; NS ϭ not significant; OA ϭ optic atrophy; OMA ϭ oculomotor apraxia; OMIM ϭ Online Mendelian Inheritance in Man; PM ϭ pigmentary maculopathy; Pt ϭ patient; RD ϭ remethylation defect; RP ϭ retinitis pigmentosa; tHcy ϭ plasma total homocysteine; THF ϭ tetrahydrofolate.

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Stable-Isotope Dilution Liquid Chromatography–Electrospray Injection Tandem Mass Spectrometry Method for Fast, Selective Measurement of S-Adenosylmethionine and S-Adenosylhomocysteine in Plasma

Cited by 104 publications

References 16 publications

Clinical-Scale High-Throughput Analysis of Urinary 8-Oxo-7,8-Dihydro-2′-Deoxyguanosine by Isotope-Dilution Liquid Chromatography–Tandem Mass Spectrometry with On-Line Solid-Phase Extraction

Clinical-Scale High-Throughput Analysis of Urinary 8-Oxo-7,8-Dihydro-2′-Deoxyguanosine by Isotope-Dilution Liquid Chromatography–Tandem Mass Spectrometry with On-Line Solid-Phase Extraction

Adenosine kinase deficiency: expanding the clinical spectrum and evaluating therapeutic options

Reduced brain choline in homocystinuria due to remethylation defects

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