Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.

Circulating concentrations of mevalonic acid (MVA) change in parallel with, and may be used as a marker of cholesterol biosynthesis. Plasma MVA levels have been quantified using a sensitive and specific capillary gas chromatography-electron capture mass spectrometric assay. The detection limit for M...

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Main Authors: A Scoppola, VM Maher, GR Thompson, NB Rendell, GW Taylor
Format: Article
Language:English
Published: Elsevier 1991-06-01
Series:Journal of Lipid Research
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520420024
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spelling doaj-03ebee744d9e43dabf85304fc3533cd12021-04-26T05:53:34ZengElsevierJournal of Lipid Research0022-22751991-06-0132610571060Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.A Scoppola0VM Maher1GR Thompson2NB Rendell3GW Taylor4Medical Research Council Lipoprotein Team, Hammersmith Hospital, London, U.K.Medical Research Council Lipoprotein Team, Hammersmith Hospital, London, U.K.Medical Research Council Lipoprotein Team, Hammersmith Hospital, London, U.K.Medical Research Council Lipoprotein Team, Hammersmith Hospital, London, U.K.Medical Research Council Lipoprotein Team, Hammersmith Hospital, London, U.K.Circulating concentrations of mevalonic acid (MVA) change in parallel with, and may be used as a marker of cholesterol biosynthesis. Plasma MVA levels have been quantified using a sensitive and specific capillary gas chromatography-electron capture mass spectrometric assay. The detection limit for MVA in plasma is 100 pg/ml; the intra-assay variation is 5.11%; the inter-assay variation is 7.7%. Using this assay, the mean plasma MVA in 15 normolipidemic subjects was 2.37 +/- 1.2 ng/ml (range 0.41-5.31 ng/ml). Administration of 40 mg of simvastatin (an HMG-CoA reductase inhibitor) significantly accenutated the diurnal decrease in plasma MVA levels. This assay may be useful in investigating cholesterol synthesis rates in different dyslipidemias and individual responses of HMG-CoA reductase-inhibiting drugs.http://www.sciencedirect.com/science/article/pii/S0022227520420024
collection DOAJ
language English
format Article
sources DOAJ
author A Scoppola
VM Maher
GR Thompson
NB Rendell
GW Taylor
spellingShingle A Scoppola
VM Maher
GR Thompson
NB Rendell
GW Taylor
Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
Journal of Lipid Research
author_facet A Scoppola
VM Maher
GR Thompson
NB Rendell
GW Taylor
author_sort A Scoppola
title Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
title_short Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
title_full Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
title_fullStr Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
title_full_unstemmed Quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
title_sort quantitation of plasma mevalonic acid using gas chromatography-electron capture mass spectrometry.
publisher Elsevier
series Journal of Lipid Research
issn 0022-2275
publishDate 1991-06-01
description Circulating concentrations of mevalonic acid (MVA) change in parallel with, and may be used as a marker of cholesterol biosynthesis. Plasma MVA levels have been quantified using a sensitive and specific capillary gas chromatography-electron capture mass spectrometric assay. The detection limit for MVA in plasma is 100 pg/ml; the intra-assay variation is 5.11%; the inter-assay variation is 7.7%. Using this assay, the mean plasma MVA in 15 normolipidemic subjects was 2.37 +/- 1.2 ng/ml (range 0.41-5.31 ng/ml). Administration of 40 mg of simvastatin (an HMG-CoA reductase inhibitor) significantly accenutated the diurnal decrease in plasma MVA levels. This assay may be useful in investigating cholesterol synthesis rates in different dyslipidemias and individual responses of HMG-CoA reductase-inhibiting drugs.
url http://www.sciencedirect.com/science/article/pii/S0022227520420024
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