期刊论文详细信息
FEBS Letters
Formation of F2‐isoprostanes during aortic endothelial cell‐mediated oxidation of low density lipoprotein
Gopaul, N.K.2  Änggård, E.E.2  Nourooz-Zadeh, J.3  Mallet, A.I.1 
[1] St John's Institute of Dermatology, Guy's and St Thomas' Medical and Dental School, Lambeth Palace Road, London SE1 7EH, UK;The William Harvey Research Institute, St Bartholomew's Hospital Medical College, Charterhouse Square, London EC1M 6BQ, UK;Department of Medicine, Division of Clinical Pharmacology and Toxicology, University College London, 5 University Street, London WC1E 6JJ, UK
关键词: F2-isoprostane;    LDL;    Cell-mediated oxidation;    Lipid peroxidation;    Atherosclerosis;    LDL;    low density lipoprotein;    NADPH;    reduced nicotinamide adenine dinucleotide phosphate oxidase;    BHT;    butylated hydroxytoluene;    SPE;    solid-phase extraction;    C18 NH2;    octadecylsilane;    aminopropyl;    PFB;    pentafluorobenzylbromide;    TMS;    trimethylsilyl;    TBARS;    thiobarbituric acid reactive substances;    FOX 2;    ferrous oxidation/xylenol orange;   
DOI  :  10.1016/0014-5793(94)00628-8
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

We investigated the formation of F2-isoprostanes produced by non-enzymatic peroxidation of arachidonic acid during rabbit aortic endothelial cell-mediated oxidation of low density lipoprotein (LDL). Free and total (sum of free and esterified) levels of F2-isoprostanes were measured using a solid-phase extraction procedure and gas chromatography-mass spectrometry. Free levels of F2-isoprostanes in native LDL were 0.06 ± 0.03 ng/mg protein (n = 4), whereas total levels were 0.28 ± 0.09 ng/mg protein (n = 4). Both free and total levels of the isoprostanes were found to increase during the oxidation. 8-epi-PGF was the major isoprostane formed (free and total concentrations after 24 h, 2.50 ± 0.24 and 6.42 ± 1.36 ng/mg protein (n = 4), respectively). The release of F2-isoprostanes during aortic endothelial cell-induced oxidation of LDL could be a contributory factor in the development of atherosclerosis.

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