Metabolism of Oxidized Phosphatidylcholines Formed in Oxidized Low Density Lipoprotein by Lecithin-Cholesterol Acyltransferase.
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概要
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The possible involvement of lecithin-cholesterol acyltransferase (LCAT) inthe metabolism of oxidized phosphatidylcholine (PC) in plasma was investigated. A variety of oxidized products are formed from PC following oxidation of low density lipoproteins (LDL). A significant increase in LDL oxidation levels in patients with familial LCAT deficiency (FLD) has been previously demonstrated by a sensitive sandwich ELISA for oxidized LDL using the monoclonal antibody DLH3 which recognizes oxidized products of PC. In the present study, we found that LCAT produces various metabolites from oxidized PC and that oxidized PC molecules in LDL particles serve as substrates. When the neutral lipid fraction was separated by TLC after the incubation of oxidized 1-palmitoy1-2-[1-14C]linoleoyl PC with human plasma, a number of radioactive bands were formed in addition to cholesteryl ester. These products were not formed from native 1-palmitoy1-2[1-14C]linoleoyl PC. Plasma from FLD patients also failed to form the additional products from oxidized PC. The addition of dithio-bis(nitrobenzoate) (DTNB), an LCAT inhibitor, or the inactivation of LCAT activity by treating the plasma at 56°C for 30min abolished the generation of these products from oxidized PC. The activity was recovered in the high density lipoprotein (HDL) fraction but not in the LDL fraction separated from normal plasma. When Ipalmitoy1-2-[1-14C](9-oxononanoyl) PC and 1-stearoy1-2-[1-14C] (5-oxovaleroyl)PC, PC oxidation products that contain short chain aldehydes, were incubated with human plasma, radioactive products in the neutral lipid fraction were observed on TLC. LDL containing oxidized PC was measured by sandwich ELISA using an anti-apolipoprotein B antibody and DLH3. The reconstituted oxidized PC-LDL particles were found to have lost their ability to bind DLH3 upon incubation with HDL, while the reactivity of the reconstituted oxidized PC-LDL remained unchanged in the presence of DTNB. These results suggest that LCAT is capable of metabolizing a variety of oxidized products of PC and preventing the accumulation of oxidized PC in circulating LDL particles.
- 社団法人 日本生化学会の論文
著者
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Imanaka Tsuneo
Department Of Biological Chemistry Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceuti
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HOSOYA Ryuta
Department of Microbiology and Molecular Pathology Teikyo University
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KARASAWA Ken
Department of Physical Chemistry, Faculty of Pharmaceutcal Sciences
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JIMI Shiro
Department of Microbiology and Molecular Pathology Teikyo University
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Itabe Hiroyuki
Department Of Biological Chemistry School Of Pharmaceutical Sciences Showa University
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Takano Tatsuya
Department Of Microbiology And Molecular Pathology Faculty Of Phamaceutical Sciences Teikyo Universi
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Saku Keijiro
Department Of Cardiology Faculty Of Medicine Fukuoka University
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Takebayash Shigeo
Department of Pathology and Internal Medicine, School of Medicine, Fukuoka University
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