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香烟烟雾会增加人低密度脂蛋白的胆固醇氧化和脂质过氧化,并在体外降低其与肝受体的结合。

Cigarette smoke increases cholesterol oxidation and lipid peroxidation of human low-density lipoprotein and decreases its binding to the hepatic receptor in vitro.

作者信息

Mahfouz M M, Hulea S A, Kummerow F A

机构信息

Burnsides Research Laboratory, University of Illinois, Urbana 61801, USA.

出版信息

J Environ Pathol Toxicol Oncol. 1995;14(3-4):181-92.

PMID:9003696
Abstract

Low-density lipoprotein (LDL) was exposed to six puffs of cigarette smoke (CS) filtered through a glass wool filter and then incubated for 6 or 20 h at 37 degrees C. Control LDL was similarly treated but exposed to air. In cigarette smoke-treated LDL (CS-LDL), compositional changes of the lipid fraction were most detectable after 20 h incubation. These changes included a decrease of polyunsaturated fatty acids (PUFA), slight degradation of phosphatidylethanolamine (PE) and phosphatidylcholine (PC) to their lysophospholipid lysoPE and lyso-PC, elevation of oxidized cholesterol content as well as thiobarbituric acid reacting substance (TBARS), indicating an oxidative effect of CS on LDL. CS-LDL also showed higher anodic electrophoretic mobility and crosslinking of its apoprotein by nondisulfide bonds. The binding affinity of CS-LDL to liver membrane receptor was much lower than control LDL as measured by the calcium-dependent binding of LDL-gold conjugate to the solubilized membrane protein dot blotted onto nitrocellulose strips. Our results indicate that CS induces changes in LDL, making it more atherogenic and cytotoxic.

摘要

将低密度脂蛋白(LDL)暴露于经玻璃棉滤器过滤的6口香烟烟雾(CS)中,然后在37℃下孵育6或20小时。对照LDL进行类似处理,但暴露于空气中。在香烟烟雾处理的LDL(CS-LDL)中,脂质部分的成分变化在孵育20小时后最明显。这些变化包括多不饱和脂肪酸(PUFA)减少、磷脂酰乙醇胺(PE)和磷脂酰胆碱(PC)轻微降解为其溶血磷脂溶血PE和溶血PC、氧化胆固醇含量以及硫代巴比妥酸反应物质(TBARS)升高,表明CS对LDL有氧化作用。CS-LDL还显示出更高的阳极电泳迁移率及其载脂蛋白通过非二硫键交联。通过LDL-金缀合物与点印迹在硝酸纤维素条上的可溶性膜蛋白的钙依赖性结合测量,CS-LDL与肝细胞膜受体的结合亲和力远低于对照LDL。我们的结果表明,CS诱导LDL发生变化,使其更具致动脉粥样硬化性和细胞毒性。

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