Oxidative Modification of Low Density Lipoproteins by Human Polymorphonuclear Leukocytes

Oxidative Modification of Low Density Lipoproteins by Human Polymorphonuclear Leukocytes Introduction r 4 peroxidation of ilow densityflipoproteinrlipids and the The pathogenesis of atherosclerosis is complex and modification of the apolipoprotein B-100 by lipid multifactorial. Hypercholesterolaemia is widely ac- peroxidation products (8, 9). It has been proposed cepted as one of the major risk factors contributing that the oxidative modification of low density lipoto the development of coronary heart disease. From proteins by cells can be mediated either by Superoxide epidemiological studies (1, 2) and animal experiments anions (10), or by the action of the 15-lipoxygenase (3, 4) it is clear that cholesterol is deposited in ath-^ enzyme (11, 12). erosclerotic * ; and that this cholesterol. is mainly T 1 u * t-i - . , c plaques . . ,. ,* * Leukocytes, t _ ^ i both polymorphonuclear neutrophil leudenved from plasma low density lipoproteins ~(5, 6). , + , have u u A ^ ., ^ ^ * * . · kocytes and monocytes, u been observed -in *u the Recent evidence suggests ari important role for the ,. 4 .. , ,. , . /~ 4 / 17, ., . r ~i « · t· earliest atherosclerotic lesions (13, 14). When +u they oxidative http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Chemistry and Laboratory Medicine de Gruyter

Oxidative Modification of Low Density Lipoproteins by Human Polymorphonuclear Leukocytes

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Publisher
de Gruyter
Copyright
Copyright © 2009 Walter de Gruyter
ISSN
1434-6621
eISSN
1437-4331
DOI
10.1515/cclm.1993.31.11.725
Publisher site
See Article on Publisher Site

Abstract

Introduction r 4 peroxidation of ilow densityflipoproteinrlipids and the The pathogenesis of atherosclerosis is complex and modification of the apolipoprotein B-100 by lipid multifactorial. Hypercholesterolaemia is widely ac- peroxidation products (8, 9). It has been proposed cepted as one of the major risk factors contributing that the oxidative modification of low density lipoto the development of coronary heart disease. From proteins by cells can be mediated either by Superoxide epidemiological studies (1, 2) and animal experiments anions (10), or by the action of the 15-lipoxygenase (3, 4) it is clear that cholesterol is deposited in ath-^ enzyme (11, 12). erosclerotic * ; and that this cholesterol. is mainly T 1 u * t-i - . , c plaques . . ,. ,* * Leukocytes, t _ ^ i both polymorphonuclear neutrophil leudenved from plasma low density lipoproteins ~(5, 6). , + , have u u A ^ ., ^ ^ * * . · kocytes and monocytes, u been observed -in *u the Recent evidence suggests ari important role for the ,. 4 .. , ,. , . /~ 4 / 17, ., . r ~i « · t· earliest atherosclerotic lesions (13, 14). When +u they oxidative

Journal

Clinical Chemistry and Laboratory Medicinede Gruyter

Published: Jan 1, 1993

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