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
Clinical Chemistry and Laboratory Medicine – de Gruyter
Published: Jan 1, 1993
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