Antioxidant properties of macrophages toward low-density lipoprotein

被引:5
作者
Baoutina, A [1 ]
Dean, RT [1 ]
Jessup, W [1 ]
机构
[1] Heart Res Inst, Cell Biol Grp, Sydney, NSW 2050, Australia
关键词
D O I
10.1016/S1050-1738(01)00075-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Oxidative modification of low-density lipoprotein (LDL) has been implicated in atherosclerosis. Intensive scientific efforts over the last two decades have focused on the elucidation of the mechanisms by which LDL is oxidized in vivo. A wealth of in vitro studies has demonstrated that the cell types present in atherosclerotic lesions, including monocyte/macrophages, quantitatively one of the most important cell types in plaque development, promote LDL oxidation. The mechanisms of cellular prooxidant activities hale been extensively investigated. Fewer studies have addressed possible protective properties of the cells in LDL oxidation. This review summarizes recent observations of antioxidant, and potentially antiatherogenic, activities of macrophages toward LDL, including macrophage-mediated detoxification of lipid and protein hydroperoxides, metal sequestration and the generation of compounds pounds with antioxidant properties. These activities could contribute to the net effect of macrophages on deleterious LDL oxidation and to the complex role of these cells in lesion development. (C) 2001, Elsevier Science Inc.
引用
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页码:1 / 7
页数:7
相关论文
共 41 条
[1]   Macrophages can decrease the level of cholesteryl ester hydroperoxides in low density lipoprotein [J].
Baoutina, A ;
Dean, RT ;
Jessup, W .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (03) :1635-1644
[2]  
Baoutina A, 1998, J LIPID RES, V39, P114
[3]  
BAOUTINA A, 2001, FASEB J EXPRESS 0507
[4]   HUMAN THIOREDOXIN REDUCTASE DIRECTLY REDUCES LIPID HYDROPEROXIDES BY NADPH AND SELENOCYSTINE STRONGLY STIMULATES THE REACTION VIA CATALYTICALLY GENERATED SELENOLS [J].
BJORNSTEDT, M ;
HAMBERG, M ;
KUMAR, S ;
XUE, J ;
HOLMGREN, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (20) :11761-11764
[5]   Nitric oxide regulation of free radical- and enzyme-mediated lipid and lipoprotein oxidation [J].
Bloodsworth, A ;
O'Donnell, VB ;
Freeman, BA .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (07) :1707-1715
[6]  
Brown AJ, 1997, J LIPID RES, V38, P1730
[7]   Systemic inflammatory parameters in patients with atherosclerosis of the coronary and peripheral arteries [J].
Erren, M ;
Reinecke, H ;
Junker, R ;
Fobker, M ;
Schulte, H ;
Schurek, JO ;
Kropf, J ;
Kerber, S ;
Breithardt, G ;
Assmann, G ;
Cullen, P .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (10) :2355-2363
[8]   Evidence for roles of radicals in protein oxidation in advanced human atherosclerotic plaque [J].
Fu, S ;
Davies, MJ ;
Stocker, R ;
Dean, RT .
BIOCHEMICAL JOURNAL, 1998, 333 :519-525
[9]  
FU SL, 1995, BIOCHEM J, V311, P821, DOI 10.1042/bj3110821
[10]   Direct copper reduction by macrophages - Its role in low density lipoprotein oxidation [J].
Garner, B ;
vanReyk, D ;
Dean, RT ;
Jessup, W .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (11) :6927-6935