Oxidized lipoproteins and nitric oxide

被引:65
作者
Jessup, W [1 ]
机构
[1] HEART RES INST,CELL BIOL UNIT,SYDNEY,NSW 2050,AUSTRALIA
关键词
D O I
10.1097/00041433-199610000-00003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nitric oxide has an important biological role as endothelium-derived relaxing factor, a key agent in the maintenance of normal vascular tone. It can also suppress lipoprotein oxidation, a potential anti-atherogenic property. However, in arteries subject to hypercholesterolemia or atherosclerosis, whereas nitric oxide synthesis is normal its biological activity is attenuated. This may be caused by its inactivation in the intima by components of oxidized lipoproteins acting both directly (by reaction with nitric oxide) and indirectly (by simulation of release of nitric oxide scavengers). Thus in hypercholesterolemia the normal balance between nitric oxide availability and lipoprotein oxidation is shifted to favour a self-reinforcing cycle of nitric oxide depletion and accelerated lipoprotein oxidation that may ultimately lead to atherosclerosis.
引用
收藏
页码:274 / 280
页数:7
相关论文
共 73 条
  • [1] On the expression of nitric oxide synthase by human macrophages. Why no NO?
    Albina, JE
    [J]. JOURNAL OF LEUKOCYTE BIOLOGY, 1995, 58 (06) : 643 - 649
  • [2] SYSTEMIC NATURE OF ENDOTHELIAL DYSFUNCTION IN ATHEROSCLEROSIS
    ANDERSON, TJ
    GERHARD, MD
    MEREDITH, IT
    CHARBONNEAU, F
    DELAGRANGE, D
    CREAGER, MA
    SELWYN, AP
    GANZ, P
    [J]. AMERICAN JOURNAL OF CARDIOLOGY, 1995, 75 (06) : B71 - B74
  • [3] EXTENSIVE NITRATION OF PROTEIN TYROSINES IN HUMAN ATHEROSCLEROSIS DETECTED BY IMMUNOHISTOCHEMISTRY
    BECKMANN, JS
    YE, YZ
    ANDERSON, PG
    CHEN, J
    ACCAVITTI, MA
    TARPEY, MM
    WHITE, CR
    BECKMAN, JS
    [J]. BIOLOGICAL CHEMISTRY HOPPE-SEYLER, 1994, 375 (02): : 81 - 88
  • [4] ENHANCED LDL OXIDATION BY MURINE MACROPHAGE FOAM CELLS AND THEIR FAILURE TO SECRETE NITRIC-OXIDE
    BOLTON, EJ
    JESSUP, W
    STANLEY, KK
    DEAN, RT
    [J]. ATHEROSCLEROSIS, 1994, 106 (02) : 213 - 223
  • [5] Brown AJ, 1996, J LIPID RES, V37, P320
  • [6] REGULATION AND FUNCTIONAL CONSEQUENCES OF ENDOTHELIAL NITRIC-OXIDE FORMATION
    BUSSE, R
    FLEMING, I
    [J]. ANNALS OF MEDICINE, 1995, 27 (03) : 331 - 340
  • [7] LIPIDS AND OXIDIZED LIPIDS IN HUMAN ATHEROSCLEROTIC LESIONS AT DIFFERENT STAGES OF DEVELOPMENT
    CARPENTER, KLH
    TAYLOR, SE
    VANDERVEEN, C
    WILLIAMSON, BK
    BALLANTINE, JA
    MITCHINSON, MJ
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM, 1995, 1256 (02): : 141 - 150
  • [8] CHRONIC INHIBITION OF NITRIC-OXIDE PRODUCTION ACCELERATES NEOINTIMA FORMATION AND IMPAIRS ENDOTHELIAL FUNCTION IN HYPERCHOLESTEROLEMIC RABBITS
    CAYATTE, AJ
    PALACINO, JJ
    HORTEN, K
    COHEN, RA
    [J]. ARTERIOSCLEROSIS AND THROMBOSIS, 1994, 14 (05): : 753 - 759
  • [9] INACTIVATION OF ENDOTHELIAL DERIVED RELAXING FACTOR BY OXIDIZED LIPOPROTEINS
    CHIN, JH
    AZHAR, S
    HOFFMAN, BB
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1992, 89 (01) : 10 - 18
  • [10] TOXICITY OF OXYSTEROLS TO HUMAN MONOCYTE-MACROPHAGES
    CLARE, K
    HARDWICK, SJ
    CARPENTER, KLH
    WEERATUNGE, N
    MITCHINSON, MJ
    [J]. ATHEROSCLEROSIS, 1995, 118 (01) : 67 - 75