The salicylate metabolite gentisic acid, but not the parent drug, inhibits glucose autoxidation‐mediated atherogenic modification of low density lipoprotein

FEBS Letters

Hermann, Marcela³  Seelos, Christian¹  Held, Irmtraud⁵  Exner, Markus²  Gmeiner, Bernhard M.K⁴  Speiser, Wolfgang²  Hofbauer, Roland²  Kapiotis, Stylianos⁶ 

[1] Institute of Tumorbiology-Cancer Research, University of Vienna, Vienna, Austria;Department of Laboratory Medicine, University of Vienna, Vienna, Austria;Institute of Molecular Genetics, University of Vienna, Vienna, Austria;Institute of Medical Chemistry, University of Vienna, Währingerstr. 10, A-1090 Vienna, Austria;BIFA, Vienna, Austria;Institute of Laboratory Medicine, Krankenhaus Neunkirchen, Neunkirchen, Austria

关键词: Glucose autoxidation;    Low density lipoprotein oxidation;    Aspirin;    Salicylate;    Gentisic acid;    2;    3-Dihydroxybenzoic acid;    2;    5-Dihydroxybenzoic acid;   

DOI  :  10.1016/S0014-5793(00)01289-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Oxidation of low density lipoprotein (LDL) by glucose-derived radicals may play a role in the aetiology of atherosclerosis in diabetes. Salicylate was shown to scavenge certain radicals. In the present study, aspirin, salicylate and its metabolites 2,5- and 2,3-dihydroxybenzoic acid (DHBA) were tested for their ability to impair LDL oxidation by glucose. Only the DHBA derivatives, when present during LDL modification, inhibited LDL oxidation and the increase in endothelial tissue factor synthesis induced by glucose oxidised LDL. The LDL glycation reaction was not affected by DHBA. The antioxidative action of DHBA may be attributed to free radical scavenging and/or chelation of transition metal ions catalysing glucose autoxidation.

【 授权许可】

Unknown