p‐Hydroxyphenylacetaldehyde, the major product of tyrosine oxidation by the activated myeloperoxidase system can act as an antioxidant in LDL

FEBS Letters

Quehenberger, P¹  Gmeiner, B²  Hofbauer, R¹  Speiser, W¹  Kapiotis, S¹  Exner, M¹  Minar, E⁵  Alt, E⁴  Hermann, M³ 

[1] Department of Laboratory Medicine, University of Vienna, Vienna, Austria;Institute of Medical Chemistry, University of Vienna, Währingerstr. 10, A-1090 Vienna, Austria;Institute of Molecular Genetics, University of Vienna, Vienna, Austria;Department of Angiology, University of Zürich, Zürich, Switzerland;Department of Angiology, University of Vienna, Vienna, Austria

关键词: p-Hydroxyphenylacetaldehyde;    Tyrosine;    LDL oxidation;    Myeloperoxidase;    Antioxidant;    CHOD;    cholesterol oxidase;    DTPA;    diethylene triamine-pentaacetate;    HOCl;    hypochlorous acid;    NaOCl;    sodium hypochlorite;    HUVEC;    human umbilical vein endothelial cell;    LDL;    low density lipoprotein;    PBS;    phosphate buffered saline;    p-HA;    p-hydroxyphenylacetaldehyde;    REM;    relative electrophoretic mobility;    TBARS;    thiobarbituric acid reactive substance;   

DOI  :  10.1016/S0014-5793(01)02131-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The oxidative modification of low density lipoprotein (LDL) may play a significant role in atherogenesis. HOCl generated by the myeloperoxidase/H₂O₂/Cl⁻ system of activated neutrophils may be operative in vivo making LDL atherogenic. Tyrosine has been found to be oxidized by HOCl to p-hydroxyphenylacetaldehyde (p-HA) capable of modifying phospholipid amino groups in LDL. As an amphiphatic phenolic compound, p-HA may have the potential to act as an antioxidant in the lipid phase of LDL. The present results show that (a) tyrosine exerts a protective effect on LDL modification by HOCl, (b) p-HA could act as antioxidant associated with the lipoprotein preventing cell- and transition metal ion-mediated LDL oxidation and (c) p-HA was able to scavenge free radicals.

【 授权许可】

Unknown