Abstract
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.
MeSH terms
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Acetaldehyde / analogs & derivatives*
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Acetaldehyde / pharmacology*
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Antioxidants / pharmacology*
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Dose-Response Relationship, Drug
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Electrophoresis, Agar Gel
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Endothelium, Vascular / cytology
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Free Radical Scavengers / metabolism
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Humans
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Hydrogen-Ion Concentration
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Hypochlorous Acid / metabolism
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Ions
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Lipid Metabolism
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Lipoproteins, LDL / metabolism*
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Neutrophils / metabolism
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Oxygen / metabolism*
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Peroxidase / metabolism*
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Phenol
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Protein Binding
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Thiobarbituric Acid Reactive Substances / metabolism
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Time Factors
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Tyrosine / metabolism*
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Umbilical Veins / cytology
Substances
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Antioxidants
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Free Radical Scavengers
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Ions
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Lipoproteins, LDL
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Thiobarbituric Acid Reactive Substances
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Phenol
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Tyrosine
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Hypochlorous Acid
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4-hydroxyphenylacetaldehyde
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Peroxidase
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Acetaldehyde
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Oxygen