Products of the reaction of HOCl with tryptophan protect LDL from atherogenic modification.

作者: Stylianos Kapiotis , Leopold Jirovetz , Marcela Hermann , Hildegard Laggner , Markus Exner

DOI: 10.1016/J.BIOCHI.2006.01.006

关键词: MyeloperoxidaseLipid oxidationChloramineLipoproteinHypochloriteMetaboliteTryptophanBiochemistryEssential amino acidChemistry

摘要: Abstract Hypochlorite (HOCl) attacks amino acid residues in LDL making the particle atherogenic. Tryptophan is prone to free radical reactions and modification by HOCl. We hypothesized, that tryptophan may quench HOCl attack therefore protecting LDL. Free inhibits apoprotein lipid oxidation. Tryptophan–HOCl metabolites associate with reducing its oxidizability initiated endothelial cells, Cu2+ peroxyl radicals. One tryptophan–HOCl metabolite was identified as 4-methyl-carbostyril which showed antioxidative activity when present during mediated oxidation, but did not Indole-3-acetaldehyde, a decomposition product of chloramine (the reaction) found increasing resistance Myeloperoxidase treatment presence chloride, H2O2 protected lipoprotein from subsequent cell-mediated conclude that, vivo, activated myeloperoxidase system can generate reaction hypochlorite this essential acid.

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