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Wiley InterScience | ||||||||||||||||||||||||||||
   Annals of the New York Academy of SciencesVolume 1043 Issue The Maillard Reaction: Chemistry at the Interface of Nutrition, Aging, and Disease, Pages 327 - 342 Published Online: 9 Jan 2006 © 2010 The New York Academy of Sciences
Abstract | References | Full Text: HTML, PDF (Size: 10051K) | Related Articles | Citation Tracking  Isolevuglandins, Oxidatively Truncated Phospholipids, and Atherosclerosis Copyright 2005 New York Academy of Sciences KEYWORDS levuglandins • isolevuglandins • isoLGs • isoprostanes • isoPs • oxidized phospholipids • lipid peroxidation • endoperoxides • atherosclerosis • foam cells • low-density lipoprotein • LDL • oxLDL • macrophages • endothelial cells • endocytosis • HNE • scavenger receptor CD36 Abstract:
Abstract: Isolevuglandins (isoLGs) and oxidatively truncated phospholipids are products of lipid peroxidation. Some of these, especially isoLGs and γ-hydroxyalkenal analogues (e.g., the 5-hydroxy-8-oxo-6-octenoic acid and 9-hydroxy-12-oxo-10-dodecenoic acid esters of 2-lysophosphatidylcholine, HOOA-PC or HODA-PC, respectively) of 4-hydroxy-2(E)-nonenal (HNE), damage proteins by covalent adduction, thereby interfering with their normal functions. These lipid-derived protein modifications may serve as dosimeters of oxidative injury. Elevated plasma levels of isoLG-protein epitopes are associated with atherosclerosis but are independent of total cholesterol, a classical risk factor. Both protein adducts and oxidatively truncated phospholipids (oxPL) can also elicit receptor-mediated cellular responses that include endocytosis of oxidized low-density lipoprotein (LDL) and expression of chemokines, which may foster infiltration of monocyte macrophages into the subendothelial space, where they become foam cells through unregulated endocytosis of oxidatively damaged LDL. | 
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