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Clin Lipidol. 2010 Dec 01;5(6):835-852. doi: 10.2217/clp.10.68.

Lipid oxidation by hypochlorous acid: chlorinated lipids in atherosclerosis and myocardial ischemia.

Clinical lipidology

David A Ford

Affiliations

  1. Department of Biochemistry & Molecular Biology, Center for Cardiovascular Research, Saint Louis University School of Medicine, Room 325, Doisy Research Center, 1100 South Grand Blvd, St Louis, MO 63104, USA, Tel.: +1 314 977 9264.

PMID: 21339854 PMCID: PMC3041592 DOI: 10.2217/clp.10.68

Abstract

Leukocytes, containing myeloperoxidase (MPO), produce the reactive chlorinating species, HOCl, and they have important roles in the pathophysiology of cardiovascular disease. Leukocyte-derived HOCl can target primary amines, alkenes and vinyl ethers of lipids, resulting in chlorinated products. Plasmalogens are vinyl ether-containing phospholipids that are abundant in tissues of the cardiovascular system. The HOCl oxidation products derived from plasmalogens are α-chlorofatty aldehyde and unsaturated molecular species of lysophosphatidylcholine. α-chlorofatty aldehyde is the precursor of both α-chlorofatty alcohol and α-chlorofatty acid. Both α-chlorofatty aldehyde and α-chlorofatty acid accumulate in activated neutrophils and have disparate chemotactic properties. In addition, α-chlorofatty aldehyde increases in activated monocytes, human atherosclerotic lesions and rat infarcted myocardium. This article addresses the pathways for the synthesis of these lipids and their biological targets.

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