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The most important known lipid mediators of inflammation are either metabolites of long-chain fatty acids, particularly arachidonic acid (AA), or l -alkyl-2-acetyl analogues of phosphatidyl choline (platelet activating factor-PAF) (1-8). Because of the scope of the subject, this chapter reviews only the mediators derived from AA and emphasizes lipoxygenase products. Arachidonate Metabolites Arachidonic acid (eicosatetraenoic acid) is a C20 fatty acid with double bonds at the 5-6, 8-9. 11-12. and 14-15 positions. The multiplicity of double bonds provides a number of potential sites for oxidation which, together with the various double bond rearrangements that are possible, permits a number of bioreactive lipids to be formed. Since AA itself and most of its initial metabolites have 20 carbons, its metabolites have been termed eicosanoids. The two major routes of AA metabolism in mam malian cells are the lipoxygenase (LO) and the cyclooxygenase (CO) path ways (Figure 1). Both enzymes act largely or entirely on unesterified AA. Lipoxygenases differ in the location of the double bond on the AA molecule where enzymatic attack is initiated (9, 10). They include the l 2-lipoxy genases (12-LO, Figure I-top left) of which the enzyme in platelets is the best characterized; the 5-lipoxygenase (5-LO,
Annual Review of Immunology – Annual Reviews
Published: Apr 1, 1987
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