Eicosanoids are lipid derivatives of three polyunsaturated 20-carbon fatty acids: dihomogammalinolenic acid (C20:3 n - 6), arachidonic acid (C20:4 n - 6) and eicosapentaenoic acid (C20:5 n - 3). The most common of them is arachidonic acid, the main precursor of eicosanoids in macrophages. In the course of eicosanoid synthesis, arachidonic acid released from membrane phospholipids is transformed via two pathways – by cyclooxygenases to cyclic compounds, i.e. prostaglandins, prostacyclins and thromboxanes, and by lipoxygenases to non-cyclic compounds - leukotrienes and hydroperoxy derivatives of arachidonic acid and linoleic acid. Two main classes of phospholipases A₂ (which are subdivided in isoforms within one class) are found in macrophages: cytoplasmatic phospholipase A₂ and secretory phospholipase A₂. Both classes participate in regulation of physiological and pathological processes, e.g. in release of pro-inflammatory mediators and stimulation of inflammatory processes. Lipoxygenases constitute a heterogeneous family of non-heme enzymes oxygenating polyunsaturated fatty acids. This family of enzymes includes a number of isoforms, including 15-lipoxygenases present in macrophages and 5-lipoxygenase. The role of lipoxygenases is to synthesise hydroperoxides of fatty acids, which play signalling functions in the body: 15S- and 12S-HpETE and 13S-and 9S-HpODE. HpODE and HpETE are labile compounds which undergo rapid reduction to hydroxyl derivatives. 5-LO is a cytoplasmatic enzyme which initiates transformation of arachidonic acid to leukotriene A₄ and its derivatives. Arachidonic acid (released from nuclear membrane by cPLA₂) is transformed by 5-LO to 5-hydroperoxyeicosatetraenoic acid (5-HpETE), which may be converted to hydroxyeicosatetraenoic acid (5-HETE) with participation of glutathion peroxydase or to leukotriene A₄ (LTA₄). LTA₄ may then be metabolised via two pathways: by cytoplasmatic hydrolase to leukotriene B₄ or by LTC₄ synthase to cysteinyl leukotrienes (LTC₄, LTD₄, LTE₄). Two cyclooxygenase isoforms are present in macrophages: cyclooxygenase-1 (COX-1) and cyclooxygenase- 2 (COX-2). COX-1 is a constitutive enzyme, COX-2 is potently stimulated by cytokines, growth factors and free radicals. Both isoforms of cyclooxygenases may be a source of prostaglandins in macrophages. Induction (and activity) of COX-2 increases significantly in the course of monocyte differentiation. A number of factors involved in this process were observed: AP2, STAT-1, STAT-3, IL-6. The best known of them is the NFκB transcription factor which is additionally responsible for induction of secretory phospholipase A₂.Expression of enzymes metabolising arachidonic acid (sPLA₂, 15-LO, COX-2 5-LO) was shown to significantly increase in advanced atherosclerotic lesions. The pro-atherogenic activity of these enzymes is related to LDL oxygenation, synthesis of pro-inflammatory leukotrienes and prostanoids, and regulation of activity of matrix metalloproteinases.

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