Leukotrienes are released in inflammatory and immediate hypersensitivity reactions. Leukotrienes are novel metabolites of arachidonic acid produced by the lungs and leucocytes. Their formation is catalyzed by a specific 5-lipoxygenase. The key compound of this pathway is leukotriene A4 which is transformed either into leukotriene B4 by enzymatic hydrolysis or into leukotriene C4 by addition of glutathione. Leukotriene D4 and E4, as well as their precursor leukotriene C4, are the myotropic constituents of the "Slow Reacting Substance of Anaphylaxis" (SRS-A). Leukotrienes are potent bronchoconstrictors in vitro and in vivo. They induce the production of mucus by the respiratory tract and decrease its transport. Leukotrienes (chiefly leukotrienes C4, D4 and E4) induce the vasoconstriction of large vessels and capillaries. Leukotriene B4 stimulates several leukocyte functions related to inflammation (chemotaxis, aggregation, release of lysosomal enzymes and production of superoxide anion). In addition, it induces the formation of suppressive and cytotoxic T-Lymphocytes. The actions of leukotrienes are mediated by specific receptors and, in certain organs, their mechanism of action involves a stimulation of the formation of prostaglandins and thromboxanes. Non-steroidal antiinflammatory drugs (aspirin) inhibit the biosynthesis of prostaglandins and thromboxanes, whereas steroidal antiinflammatory agents (dexamethasone) should inhibit the production of leukotrienes as well as of prostaglandins and thromboxanes (through an indirect action on phospholipase A2).
白三烯在炎症和速发型超敏反应中释放。白三烯是肺和白细胞产生的花生四烯酸的新型代谢产物。它们的形成由一种特定的5-脂氧合酶催化。该途径的关键化合物是白三烯A4,它通过酶促水解转化为白三烯B4,或通过添加谷胱甘肽转化为白三烯C4。白三烯D4和E4以及它们的前体白三烯C4是“过敏反应慢反应物质”(SRS-A)的致肌成分。白三烯在体外和体内都是强效支气管收缩剂。它们诱导呼吸道产生黏液并减少其运输。白三烯(主要是白三烯C4、D4和E4)诱导大血管和毛细血管的血管收缩。白三烯B4刺激与炎症相关的几种白细胞功能(趋化性、聚集、溶酶体酶释放和超氧阴离子产生)。此外,它诱导抑制性和细胞毒性T淋巴细胞的形成。白三烯的作用由特定受体介导,在某些器官中,它们的作用机制涉及刺激前列腺素和血栓素的形成。非甾体抗炎药(阿司匹林)抑制前列腺素和血栓素的生物合成,而甾体抗炎剂(地塞米松)应抑制白三烯以及前列腺素和血栓素的产生(通过对磷脂酶A2的间接作用)。