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).