Modulation of the Release of Leukotrienes and Prostaglandins and of their Functional Effects in Human and Guinea-Pig Lung Parenchyma

Abstract

The elucidation of the structure of SRS-A (slow reacting substance of anaphylaxis) has led to the discovery of Leukotrienes (LTs), a family of arachidonate metabolites produced by the enzyme 5-lipoxygenase (1) (2). A stereospecific synthesis brings about formation of two classes of LTs, one major class composed of the sulfidopeptide leukotrienes, LTC4, LTD4 and LTE4, and another class represented solely by LTB4. A variety of stimuli, cleaving arachidonate from membrane phospholipids, provide the necessary substrate for the synthesis of prostaglandins (PGs), thromboxanes (TX) and LTs (3). PGs and to a minor extent TX are formed ubiquitarily, whereas the synthesis of LTs seems to require a considerable cellular specificity (4) (5): all of them are formed by normal and asthmatic human lung where they may play a role as potent bronchoconstrictors as well as primary mediators of airway hyperreactivity (6).