Cysteinyl leukotrienes are lipid mediators released during the allergic response primarily from mast cells, eosinophils and macrophages [1]. LTC_4 is produced from arachidonic acid stored in the membrane phos-pholipids [2]. Extracellular LTC_4 is converted to LTD4, which is then quickly converted to LTE_4, the most stable of the three mediators [3]. The effects of CysLT are mainly considered to occur through two G-protein coupled receptors [CysLT_1 receptor (R) and CysLT_2R], which have relatively high affinities for LTC_4 and LTD_4, whereas LTE_4 is considered a weak agonist [4, 5]. With the development of drugs blocking the CysLT_1 receptor, the role of leukotrienes in asthma has focused largely on LTC_4 and LTD_4.
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