Leukotriene C4 (LTC4), leukotriene D4 (LTD4), and leukotriene E4 (LTE4), collectively known as cysteinyl leukotrienes, are members of the eicosanoid group of lipid mediators1. They have been implicated in a wide variety of acute and chronic inflammatory conditions including asthma, tissue injury, cardiac and liver diseases, and shock2,3. Production of LTC4 is initiated by the conjugation of the epoxide intermediate LTA4 with glutathione (GSH). LTC4 is further metabolized to the cysteinyl glycine conjugate of LTA4 known as LTD4 by the actions of two plasma-membrane-bound ectoenzymes, γ-glutamyl transpeptidase (GGT) and γ-glutamyl leukotrienase (GGL)4,5. LTD4 is believed to be converted to the less active cysteinyl glycine conjugate of LTA4 called LTE4 by a dipeptidase6. The rank order of molar potencies of cysteinyl leukotrienes is LTD4>LTC4 >LTE4. LTD4 is considered to be at least 10 to 100-fold more potent than LTE4 7. Consequently, conversion of LTD4 to LTE4 is a critical step in the cysteinyl leukotriene metabolism. LTC4, LTD4, and LTE4 are eliminated from the blood circulation with initial half-lives of 30–40 s. They are mainly taken up by kidney and liver and excreted into the urine and bile, respectively8. Thus, the liver seems to be the major site of their metabolic inactivation.