Molecular determinants for functional responses to the sulfidopeptide leukotrienes: metabolism and receptor subclasses.

The end-organ effects of generated leukotriene C4 (LTC4) are regulated by a number of events subsequent to LTC4 biosynthesis. Ongoing peptide cleavage of LTC4 to the other sulfidopeptide leukotrienes, D4 and E4, would be regulatory, since LTC4 and LTD4 possess unique separate tissue receptors, as demonstrated on nonvascular smooth muscle. Further, both neutrophils and eosinophils possess a mechanism, dependent upon triggering of the respiratory burst, that modifies the structures and functional activities of the sulfidopeptide leukotrienes. This rapid inactivation process extends the previous appreciation that the sulfidopeptide leukotrienes function as local mediators of inflammation, rather than as hormones.