Abstract-3-Morpholino-sydnonimine (SIN-l) is a NO-releasing compound which mimics the effects of cGMP through activation of soluble guanylyl cyclase. Its prodrug, molsidomine (SIN-lo), does not release NO but does modulate various cell functions. These findings prompted us to study the effects of SIN-10 and SIN-1 on the respiratory burst in human neutrophils. SIN-10 was more effective than SIN-1 in inhibiting superoxide anion (0;) formation induced by N-formyl-L-methionyl-L-leucyl-Lphenylalanine (fMet-Leu-Phe) and by C5a. The effects of SIN-l and SIN-10 on 0; formation were additive or less than additive, indicating the sydnonimines acted through a common mechanism. The sydnonimines showed no effect on 0; formations induced by y-hexachlorocyclohexane, arachidonic acid and a phorbol ester. They did not inhibit 0; formation induced by xanthine oxidase, by autoxidation of pyrogallol and in a cell-free system from HL-60 leukemic cells. Neutrophils did not convert SIN-10 to SIN-1 as assessed by 0, consumption which accompanies NO release from SIN-l.
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