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Formation and release of nitric oxide from human neutrophils and HL‐60 cells induced by a chemotactic peptide, platelet activating factor and leukotriene B 4
Author(s) -
Schmidt Harald H.H.W.,
Seifert Roland,
Böhme Eycke
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80562-9
Subject(s) - superoxide , leukotriene b4 , nitric oxide , chemistry , chemotaxis , platelet activating factor , endothelium derived relaxing factor , superoxide dismutase , peptide , arginine , biochemistry , platelet , enzyme , inflammation , amino acid , immunology , biology , receptor , organic chemistry
Vascular endothelial cells and neutrophils synthesize and release potent vasodilatatory factors, i.e. endothelium‐derived relaxing factors (EDRF) and neutrophil‐derived relaxing factors (NDRF). One EDRF has been identified as nitric oxide (NO) derived from arginine. We studied the synthesis and release of NO from human neutrophils stimulated with the chemotactic peptide N ‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine, platelet activating factor or leukotriene B 4 . The formation and release of NO was enhanced several‐fold in the presence of superoxide dismutase, probably by inhibiting superoxide‐induced breakdown of NO. The formation and release of NO but not the formation of superoxide anions was decreased in neutrophils pretreated with L‐canavanine, an inhibitor of arginine‐utilizing enzymes. Our data suggest that at least one NDRF is identical with NO or another labile NO containing compound derived from arginine.