Studies on the mechanism of inhibition of chemotactic tripeptide stimulated human neutrophil polymorphonuclear leucocyte superoxide production by chloroquine and hydroxychloroquine.
The effect of chloroquine and hydroxychloroquine on neutrophil superoxide release stimulated by the chemotactic tripeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) was examined. Both drugs caused time and dose dependent inhibition of superoxide release but had no effect on equilibrium binding of [3H]FMLP to its receptor. Preliminary experiments suggest that these drugs may exert their inhibitory effect on superoxide release by inhibiting the FMLP stimulated hydrolysis of phosphoinositides.
Hurst
N P
NP
Queen Elizabeth Hospital Rheumatology Unit, Woodville, South Australia.
French
J K
JK
Gorjatschko
L
L
Betts
W H
WH
D002634:Chemotaxis, Leukocyte; D002738:Chloroquine / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006886:Hydroxychloroquine / Q000494:pharmacology*; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000378:metabolism / Q000494:pharmacology*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D013481:Superoxides / Q000493:pharmacokinetics*
D013481:Superoxides; D006886:Hydroxychloroquine; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002738:Chloroquine