Dissociation of human neutrophil membrane depolarization, respiratory burst stimulation and phospholipid metabolism by quinacrine.
Human neutrophils generate a respiratory burst with the elaboration of toxic oxygen metabolites upon appropriate stimulation. Subsequent to receptor-ligand interaction, the activation pathway of this burst is unknown. Here, attempts to correlate phospholipid turnover have demonstrated dissociation of lipid flux and burst activation. Quinacrine inhibited membrane depolarization, superoxide (O-2) generation, and net phosphatidylserine production with ID50-values of 16 microM and greater than 500 microM, respectively. The inhibitory profiles of these neutrophil activation parameters demonstrate a dissociation between membrane depolarization, respiratory burst stimulation, and phospholipid turnover.
D004305:Dose-Response Relationship, Drug; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D009504:Neutrophils / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects*; D010718:Phosphatidylserines / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism*; D011796:Quinacrine / Q000494:pharmacology*; D013481:Superoxides / Q000378:metabolism
D010718:Phosphatidylserines; D010743:Phospholipids; D013481:Superoxides; D011796:Quinacrine