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 μM, 73 μM and >500 μM, respectively. The inhibitory profiles of these neutrophil activation parameters demonstrate a dissociation between membrane depolarization, respiratory burst stimulation, and phospholipid turnover. © 1983.
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