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Dissociation of human neutrophil membrane depolarization, respiratory burst stimulation and phospholipid metabolism by quinacrine
Author(s) -
Tauber Alfred I.,
Simons Elizabeth R.
Publication year - 1983
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(83)80269-5
Subject(s) - depolarization , phospholipid , respiratory burst , stimulation , phosphatidylserine , chemistry , biophysics , superoxide , biochemistry , membrane potential , membrane , biology , endocrinology , enzyme
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 ID 50 ‐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.