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Benoxaprofen activates membrane‐associated oxidative metabolism in human polymorphonuclear leucocytes by apparent modulation of protein kinase C
Author(s) -
Lukey Pauline T.,
Anderson Ronald,
Dippenaar Ursula H.
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11433.x
Subject(s) - protein kinase c , superoxide , cytosol , oxidative phosphorylation , chemistry , phosphatidylserine , biochemistry , pharmacology , in vitro , platelet , stimulation , metabolism , kinase , biology , endocrinology , enzyme , membrane , immunology , phospholipid
1 The non‐steroidal anti‐inflammatory drug (NSAID) benoxaprofen at concentrations of 15, 30 and 60 μg ml −1 caused a dose‐related activation of superoxide generation by human polymorphonuclear leucocytes (PMNL) in vitro.2 The protein kinase C (PKC) inhibitor H‐7 prevented benoxaprofen‐mediated activation of superoxide generation by PMNL. 3 Benoxaprofen, by apparent substitution for phosphatidylserine, caused a dose‐related activation of purified PKC from rat brain and in cytosolic extracts from human platelets. 4 Benoxaprofen‐mediated stimulation of PMNL membrane‐associated oxidative metabolism is due to apparent activation of PKC by this NSAID. These findings establish the molecular basis of the pro‐oxidative properties of benoxaprofen.