{'fraction_non_alphanumeric': 0.027995520716685332, 'fraction_numerical': 0.013437849944008958, 'mean_word_length': 6.327868852459017, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Benoxaprofen activates membrane‐associated oxidative metabolism in human polymorphonuclear leucocytes by apparent modulation of protein kinase C

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.