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THE PHOTOTOXIC EFFECT OF BENOXAPROFEN AND ITS ANALOGS ON HUMAN ERYTHROCYTES AND RAT PERITONEAL MAST CELLS
Author(s) -
Sik Robert H.,
Paschall Carl S.,
Chignell Colin F.
Publication year - 1983
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1983.tb03360.x
Subject(s) - chemistry , histamine , degranulation , phototoxicity , pharmacology , butylated hydroxyanisole , mast cell , lysis , superoxide dismutase , biochemistry , glutathione , immunology , antioxidant , biology , receptor , in vitro , enzyme
— Benoxaprofen [2‐(4‐chlorophenyl)‐α‐methyl‐5‐benzoxazoleacetic acid] is a phototoxic non‐steroidal anti‐inflammatory agent. Irradiation of human erythrocytes in the presence of benoxaprofen (8 μ M ) and oxygen resulted in rapid cell lysis which began after 10 min and was complete within 30 min. While photohemolysis was also observed under anerobic conditions, its onset was delayed for more than 20 min and it took nearly 100 min for complete lysis to occur. Photohemolysis was also delayed by butylated hydroxyanisole but was unaffected by reduced glutathione. 1,4‐diazabicyclo[2.2.2]octane, D 2 O. β‐carotene, or superoxide dismutase. The main photoproduct of benoxaprofen, 2‐(4‐chlorophenyl)‐5‐ethylbenzoxazole, was almost as effective in causing photohemolysis as benoxaprofen itself. In the presence of UV irradiation, benoxaprofen (10 (μ M ) caused the degranulation of rat peritoneal mast cells and the release of histamine. The release of mast cell histamine may provide a reasonable explanation for the urticarial response to benoxaprofen and irradiation seen in human subjects.