Benoxaprofen photosensitization of cell membrane disruption.
Benoxaprofen (BXP) is a nonsteroidal anti-inflammatory drug which causes cutaneous phototoxicity. Because the in vivo phototoxicity may involve photosensitized damage to mast cell membranes, the mechanism for photosensitized damage was studied in a single model system, the red blood cell. Oxygen-dependent and oxygen-independent mechanisms for membrane disruption were detected. Oxygen-dependent lysis was not quenched by superoxide dismutase and was quenched only at high sodium azide concentrations. A two-step mechanism is proposed involving initial photodecarboxylation of BXP to form a lipophilic photoproduct which subsequently photosensitizes membrane damage. Human serum albumin at 0.03% totally inhibited BXP-photosensitized lysis.
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001386:Azides / Q000494:pharmacology; D002851:Chromatography, High Pressure Liquid; D003879:Dermatologic Agents / Q000494:pharmacology*; D004910:Erythrocyte Membrane / Q000187:drug effects*; D006461:Hemolysis; D006801:Humans; D066298:In Vitro Techniques; D010787:Photosensitivity Disorders / Q000139:chemically induced* / Q000473:pathology; D011422:Propionates / Q000494:pharmacology*; D012709:Serum Albumin / Q000494:pharmacology; D019810:Sodium Azide; D013050:Spectrometry, Fluorescence; D013482:Superoxide Dismutase / Q000494:pharmacology; D014466:Ultraviolet Rays
D000893:Anti-Inflammatory Agents; D001386:Azides; D003879:Dermatologic Agents; D011422:Propionates; D012709:Serum Albumin; C011677:benoxaprofen; D019810:Sodium Azide; D013482:Superoxide Dismutase