Kochevar I E, Hoover K W, Gawienowski M
J Invest Dermatol. 1984 Mar;82(3):214-8. doi: 10.1111/1523-1747.ep12260034.
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.
苯恶洛芬（BXP）是一种会引起皮肤光毒性的非甾体抗炎药。由于体内光毒性可能涉及对肥大细胞膜的光敏损伤，因此在单一模型系统红细胞中研究了光敏损伤的机制。检测到了膜破坏的氧依赖性和非氧依赖性机制。氧依赖性裂解不能被超氧化物歧化酶淬灭，仅在高浓度叠氮化钠时才被淬灭。提出了一种两步机制，涉及BXP的初始光脱羧作用以形成亲脂性光产物，该光产物随后使膜损伤发生光敏化。0.03%的人血清白蛋白完全抑制了BXP光敏化裂解。
