Ribeiro C A, Figueiredo A, Tavares P, Poiares-Baptista A, Teixeria F
Institute of Pharmacology and Experimental Therapeutics, Faculty of Medicine, University of Coimbra, Portugal.
Drug Metabol Drug Interact. 1992;10(4):293-305. doi: 10.1515/dmdi.1992.10.4.293.
The effect of nimesulide on red blood cell (RBC) lysis photosensitized by tiaprofenic acid was investigated. The tiaprofenic acid-induced photohemolysis rate was enhanced by exposure to oxygen but lysis was also observed under anaerobic conditions. Photohemolysis was decreased by reduced glutathione (GSH) and reduced even more by butylated hydroxyanisole (BHA); sodium azide, superoxide dismutase and mannitol did not show a significant effect. Nimesulide did not cause any RBC lysis and inhibited this action of tiaprofenic acid by 20-30%, depending on the concentration of nimesulide and the intensity of ultraviolet A light. The protective effect of GSH, but not of BHA, was increased by nimesulide. Our findings suggest that free radicals are generated in this in vitro model of phototoxicity and are involved in the photoaggression to the red blood cell membrane, this effect being partially inhibited by nimesulide.
研究了尼美舒利对噻洛芬酸致敏的红细胞（RBC）裂解的影响。噻洛芬酸诱导的光溶血率在暴露于氧气时会增强，但在厌氧条件下也可观察到裂解。还原型谷胱甘肽（GSH）可降低光溶血，丁基羟基茴香醚（BHA）的降低作用更强；叠氮化钠、超氧化物歧化酶和甘露醇未显示出显著作用。尼美舒利不会引起任何红细胞裂解，并根据尼美舒利的浓度和紫外线A光的强度，将噻洛芬酸的这种作用抑制20%-30%。尼美舒利可增强GSH而非BHA的保护作用。我们的研究结果表明，在这个光毒性体外模型中会产生自由基，并且自由基参与了对红细胞膜的光损伤，尼美舒利可部分抑制这种作用。
