Facorro G, Aguirre F, Florentin L, Díaz M, De Paoli T, Ihlo J E, Hager A A, Sánchez Avalos J C, Farach H A, Poole C P
Cátedra de Física, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
Acta Physiol Pharmacol Ther Latinoam. 1997;47(3):137-46.
In order to investigate the implications of oxidative disturbances in the hemolysis associated with the Hemolytic Uremic Syndrome (HUS), basal levels of lipid peroxidation products, the response to t-butyl hydroperoxide induced damage and membrane fluidity were assayed by the technique of electron spin resonance in erythrocytes spin labeled with 5-Doxyl stearic acid obtained from eight children with HUS, during the 1st, 2nd, 4th and 12th weeks after diagnosis. During the acute phase of the disease, red blood cells (RBC) showed increased initial lipid peroxidation products, a higher susceptibility to oxidative insult and a lower membrane fluidity. All parameters reached control values the 12th week after diagnosis. The results suggest that in the acute phase of HUS, RBCs are exposed to an oxidative imbalance that could contribute to hemolysis directly through oxidative damage and/or by decreasing membrane fluidity.
为了研究氧化紊乱在与溶血性尿毒症综合征(HUS)相关的溶血中的影响,我们采用电子自旋共振技术,对8名HUS患儿诊断后第1、2、4和12周时,用5-硬脂酰氧基-1-氧基-3-甲基-5-氮杂环戊烷标记的红细胞中的脂质过氧化产物基础水平、对叔丁基过氧化氢诱导损伤的反应以及膜流动性进行了检测。在疾病急性期,红细胞(RBC)显示出初始脂质过氧化产物增加、对氧化损伤的敏感性更高以及膜流动性更低。所有参数在诊断后第12周达到对照值。结果表明,在HUS急性期,红细胞暴露于氧化失衡状态,这可能直接通过氧化损伤和/或降低膜流动性导致溶血。