摘要
目的研究G6PD缺乏患者红细胞膜蛋白氨基酸残基的氧化修饰,定量分析红细胞膜蛋白的氧化损伤程度.方法设置3组研究对象,分别是G6PD正常组和G6PD缺乏无急性溶血组;G6PD缺乏急性溶血组,用NDPH法分别测定各组红细胞膜蛋白活性羰基含量,荧光比色法测定色氨酸残基荧光强度的改变.结果(1)与正常组比较,G6PD缺乏无急性溶血组、G6PD缺乏急性溶血组的红细胞还原型谷胱甘肽含量下降,硫代巴比妥酸反应产物(TBARS)水平显著升高;(2)G6PD缺乏无急性溶血组、G6PD缺乏急性溶血组的红细胞膜蛋白羰基含量均显著增加,色氨酸残基荧光强度显著下降;(3)G6PD缺乏急性溶血组与非急性溶血组差异之间红细胞TBARS、膜蛋白羰基含量、色氨酸残基荧光强度差异均无显著性(P>0.005).结论G6PD缺乏可引起红细胞膜脂质和蛋白氧化损伤,但这些损伤不是急性溶血的直接原因.
Objective To residues of the membrane proteins study the oxidative insults in erythrocytes and oxidative modification of amino acid in erythrocytes with glucose-6-phosphate dehydrogenises (G6PD) deficiency. ed, including control group, G6PD deficiency group with acute hemolysis and G6PD deficiency group with non -acute hemolysis. The amount of active carbonyls and fluorescence intensity of tryptophan residues in erythrocyte membrane proteins were determined by using NADP method . The levels TBABS and GSH in erythrocytes were also measured. Results Compared with control group, both the two G6PD deficiency groups had significant ally higher levels of carbonyls and TBARS, and lower levers of fluorescence intensity of tryptophan residues and GSH; the level of TBARS and GSH in erythrocyte and the level of active carbonyls and fluorescence intensity of tryptophan residues have no significant differences between the two G6PD deficiency groups. Conclusions G6PD deficiency can result in oxidative damage to erythrocyte and membrane proteins. Although oxidative damages are probably the molecular medinism of hemolysis, they are not direct causes of acute hemolysis.
出处
《昆明医学院学报》
2007年第2期22-26,共5页
Journal of Kunming Medical College
基金
云南省教育厅基金资助(No03Y445C)
关键词
葡萄糖-6-磷酸脱氢酶
膜蛋白
氨基酸残基修饰
Glucose -6 - phosphate dehydrogenises
Membrane protein
Modification of amino acid residues