Yu Guoyu, Li Jialin, Tian Xingya, Lin Hong, Wang Xiaoying
Department of Biochemistry, Kunming Medical College, Kunming 650031, China.
Zhonghua Xue Ye Xue Za Zhi. 2002 Nov;23(11):565-7.
To explore the hemolytic mechanism of glucose-6-phosphate dehydrogenase (G6PD) deficient erythrocytes in the view of phosphorylation of membrane protein.
The alternation of membrane protein phosphorylation and the effect of dithiothreitol (DTT) on protein phosphorylation were analysed by Western blot technique. The activity of phosphotyrosine phosphatase (PTPs) was determined by using p-nitrophenyl phosphate as substrate.
Tyrosine phosphorylation of band 3 protein was obviously enhanced in G6PD-deficient erythrocytes. The activity of PTPs was low compared to the normal erythrocytes. The level of phosphotyrosine in G6PD-deficient erythrocytes incubated with DTT was almost the same as in those without DTT. The results were consistent with the activity of PTPs.
PTPs activity reduction and tyrosine phosphorylation enhancement induced by oxidation in G6PD deficiency play an important role in erythrocytes hemolysis. However, the alternation of thiol group is not the only factor affecting the activity of PTPs in G6PD-deficient erythrocytes.
从膜蛋白磷酸化角度探讨葡萄糖-6-磷酸脱氢酶（G6PD）缺乏红细胞的溶血机制。
采用蛋白质免疫印迹技术分析膜蛋白磷酸化的变化以及二硫苏糖醇（DTT）对蛋白质磷酸化的影响。以对硝基苯磷酸为底物测定磷酸酪氨酸磷酸酶（PTPs）的活性。
G6PD缺乏红细胞中带3蛋白的酪氨酸磷酸化明显增强。与正常红细胞相比，PTPs的活性较低。用DTT孵育的G6PD缺乏红细胞中磷酸酪氨酸水平与未用DTT处理的几乎相同。结果与PTPs的活性一致。
G6PD缺乏时氧化诱导的PTPs活性降低和酪氨酸磷酸化增强在红细胞溶血中起重要作用。然而，硫醇基团的变化不是影响G6PD缺乏红细胞中PTPs活性的唯一因素。
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