Horn S, Bashan N, Peleg N, Gopas J
Department of Microbiology, Faculty of Health Sciences, Ben-Gurion University, Beer Sheva, Israel.
Eur J Clin Invest. 1995 Jan;25(1):32-8. doi: 10.1111/j.1365-2362.1995.tb01522.x.
In this study, the composition and the role of membrane glycoproteins in phagocytosis were determined in G6PD deficient RBCs. G6PD deficient RBCs were recognized and significantly phagocytosed by murine macrophages, without pre-exposure to oxidants in vivo. Phagocytosis was partially (60%) inhibited by incubating macrophages with either galactose or mannose, or by incubating RBCs with beta-galactosidase, indicating the involvement of lectin-like receptors in the recognition of G6PD deficient RBCs. Membrane glycoproteins on G6PD deficient cells were detected by binding of Con A to both intact RBCs and to purified membrane proteins. The results demonstrated modifications in the glycoprotein pattern of G6PD deficient RBCs compared to untreated controls. These included reduction in the amounts of several high molecular weight glycoproteins and appearance of lower molecular weight bands. These results suggest that G6PD deficient RBCs undergo glycoprotein modifications, which may lead to premature removal from circulation, even in non-acute hemolysis.
在本研究中，测定了葡萄糖-6-磷酸脱氢酶（G6PD）缺乏的红细胞中膜糖蛋白的组成及其在吞噬作用中的作用。G6PD缺乏的红细胞在体内未预先暴露于氧化剂的情况下，能够被小鼠巨噬细胞识别并显著吞噬。用半乳糖或甘露糖孵育巨噬细胞，或用β-半乳糖苷酶孵育红细胞，吞噬作用会部分（60%）受到抑制，这表明凝集素样受体参与了对G6PD缺乏红细胞的识别。通过伴刀豆球蛋白A（Con A）与完整红细胞及纯化膜蛋白的结合，检测G6PD缺乏细胞上的膜糖蛋白。结果表明，与未处理的对照相比，G6PD缺乏红细胞的糖蛋白模式发生了改变。这些改变包括几种高分子量糖蛋白数量的减少以及低分子量条带的出现。这些结果表明，G6PD缺乏的红细胞会发生糖蛋白修饰，这可能导致即使在非急性溶血情况下也会过早地从循环中清除。
