Simmons N L, Naftalin R J
Biochim Biophys Acta. 1976 Feb 6;419(3):493-511. doi: 10.1016/0005-2736(76)90261-3.
Sugar-dependent increments in red cell stability under osmotic stress can be ascribed to changes either in the membrane or in the intracellular matrix. These two possible modes of action have been tested and characterized. Rheological investigation of membrane-free haemoglobin solutions has shown that D-glucose, but not D-fructose, promotes the formation of a visco-plastic gel structure. Gel strength is a function of glucose concentration, haemoglobin concentration and temperature. The ability of various sugars to promote gel formation correlates with their solution properties. The existence of gel structure reduces K+ and haemoglobin leak from red cells whose membranes were partially destroyed by gamma-radiation. Reduced osmotic swelling in the presence of glucose is also due to gel formation since the glucose effect is lost in resealed red cell ghosts. D-Fructose does not protect red cells against radiation damage; its mode of action in increasing red cell stability under osmotic stress is a membrane effect. Cell sizing using the Coulter Counter has shown that fructose, but not glucose, can increase the maximal volume at lysis. At 50 mM, D-fructose expands the red cell ghost volume by 11.2%; this represents a 7.2% increase in membrane area. Ghost expansion by fructose is fructose concentration dependent (0-100 mM) and is insensitive to temperature variation (0-37 degrees C).
在渗透应激下，红细胞稳定性的糖依赖性增加可归因于细胞膜或细胞内基质的变化。这两种可能的作用模式已得到测试和表征。对无膜血红蛋白溶液的流变学研究表明，D-葡萄糖而非D-果糖能促进粘塑性凝胶结构的形成。凝胶强度是葡萄糖浓度、血红蛋白浓度和温度的函数。各种糖类促进凝胶形成的能力与其溶液性质相关。凝胶结构的存在减少了钾离子和血红蛋白从其膜被γ射线部分破坏的红细胞中的泄漏。在葡萄糖存在下渗透肿胀的减少也是由于凝胶形成，因为在重新封闭的红细胞血影中葡萄糖的作用消失了。D-果糖不能保护红细胞免受辐射损伤；其在渗透应激下增加红细胞稳定性的作用模式是一种膜效应。使用库尔特计数器进行的细胞大小测定表明，果糖而非葡萄糖能增加溶血时的最大体积。在50 mM时，D-果糖使红细胞血影体积增加11.2%；这代表膜面积增加7.2%。果糖引起的血影膨胀依赖于果糖浓度（0-100 mM），并且对温度变化（0-37℃）不敏感。
