Clark M R, Mohandas N, Caggiano V, Shohet S B
J Supramol Struct. 1978;8(4):521-32. doi: 10.1002/jss.400080414.
We have studied the deformability of subpopulations of red cells from a patient with "desiccytosis," a disorder characterized by increased membrane permeability to potassium and associated with a probable increase in sodium-sodium exchange. Cells become increasingly dehydrated after maturation because of continued potassium loss without compensatory sodium gain, and they exhibit a progressive increase in mean cell hemoglobin concentration (MCHC). This increase in MCHC causes the cells to become underformable at shear stress values which result in extensive deformation of normal cells. Reduction of MCHC to approximately normal levels by suspending the cells in hypotonic medium restores normal deformability to all but 0.1--0.2% of the cells. These results suggest that the major factor leading to premature destruction in this disorder is whole cell rigidity conferred by increased intracellular hemoglobin concentrations, rather than any associated membrane rigidity.
我们研究了一名患有“干燥细胞症”患者红细胞亚群的变形能力。该病症的特征是细胞膜对钾的通透性增加,并可能伴有钠-钠交换增加。细胞成熟后,由于持续失钾而无代偿性钠摄入,会变得越来越脱水,并且平均细胞血红蛋白浓度(MCHC)会逐渐升高。MCHC的这种升高导致细胞在切应力值下变得不可变形,而该切应力值会使正常细胞发生广泛变形。通过将细胞悬浮在低渗介质中,将MCHC降低至大致正常水平,除了0.1%-0.2%的细胞外,其余细胞的正常变形能力得以恢复。这些结果表明,导致该病症中细胞过早破坏的主要因素是细胞内血红蛋白浓度增加所赋予的全细胞刚性,而非任何相关的膜刚性。