Nash G B, Meiselman H J
Biophys J. 1983 Jul;43(1):63-73. doi: 10.1016/S0006-3495(83)84324-0.
To assess the influence of intracellular hemoglobin concentration on red cell viscoelasticity and to better understand changes related to in vivo aging, membrane shear elastic moduli (mu) and time constants for cell shape recovery (tc) were measured for age-fractionated human erythrocytes and derived ghosts. Time constants were also measured for osmotically shrunk cell fractions. Young and old cells had equal mu, but tc was longer for older cells. When young cells were shrunk to equal the volume (and hence hemoglobin concentration and internal viscosity) of old cells, tc increased only slightly. Thus membrane viscosity (eta = mu . tc) increases during aging, regardless of increased internal viscosity. However, further shrinkage of young cells, or slight shrinkage of old cells, caused a sharp increase in tc. Because this increased tc is not explainable by elevated internal viscosity, eta increased, possibly due to a concentration-dependent hemoglobin-membrane interaction. Ghosts had a greater mu than intact cells, with proportionally faster tc; their membrane viscosity was therefore similar to intact cells. However, the ratio of old/young membrane viscosity was less for ghosts than for intact cells, indicating that differences between young and old cell eta may be partly explained by altered hemoglobin-membrane interaction during aging. It is postulated that these changes in viscoelastic behavior influence in vivo survival of senescent cells.
为评估细胞内血红蛋白浓度对红细胞粘弹性的影响,并更好地理解与体内衰老相关的变化,对按年龄分级的人红细胞及其衍生的空壳测量了膜剪切弹性模量(μ)和细胞形状恢复的时间常数(tc)。还测量了渗透性收缩细胞组分的时间常数。年轻细胞和衰老细胞的μ相等,但衰老细胞的tc更长。当年轻细胞收缩至与衰老细胞体积相同(从而血红蛋白浓度和内部粘度相同)时,tc仅略有增加。因此,无论内部粘度增加与否,衰老过程中膜粘度(η = μ·tc)都会增加。然而,年轻细胞的进一步收缩或衰老细胞的轻微收缩会导致tc急剧增加。由于这种增加的tc无法用升高的内部粘度来解释,η增加,可能是由于浓度依赖性的血红蛋白-膜相互作用。空壳的μ比完整细胞大,tc相应更快;因此它们的膜粘度与完整细胞相似。然而,空壳的衰老/年轻膜粘度比低于完整细胞,这表明年轻细胞和衰老细胞η之间的差异可能部分由衰老过程中血红蛋白-膜相互作用的改变所解释。据推测,这些粘弹性行为的变化会影响衰老细胞在体内的存活。