Zhelev D V
Department of Mechanical Engineering and Materials Science, Duke University, Durham, North Carolina 27708-0300, USA.
Biophys J. 1996 Jul;71(1):257-73. doi: 10.1016/S0006-3495(96)79222-6.
In a previous paper we described the experiments and the framework of a model for the exchange of monooleoylphosphatidylcholine with a single egg phosphatidylcholine membrane. In the present paper a model is presented that relates the experimentally measured apparent characteristics of the overall kinetics of lysolipid exchange to the true rates of lysolipid exchange and interbilayer transfer. It is shown that the adsorption of the lysolipid follows two pathways: one through the adsorption of lipid monomers and other through the fusion of micelles. The desorption of lysolipid follows a single pathway, namely, the desorption of monomers. The overall rate of fast desorption under convective flow conditions gives the true rate of monomer desorption from the outer membrane monolayer. The overall rate of both slow lysolipid uptake and slow desorption gives the rate of interbilayer transfer. Because of the uneven distribution of lysolipid between the two monolayers during its uptake, one of the membrane monolayers is apparently extended relative to the other. This relative extension of one of the monolayers induces a monolayer tension. The induced monolayer tension can increase up to 7 mN.m-1, when most of the intercalated lysolipid only partitions into the monolayer facing the lysolipid solution. This value is similar to the measured value for the critical monolayer tension of membrane failure, which is on the order of 5 mN.m-1. The similarity of the magnitudes of the induced monolayer tension during monooleoylphosphatidylcholine exchange and the monolayer tension of membrane failure suggests that the interbilayer lipid transfer may be affected by the formation of short living membrane defects. Furthermore, the pH-induced interbilayer exchange of phosphatidylglycerol is considered. In this case, it is shown that the rate of interbilayer transfer is a function of the phosphatidylglycerol concentration in the membrane.
在之前的一篇论文中,我们描述了单油酰磷脂酰胆碱与单个卵磷脂酰胆碱膜交换的实验及模型框架。在本文中,我们提出了一个模型,该模型将实验测量的溶血磷脂交换总体动力学的表观特征与溶血磷脂交换及双层间转移的真实速率联系起来。结果表明,溶血磷脂的吸附遵循两条途径:一条是通过脂质单体的吸附,另一条是通过胶束的融合。溶血磷脂的解吸遵循单一途径,即单体的解吸。对流条件下快速解吸的总体速率给出了单体从外膜单层解吸的真实速率。缓慢的溶血磷脂摄取和缓慢解吸的总体速率给出了双层间转移的速率。由于溶血磷脂摄取过程中在两个单层之间分布不均,其中一个膜单层相对于另一个明显伸展。一个单层的这种相对伸展会诱导单层张力。当大多数插入的溶血磷脂仅分配到面向溶血磷脂溶液的单层中时,诱导的单层张力可增加至7 mN·m-1。该值与测得的膜破坏临界单层张力值相似,约为5 mN·m-1。单油酰磷脂酰胆碱交换过程中诱导的单层张力大小与膜破坏的单层张力大小相似,这表明双层间脂质转移可能受短寿命膜缺陷形成的影响。此外,还考虑了pH诱导的磷脂酰甘油双层间交换。在这种情况下,结果表明双层间转移速率是膜中磷脂酰甘油浓度的函数。