Burt H M, Jackson J K, Wu W
Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
Scanning Microsc. 1991 Mar;5(1):273-9; discussion 279-80.
Studies of the interactions of monosodium urate monohydrate (MSUM) crystals and calcium pyrophosphate dihydrate triclinic (CPPD) crystals with biomembranes have been reviewed. Crystal-membrane binding and crystal-induced membranolysis have been studied using human erythrocytes as a model membrane system. The extent of MSUM-membrane binding was determined by incorporating a hydrophobic, fluorescent probe into the membranes, centrifugation to separate free membranes from membranes with bound crystals and quantitation of free membranes by measuring the total fluorescence intensity. The ability of MSUM and CPPD to hemolyse red cells was used as a measure of the membranolytic potential of the crystals. Fluorescence polarization studies showed that MSUM-membrane binding resulted in fluidization of the membrane. Cross-linking of the membrane proteins of the erythrocyte or the presence of divalent cations in the incubation medium inhibited MSUM induced hemolysis. These findings were explained by hypothesizing a "pore" model mechanism for MSUM induced membranolysis as follows. Binding of crystals to membranes induces the redistribution of transmembrane proteins into clusters or aggregates leading to "pore" formation. The "pores" permit the leakage of low molecular weight soluble compounds and ions acoss the membrane which is followed by osmotic rupture of the membrane.
关于一水合尿酸钠（MSUM）晶体和三斜二水焦磷酸钙（CPPD）晶体与生物膜相互作用的研究已有综述。利用人红细胞作为模型膜系统，对晶体 - 膜结合及晶体诱导的膜溶解进行了研究。通过将疏水性荧光探针掺入膜中、离心分离游离膜与结合晶体的膜，并通过测量总荧光强度对游离膜进行定量，来确定MSUM与膜的结合程度。将MSUM和CPPD使红细胞溶血的能力用作晶体膜溶解潜能的指标。荧光偏振研究表明，MSUM与膜的结合导致膜的流动性增加。红细胞膜蛋白的交联或孵育介质中存在二价阳离子会抑制MSUM诱导的溶血。通过假设MSUM诱导膜溶解的“孔”模型机制来解释这些发现，具体如下。晶体与膜的结合诱导跨膜蛋白重新分布形成簇或聚集体，从而导致“孔”的形成。“孔”允许低分子量可溶性化合物和离子跨膜泄漏，随后膜发生渗透破裂。
