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Microvesicle release and micellar attack as the alternative mechanisms involved in the red-blood-cell-membrane solubilization induced by arginine-based surfactants

机译:微囊泡释放和胶束攻击是基于精氨酸的表面活性剂诱导的红细胞膜溶解的替代机制

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Two novel arginine-based surfactants, Bz-Arg-NHC10 and Bz-Arg-NHC12, were characterized with respect to surface properties and their interaction with human red-blood-cell (HRBC) membranes. The values for critical micellar concentration (CMC), the maximum surfactant adsorption at the air–liquid interface, and the area per molecule indicated better surface properties for Bz-Arg-NHC12. The observation of cylindrical worm-like aggregates of Bz-Arg-NHCn via atomic-force microscopy supported the predictions based on the value of the surfactant-packing parameter (SPP). Erythrocyte-membrane solubilization was effected by surfactant aggregates since cell lysis became evident at only surfactant concentrations above the CMC. Changes in HRBC shape observed at different surfactant concentrations led to the conclusion that a slow mechanism based on the insertion of surfactant monomers into the HRBC membrane, followed by a shedding of microvesicles was responsible for the hemolysis produced by both surfactants at the lower concentrations tested. In contrast, the extraction of membrane lipids upon collisions between HRBCs and surfactant aggregates competes with and prevents microvesicle release at the higher concentrations assayed.
机译:两种基于精氨酸的新型表面活性剂分别为Bz-Arg-NHC 10 和Bz-Arg-NHC 12 在表面特性及其与人红细胞(HRBC)膜的相互作用方面进行了表征。临界胶束浓度(CMC),表面活性剂在气液界面的最大吸附量以及每分子面积的值表明Bz-Arg-NHC 12 。通过原子力显微镜观察Bz-Arg-NHC n 的圆柱蠕虫状聚集体基于表面活性剂填充参数(SPP)值的预测。由于仅在高于CMC的表面活性剂浓度下细胞裂解才变得明显,因此表面活性剂聚集体影响红细胞膜的溶解。在不同的表面活性剂浓度下观察到的HRBC形状变化得出这样的结论:在较低的测试浓度下,两种表面活性剂产生的溶血是基于将表面活性剂单体插入HRBC膜的缓慢机制,随后脱落的微泡。相反,HRBC与表面活性剂聚集体发生碰撞时,膜脂质的提取会与较高浓度的竞争性竞争,并阻止微囊泡的释放。

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