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本文在质子泵驱动膜融合模型的基础上,进一步研究了小鼠艾氏腹水癌细胞质膜质子转运活性驱动的质膜和脂质体的融合.结果表明:在对照条件下,艾氏腹水癌细胞可以利用内源底物引起质子跨膜转运,后者可以驱动细胞和脂质体的融合.CCCP和尼日利亚菌素对质膜质子转运活性的抑制率分别为69.0％和80.1％,同时膜融合程度亦分别降低了85.7％和90.4％,证明质膜质子转运活性是驱动膜融合的主要因素.与此同时,在CCCP和尼日利亚菌素的影响下,细胞膜表面电位由对照条件下的17.7mV分别升高为27.2mV和27.5mV,膜表面电荷密度由对照条件下的0.86μC/cm~2分别升高为1.37μC/cm~2和1.39μC/cm~2,提示质膜质子转运活性可能引起膜表面质子化,从而为质子泵驱动膜融合模型提供了另一个实验证据.
Based on the proton pump driving membrane fusion model, this study further investigated the plasma membrane and liposome fusion driven by the proton transport activity of Ehrlich ascites carcinoma cell. The results showed that Ehrlich ascites carcinoma cells under control conditions. The proton transmembrane transport can be induced by endogenous substrates, which can drive the fusion of cells and liposomes. The inhibitory rates of CCCP and nigericin on the proton membrane proton transport activity were 69.0% and 80.1%, respectively, and the extent of membrane fusion was also Respectively decreased by 85.7% and 90.4% respectively, proving that the proton transport activity of the plasma membrane is the main factor driving membrane fusion. At the same time, under the influence of CCCP and nigericin, the cell membrane surface potential was increased by 17.7mV under control conditions. For 27.2mV and 27.5mV, the surface charge density of the film was increased to 1.37μC/cm~2 and 1.39μC/cm~2, respectively, from 0.86μC/cm~2 under the control conditions, suggesting that proton transport activity of the plasma membrane may cause membrane surface Protonation provides another experimental evidence for the proton pump driven membrane fusion model.