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首页> 外文期刊>Chinese science bulletin >Transmembrane proton translocation decreases hydrophilicity of plasma membrane surface in Ehrlich ascites cells
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Transmembrane proton translocation decreases hydrophilicity of plasma membrane surface in Ehrlich ascites cells

机译：跨膜质子移位降低了艾氏腹水细胞质膜表面的亲水性

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We reported previously that proton pumping activities of different biological membrane systems could induce membrane fusion of biological membranes with liposomes and that the proton pumping activity of the respiratory chain initiated by succinate oxidation in mitochondria could decrease 0.6 pH units on the mitochondrial outer membrane surface. On these bases, a hypothetical model for proton pumping inducing membrane fusion was proposed by Liu. This model emphasizes that the mechanism of membrane fusion induced by proton pumping was mainly due to the membrane surface protonation, which may serve as a driving force to break the hydrogen bond between water molecules in the membrane surface hydration layer and the polar head of phospholipids, resultingin occurrence of local and transient dehydration of the membrane surface, Dehydration at the contact site between two opposite membranes resulted in both membranes' tight contact and membrane fusion, Recently, we presented further experimental evidenceto show that proton translocation of Ehrlich ascites cells could induce the membrane surface protonation leading to membrane fusion and that proton pumping of rat liver mitochondria could decrease the dielectric constant on the membrane surface and the hydrophilicity of the mitoplast surface. In this note, it will be shown that the protonation of the plasma membrane surface of Ehrlich ascites cell could decrease the hydrophilicity of the membrane surface through observing the relationship between the dielectric constant of the membrane surface and the transmembrane proton translocation by using a fluorescent probe (DPE) labelling the cell membrane surface. The results obtained are considered as new evidence for supporting the hypothetical model of proton pumping inducing membrane fusion.
机译：我们以前曾报道过，不同生物膜系统的质子泵送活性可以诱导生物膜与脂质体的膜融合，并且线粒体中琥珀酸氧化引发的呼吸链的质子泵送活性可以降低线粒体外膜表面上的0.6 pH单位。在这些基础上，Liu提出了质子泵诱导膜融合的假设模型。该模型强调质子泵激引起的膜融合机制主要是由于膜表面质子化，它可能是破坏膜表面水化层中水分子与磷脂极性头之间氢键的驱动力，导致膜表面发生局部和瞬时脱水，两个相对膜之间的接触位点处的脱水导致膜的紧密接触和膜融合。最近，我们提供了进一步的实验证据，以证明Ehrlich腹水细胞的质子易位可以诱导膜表面质子化导致膜融合，并且大鼠肝线粒体的质子泵送可降低膜表面的介电常数和线粒体表面的亲水性。在此说明中，将显示出通过使用荧光探针观察膜表面介电常数与跨膜质子移位之间的关系，Ehrlich腹水细胞质膜表面的质子化可降低膜表面的亲水性。 （DPE）标记细胞膜表面。所获得的结果被认为是支持质子泵诱导膜融合的假设模型的新证据。

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