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聚乙二醇对脂质体和红细胞的影响。通透性变化和膜融合。

Effects of poly(ethylene glycol) on liposomes and erythrocytes. Permeability changes and membrane fusion.

作者信息

Aldwinckle T J, Ahkong Q F, Bangham A D, Fisher D, Lucy J A

出版信息

Biochim Biophys Acta. 1982 Aug 12;689(3):548-60. doi: 10.1016/0005-2736(82)90313-3.

Abstract

Poly(ethylene glycol) 6000 induced a concentration-dependent, time-dependent decrease in the latency of the reaction between Arsenazo III sequestered in liposomes and extraliposomal Ca2+. This was mediated by a gross change in liposomal permeability, i.e. by a release of Arsenazo III from liposomes rather than simply by an entry of Ca2+. The loss of latency was strongly temperature-dependent, and it was markedly diminished on increasing the cholesterol content of the liposomes. It was apparently not due to an osmotic stress of the polymer. The high activation energy found (63 kJ . mol-1) is thought to indicate that the loss of latency resulted from local discontinuities in the lipid bilayers, caused by dehydration, rather than from partial or total lysis. Related microscopy experiments indicated that the polymer also caused the liposomes to fuse, and it is suggested that membrane fusion may have occurred at the sites of dehydration-induced discontinuities in adjacent bilayers. In addition, the polymer was found to enhance the permeability of hen erythrocytes of Ca2+ in a manner that was comparable to its effect on liposomal latency, and it is proposed that gel fusion induced by poly(ethylene glycol) may occur at the sites of similarly induced discontinuities in the phospholipid bilayers of two closely adjacent cells.

摘要

聚乙二醇6000诱导包封于脂质体中的偶氮胂III与脂质体外Ca2+之间反应的延迟时间呈浓度和时间依赖性降低。这是由脂质体通透性的总体变化介导的,即偶氮胂III从脂质体中释放出来,而不仅仅是Ca2+的进入。延迟时间的丧失强烈依赖于温度,并且随着脂质体胆固醇含量的增加而显著减少。这显然不是由于聚合物的渗透应激所致。所发现的高活化能(63 kJ·mol-1)被认为表明延迟时间的丧失是由脱水引起的脂质双层局部不连续所致,而不是由部分或完全裂解引起的。相关的显微镜实验表明,该聚合物还导致脂质体融合,并且有人提出膜融合可能发生在相邻双层中脱水诱导的不连续部位。此外,发现该聚合物以与其对脂质体延迟时间的影响相当的方式增强鸡红细胞对Ca2+的通透性,并且有人提出聚乙二醇诱导的凝胶融合可能发生在两个紧密相邻细胞的磷脂双层中类似诱导的不连续部位。

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