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海葵毒素II对冠状动脉平滑肌膜流动性的影响。

Influence of equinatoxin II on coronary smooth muscle membrane fluidity.

作者信息

Sentjurc M, Stalc A, Suput D

机构信息

Institute J. Stefan, Ljubljana, Slovenia.

出版信息

Pflugers Arch. 1996;431(6 Suppl 2):R317-8. doi: 10.1007/BF02346396.

Abstract

Equinatoxin II forms pores in artificial as well as in natural phospholipid bylayers. As it also reduces the perfusion through the coronary arteries it seemed reasonable to investigate the interaction of this protein with the plasmalemma of the vascular smooth muscle cells more directly with the patch-clamp method and with EPR using the spin probe methyl ester of 5-doxylpalmitate. In the EPR spectra at least three regions in the membranes were identified with different membrane fluidity. Application of 0.1 microM or 1 microM equinatoxin II increases the portion with the lower membrane fluidity, and irreversibly increases the unspecific membrane conductance. This is compatible with the view that equinatoxin II forms pores in the membrane bilayer.

摘要

海葵毒素II可在人工磷脂双分子层以及天然磷脂双分子层中形成孔道。由于它还会降低冠状动脉的灌注,因此,采用膜片钳技术并使用自旋探针5-二氧棕榈酸甲酯通过电子顺磁共振(EPR)更直接地研究这种蛋白质与血管平滑肌细胞质膜之间的相互作用似乎是合理的。在EPR光谱中,至少在膜中鉴定出了三个具有不同膜流动性的区域。施加0.1微摩尔或1微摩尔的海葵毒素II会增加膜流动性较低部分的比例,并不可逆地增加非特异性膜电导。这与海葵毒素II在膜双层中形成孔道的观点相符。

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