Hof D, Fox J M
J Membr Biol. 1984;79(1):1-6. doi: 10.1007/BF01868521.
The modification of the ultraviolet blocking of sodium channels and of the ultraviolet-induced potential shift of the gating parameters by means of the sulfhydryl compounds l-cysteine and 2-mercaptoethanol was investigated in the node of Ranvier under voltage-clamp conditions. The UV wavelength was 280 nm. The radiation-induced potential shift of the voltage-dependent gating parameters was prevented or even reversed by the action of the sulfhydryl compounds (internal application), while the blocking effect was not affected. It is concluded that the two radiation effects are caused by two separate photoreactions. Internally applied N-ethylmaleimide, binding specifically to protein-SH groups, exhibits an effect similar to the ultraviolet-induced potential shift, without affecting the maximum sodium permeability. Therefore, the ultraviolet-induced potential shift might be caused by a photocatalyzed oxidation of -SH groups of membrane proteins changing the surface charge density at the inner side of the nodal membrane.
在电压钳制条件下，于郎飞结处研究了巯基化合物L-半胱氨酸和2-巯基乙醇对钠通道紫外线阻断作用以及紫外线诱导的门控参数电位变化的影响。紫外线波长为280nm。巯基化合物（内部应用）的作用可防止甚至逆转辐射诱导的电压依赖性门控参数的电位变化，而阻断作用不受影响。得出的结论是，这两种辐射效应是由两个独立的光反应引起的。内部应用的N-乙基马来酰亚胺特异性结合蛋白质-SH基团，表现出与紫外线诱导的电位变化类似的效应，而不影响最大钠通透性。因此，紫外线诱导的电位变化可能是由膜蛋白-SH基团的光催化氧化引起的，从而改变了结膜内侧的表面电荷密度。
