RADIATION INACTIVATION OF ION CHANNELS FORMED BY GRAMICIDIN-A - PROTECTION BY LIPID DOUBLE-BONDS AND BY ALPHA-TOCOPHEROL
RADIATION INACTIVATION OF ION CHANNELS FORMED BY GRAMICIDIN-A - PROTECTION BY LIPID DOUBLE-BONDS AND BY ALPHA-TOCOPHEROL
复制标题
DOI：
10.1016/0005-2736(91)90249-8
复制
发表时间：
1991-07-01
期刊：
影响因子：
--
通讯作者：
STARK, G
中科院分区：
文献类型：
--
作者：
BARTH, C;STARK, G
在脂质膜中由通道形成肽短杆菌肽A诱导的电导在膜及其水性环境暴露于电离辐射时降低许多数量级。这是水辐解的自由基与短杆菌肽A的色氨酸残基相互作用的结果。在维生素E或高度不饱和脂质的存在下，离子通道对辐射的敏感性大大降低。发现D37剂量的增加高达50倍。通过自由基（如OH）的有效浓度的减少解释了这种现象。通过与不饱和脂肪酸残基或与维生素E反应在膜中。
The conductance induced by the channel-forming peptide gramicidin A in lipid membranes is reduced by many orders of magnitude on exposure of the membrane and its aqueous environment to ionizing radiation. This results from an interaction of free radicals of water radiolysis with the tryptophan residues of gramicidin A. The sensitivity of the ion channels towards irradiation is strongly reduced in the presence of either vitamin E or of highly unsaturated lipids. An increase of the D37 dose up to a factor of 50 was found. The phenomena are interpreted via a reduction of the effective concentration of free radicals (such as OH.) in the membrane by reaction with unsaturated fatty acid residues or with vitamin E.