Sedgwick E G, Bragg P D
Department of Biochemistry, University of British Columbia, Vancouver, Canada.
Biochim Biophys Acta. 1992 Jan 30;1099(1):51-6.
The mechanism of uptake of the fluorescent dye 2-(4-dimethylaminostyryl)-1-ethylpyridinium cation (DMP+) into cells and vesicles of the acrA strain AS-1 of Escherichia coli was examined. Uptake was energized by substrate oxidation and discharged by uncouplers. Uptake was enhanced by the presence of tetraphenylphosphonium cation, tetraphenylboron anion and tributyltin chloride, which may inhibit the efflux system for DMP+. Uptake was inhibited by 5-methoxyindole-2-carboxylic acid (MIC). By the use of ionophores with right-side-out vesicles loaded with monovalent cations it was shown that DMP+ uptake could be driven both by the establishment of a membrane potential across the vesicle membrane and by a H+/DMP+ antiport system. Attempts to demonstrate the latter mechanism in everted membrane vesicles were unsuccessful.
研究了荧光染料2-（4-二甲基氨基苯乙烯基）-1-乙基吡啶鎓阳离子（DMP +）进入大肠杆菌acrA菌株AS-1的细胞和囊泡的机制。摄取由底物氧化提供能量，并由解偶联剂释放。四苯基鏻阳离子、四苯基硼阴离子和三丁基氯化锡的存在增强了摄取，它们可能抑制DMP +的外排系统。摄取受到5-甲氧基吲哚-2-羧酸（MIC）的抑制。通过使用装载单价阳离子的外翻囊泡的离子载体表明，DMP +摄取可以由跨囊泡膜的膜电位的建立和H + / DMP +反向转运系统驱动。在翻转膜囊泡中证明后一种机制的尝试未成功。
