Mehta B M, Gravelle M J, Kushner D J
Antimicrob Agents Chemother. 1973 Sep;4(3):332-6. doi: 10.1128/AAC.4.3.332.
Proflavine inhibited the aerobic and anaerobic utilization of glucose by sensitive but not by resistant Escherichia coli. In resistant cells that had bound proflavine, glucose utilization was accompanied by release of the dye. After glucose was used up, the cells could again take up proflavine. If the amount of proflavine bound to sensitive cells was too low to inhibit glucose utilization, adding glucose to these cells caused them to release the dye. With higher proflavine concentrations, inhibitory to glucose utilization, the dye remained cell bound. Thus, metabolic energy causes the release of proflavine by both sensitive and resistant cells. In the former, energy production is inhibited by proflavine, and thus the dye prevents its own release. Chloramphenicol did not interfere with metabolically induced release of proflavine from resistant cells. Cyanide inhibited the glycerol-induced loss of proflavine, but not the glucose-induced loss. Azide and carbonyl cyanide m-chlorophenylhydrazone could prevent proflavine release without inhibiting glucose utilization.
硫酸原黄素抑制敏感型大肠杆菌对葡萄糖的需氧和厌氧利用,但不抑制耐药型大肠杆菌。在已结合硫酸原黄素的耐药细胞中,葡萄糖利用伴随着染料的释放。葡萄糖耗尽后,细胞可再次摄取硫酸原黄素。如果与敏感细胞结合的硫酸原黄素量过低而无法抑制葡萄糖利用,向这些细胞中添加葡萄糖会导致它们释放染料。在较高的硫酸原黄素浓度下,对葡萄糖利用有抑制作用,染料仍与细胞结合。因此,代谢能量导致敏感细胞和耐药细胞释放硫酸原黄素。在前者中,能量产生被硫酸原黄素抑制,因此染料阻止自身释放。氯霉素不干扰耐药细胞中代谢诱导的硫酸原黄素释放。氰化物抑制甘油诱导的硫酸原黄素损失,但不抑制葡萄糖诱导的损失。叠氮化物和羰基氰化物间氯苯腙可在不抑制葡萄糖利用的情况下阻止硫酸原黄素释放。