Mukherjee U, Basak J, Chatterjee S N
Biophysics Division, Saha Institute of Nuclear Physics, Calcutta, India.
Cancer Biochem Biophys. 1990 Nov;11(4):275-87.
Nitrofurantoin inhibited growth and produced loss of viability of Vibrio cholerae cells in a dose-dependent manner, the 10% (D10) and 37% (D37) survival doses being 18.0 and 5.5 micrograms/ml x hr. respectively. The drug also caused filamentation of the cells in a very significant manner. Ultraviolet absorption data and thermal chromatography through hydroxyapatite column revealed that nitrofurantoin treatment of Vibrio cholerae cells produced a maximum amount of 55% of DNA reversibly bihelical due to the formation of inter-strand cross-links. Helix-coil transition studies carried out by viscometric and also, spectrophotometric methods revealed that the nitrofurantoin-induced cross-links in Vibrio cholerae DNA, imparted to this DNA greater thermal stability than that of native DNA. The quantitative aspect and also the mode of nitrofurantoin action on DNA of Vibrio cholerae and Escherichia coli cells vis-à-vis the carcinogenic potential of the drug were discussed.
呋喃妥因以剂量依赖方式抑制霍乱弧菌细胞生长并导致其活力丧失,10%(D10)和37%(D37)存活剂量分别为18.0和5.5微克/毫升×小时。该药物还非常显著地导致细胞丝状化。紫外吸收数据和通过羟基磷灰石柱的热色谱分析表明,用呋喃妥因处理霍乱弧菌细胞会因链间交联的形成而产生高达55%的可逆双螺旋DNA。通过粘度测定法和分光光度法进行的螺旋-线圈转变研究表明,呋喃妥因诱导的霍乱弧菌DNA交联赋予该DNA比天然DNA更高的热稳定性。文中讨论了呋喃妥因对霍乱弧菌和大肠杆菌细胞DNA作用的定量方面及其作用方式,以及该药物的致癌潜力。