呋喃唑酮引起的DNA损伤、原噬菌体诱导和突变。

DNA damage, prophage induction and mutation by furazolidone.

作者信息

Chatterjee S N, Banerjee S K, Pal A K, Basak J

出版信息

Chem Biol Interact. 1983 Aug 1;45(3):315-26. doi: 10.1016/0009-2797(83)90078-9.

Abstract

Ultraviolet absorption data and thermal chromatography through hydroxyapatite (HAP) column revealed that furazolidone treatment of Vibrio cholerae cells produced more than 80% of DNA reversibly bihelical due to the formation of interstrand cross-links and the reaction obeyed a first order relation. Sensitivities of the Escherichia coli strains to the lethal action of the drug were in the order: AB 2480(uvr- rec-) greater than AB 2463(rec-) greater than AB 1886(uvr-) greater than AB 1157(repair proficient) or AB 4401(wild type). Furazolidone was 'Rec test' positive, produced dose-dependent prophage induction in E. coli cells and also dose-dependent streptomycin-resistance forward mutation in V. cholerae cells. The quantitative aspect and also the mode of furazolidone action on DNA were discussed.

摘要

紫外吸收数据以及通过羟基磷灰石柱的热色谱分析表明，呋喃唑酮处理霍乱弧菌细胞会因链间交联的形成而使80%以上的DNA产生可逆双螺旋结构，且该反应符合一级反应关系。大肠杆菌菌株对该药物致死作用的敏感性顺序为：AB 2480（uvr- rec-）＞AB 2463（rec-）＞AB 1886（uvr-）＞AB 1157（修复 proficient）或AB 4401（野生型）。呋喃唑酮为“Rec测试”阳性，在大肠杆菌细胞中产生剂量依赖性的原噬菌体诱导作用，在霍乱弧菌细胞中也产生剂量依赖性的链霉素抗性正向突变。文中讨论了呋喃唑酮对DNA作用的定量方面以及作用方式。