Winshell E, Shaw W V
J Bacteriol. 1969 Jun;98(3):1248-57. doi: 10.1128/jb.98.3.1248-1257.1969.
Plasmid-mediated chloramphenicol resistance in Staphylococcus aureus has been shown to involve acetylation of chloramphenicol by an enzyme induced by growth in the presence of the antibiotic and certain analogues. Analysis of the kinetics of induction has been complicated by (i) the intrinsic inhibitory effects of chloramphenicol on induced enzyme synthesis and (ii) the rapid disappearance of inducer after synthesis of the acetylating enzyme. The compound related to d-threo chloramphenicol which lacks a C(3) hydroxyl substituent (3-deoxychloramphenicol) is a potent inducer of chloramphenicol acetyltransferase but is ineffective as an antibiotic and is not a substrate for the enzyme. The availability of such a "gratuitous" inducer has simplified an analysis of the kinetics of induction of chloramphenicol acetyltransferase. The enzyme from induced bacteria has been purified to homogeneity and has been compared with the analogous enzyme present in E. coli which harbors a resistance transfer factor with the chloramphenicol resistance determinant.
已证明金黄色葡萄球菌中质粒介导的氯霉素抗性涉及一种酶对氯霉素的乙酰化作用，该酶由在抗生素及某些类似物存在下生长诱导产生。诱导动力学分析因以下情况而变得复杂：（i）氯霉素对诱导酶合成的内在抑制作用；（ii）乙酰化酶合成后诱导剂迅速消失。与缺乏C(3)羟基取代基的d-苏型氯霉素相关的化合物（3-脱氧氯霉素）是氯霉素乙酰转移酶的有效诱导剂，但作为抗生素无效，且不是该酶的底物。这种“ gratuitous”诱导剂的可得性简化了氯霉素乙酰转移酶诱导动力学的分析。来自诱导细菌的酶已纯化至同质，并与存在于携带氯霉素抗性决定簇的抗性转移因子的大肠杆菌中的类似酶进行了比较。
