Kirschmann C, Davis B D
J Bacteriol. 1969 Apr;98(1):152-9. doi: 10.1128/jb.98.1.152-159.1969.
Antibiotics that interfere reversibly with various aspects of ribosomal function (chloramphenicol, tetracycline, erythromycin, and spectinomycin) are shown to antagonize, at barely inhibitory concentrations, the inhibitory effect of low concentrations of streptomycin (SM) on the growth of Escherichia coli. Paradoxically, these compounds can also replace SM in supporting the growth of conditionally SM-dependent mutants. Chloramphenicol produced about as much phenotypic suppression as SM in SM-sensitive strains, but less than that attainable with high concentrations of SM in resistant strains. The antagonism to SM inhibition and the phenotypic suppression appear to be specific for those growth inhibitors that act on the ribosome. Since inhibitors of the 50S subunit of the ribosome (chloramphenicol, erythromycin) are as active as inhibitors of the 30S subunit, it is suggested that phenotypic suppression by borderline concentrations of ribosome inhibitors does not necessarily depend on an alteration of the recognition region of the ribosome. Alternatively, partial inhibition of the ribosomes might change the environment in a way that would influence the frequency of misreading. Phenotypic suppression by a low concentration of SM as well as by chloramphenicol was found to depend on the presence of a trace of the required growth factor.
那些可逆地干扰核糖体功能各个方面的抗生素(氯霉素、四环素、红霉素和壮观霉素)显示,在几乎抑制浓度时,能拮抗低浓度链霉素(SM)对大肠杆菌生长的抑制作用。矛盾的是,这些化合物在支持条件性依赖SM的突变体生长方面也能替代SM。在对SM敏感的菌株中,氯霉素产生的表型抑制作用与SM大致相同,但在抗性菌株中,其产生的表型抑制作用小于高浓度SM所能达到的程度。对SM抑制作用的拮抗和表型抑制似乎对那些作用于核糖体的生长抑制剂具有特异性。由于核糖体50S亚基的抑制剂(氯霉素、红霉素)与30S亚基的抑制剂活性相同,因此有人提出,核糖体抑制剂的临界浓度产生的表型抑制不一定取决于核糖体识别区域的改变。或者,核糖体的部分抑制可能会以某种方式改变环境,从而影响错读频率。发现低浓度的SM以及氯霉素产生的表型抑制取决于微量所需生长因子的存在。