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亚致死浓度的氯霉素对酶合成的刺激作用并非由核糖核苷酸池介导。

Stimulation of enzyme synthesis by sublethal concentrations of chloramphenicol is not mediated by ribonucleotide pools.

作者信息

Ford S R, Switzer R L

出版信息

Antimicrob Agents Chemother. 1975 May;7(5):564-70. doi: 10.1128/AAC.7.5.564.

Abstract

Growth of Salmonella typhimurium LT-2 strain pyrA81 in minimal medium containing 0.8 mug of chloramphenicol (CAP) per ml resulted in a 50 to 100% increase in the steady-state nucleotide pools in the cells. When such a culture was starved for uracil, the pyrimidine nucleotide pools decayed much more slowly in CAP-treated cells than in controls. An attempt was made to determine whether this effect of CAP on nucleotide pools could account for enhanced enzyme derepression observed under the same conditions (8). Treatment with low levels of puromycin also resulted in elevation of nucleotide pools but did not lead to enhanced enzyme synthesis. CAP treatment during arginine starvation has been shown to enhance enzyme synthesis, but nucleotide pools were not significantly affected by CAP nor was the stringent response relieved under these conditions. Thus, the effects of CAP on enzyme synthesis cannot be the result of effects of the antibiotic on nucleotide pools in all cases. The elevation of nucleotide pools was shown not to be due to enhanced conversion of exogeneous uracil into nucleotides, but to result from the enhanced turnover of ribonucleic acid in CAP-treated cells.

摘要

鼠伤寒沙门氏菌LT - 2菌株pyrA81在每毫升含有0.8微克氯霉素(CAP)的基本培养基中生长,导致细胞内稳态核苷酸池增加50%至100%。当这样的培养物缺乏尿嘧啶时,与对照相比,经CAP处理的细胞中嘧啶核苷酸池的衰减要慢得多。人们试图确定CAP对核苷酸池的这种作用是否可以解释在相同条件下观察到的增强的酶去阻遏现象(8)。用低水平的嘌呤霉素处理也导致核苷酸池升高,但并未导致酶合成增强。已表明在精氨酸饥饿期间用CAP处理可增强酶合成,但在这些条件下CAP对核苷酸池没有显著影响,也没有解除严格反应。因此,在所有情况下,CAP对酶合成的作用不可能是抗生素对核苷酸池作用的结果。核苷酸池的升高并非由于外源尿嘧啶向核苷酸的转化增强,而是由于经CAP处理的细胞中核糖核酸周转增强所致。

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