Clark V L, Young F E
Antimicrob Agents Chemother. 1977 May;11(5):871-6. doi: 10.1128/AAC.11.5.871.
Resistance to d-cycloserine could be induced in Bacillus subtilis 168 by sublethal concentrations of d-cycloserine. Sensitivity to the antibiotic could be regained by growth in the absence of d-cycloserine. The bactericidal activity of d-cycloserine apparently was not altered by resistant cells, and peptidoglycan synthesis was still inhibited by d-cycloserine in resistant cells. The d-cycloserine resistance apparently resulted from a decreased uptake of the antibiotic. The decrease in d-cycloserine transport could be prevented by simultaneous treatment of the cells with rifampin and d-cycloserine. d-Cycloserine was transported by the same system as glycine in B. subtilis. d-Cycloserine was able to exchange for intracellular glycine in both sensitive and resistant cells, suggesting that d-cycloserine is not excluded from the cell in resistant cultures.
在枯草芽孢杆菌168中，亚致死浓度的d-环丝氨酸可诱导其产生对d-环丝氨酸的抗性。在无d-环丝氨酸的条件下生长，对抗生素的敏感性可恢复。d-环丝氨酸的杀菌活性显然未被抗性细胞改变，且在抗性细胞中d-环丝氨酸仍能抑制肽聚糖合成。d-环丝氨酸抗性显然是由于抗生素摄取减少所致。同时用利福平和d-环丝氨酸处理细胞可防止d-环丝氨酸转运的减少。在枯草芽孢杆菌中，d-环丝氨酸与甘氨酸通过同一系统转运。d-环丝氨酸能够在敏感细胞和抗性细胞中与细胞内的甘氨酸进行交换，这表明在抗性培养物中d-环丝氨酸不会被细胞排除在外。
