Takayama K, Kilburn J O
Mycobacteriology Research Laboratory, William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin 53705.
Antimicrob Agents Chemother. 1989 Sep;33(9):1493-9. doi: 10.1128/AAC.33.9.1493.
Ethambutol at 3.0 micrograms/ml inhibited the transfer of label from D-[14C]glucose into the D-arabinose residue of arabinogalactan in whole cells of a drug-susceptible strain of Mycobacterium smegmatis. This inhibition began almost immediately after exposure of the cells to the drug. When drug-resistant M. smegmatis was used in a similar experiment, no such drug inhibition was detected. A much higher concentration of ethambutol (greater than 50 micrograms/ml) was required to show this inhibition. The drug also inhibited synthesis of arabinose-containing oligosaccharides when a cell-free enzyme system was used. These results suggest that the site of action of ethambutol is somewhere on the pathway between the conversion of D-glucose to D-arabinose and the transfer of arabinose into arabinogalactan. The primary mode of action of ethambutol appears to be inhibition of arabinogalactan synthesis.
在3.0微克/毫升浓度下，乙胺丁醇抑制了放射性标记从D-[14C]葡萄糖转移至耻垢分枝杆菌药物敏感株全细胞中阿拉伯半乳聚糖的D-阿拉伯糖残基。这种抑制作用在细胞接触药物后几乎立即开始。当在类似实验中使用耐药性耻垢分枝杆菌时，未检测到这种药物抑制作用。需要更高浓度的乙胺丁醇（大于50微克/毫升）才能显示出这种抑制作用。当使用无细胞酶系统时，该药物也抑制含阿拉伯糖寡糖的合成。这些结果表明，乙胺丁醇的作用位点位于D-葡萄糖转化为D-阿拉伯糖以及阿拉伯糖转移至阿拉伯半乳聚糖的途径中的某个位置。乙胺丁醇的主要作用方式似乎是抑制阿拉伯半乳聚糖的合成。
