Reinicke B, Blümel P, Labischinski H, Giesbrecht P
Arch Microbiol. 1985 May;141(4):309-14. doi: 10.1007/BF00428842.
In contrast to what has been postulated, penicillin G at its optimal lytic concentration of 0.1 microgram per ml did not lead to a detectable activation of autolytic wall processes in staphylococci in terms of the release of uniformly labelled wall fragments from cells pretreated with the drug for 1 h. Rather a considerable inhibition of this release was observed. A similarly profound inhibition of the release of peptidoglycan fragments occurred when staphylococci pretreated for 1 h with 0.1 microgram penicillin per ml acted as a source of crude autolysins on peptidoglycan isolated from labelled normal cells of the same strain. This clearly demonstrated that the overall inhibition of autolytic wall processes caused by penicillin was mainly due to a decreased total autolysin action rather than to an altered wall structure. Furthermore, no substantial penicillin-induced inhibition of the incorporation of 14C-N-acetylglucosamine into the staphylococcal wall could be observed before bacteriolysis started, i.e., approximately during the first 80 min of penicillin action. These results are not consistent with any of the models hitherto proposed for the action of penicillin.
与所假设的情况相反，青霉素G在其每毫升0.1微克的最佳溶菌浓度下，就从用该药物预处理1小时的细胞中释放均匀标记的细胞壁片段而言，并未导致葡萄球菌中自溶细胞壁过程的可检测激活。相反，观察到这种释放受到了相当大的抑制。当每毫升用0.1微克青霉素预处理1小时的葡萄球菌作为从同一菌株的标记正常细胞中分离的肽聚糖上的粗制自溶素来源时，肽聚糖片段的释放也出现了类似的深度抑制。这清楚地表明，青霉素对自溶细胞壁过程的总体抑制主要是由于总自溶素作用的降低，而不是由于细胞壁结构的改变。此外，在细菌溶解开始之前，即在青霉素作用的大约前80分钟内，未观察到青霉素对14C-N-乙酰葡糖胺掺入葡萄球菌细胞壁的实质性抑制。这些结果与迄今为止提出的任何青霉素作用模型均不一致。
