Mirelman D, Nuchamowitz Y
Eur J Biochem. 1979 Mar;94(2):549-56. doi: 10.1111/j.1432-1033.1979.tb12924.x.
The intrinsic effect of various beta-lactam antibiotics on the biosynthesis of peptidoglycan of Pseudomonas aeruginosa X-48 was investigated. Most of the cephalosporins and penicillins tested already at 0.5 microgram/ml strongly inhibited (a) the incorporation of nascent peptidoglycan into the detergent-insoluble fraction (greater than 75%), (b) the formation of peptide crosslinkages (greater than 60%) and (c) the activity of the DD-carboxypeptidase and partially that of the transpeptidase (approximately 90% and approximately 40% respectively). Another group of beta-lactum drugs did not inhibit incorporation into the material insoluble in sodium dodecylsulfate, the formation of peptide crosslinkages nor transpeptidase activity. They only partially inhibited the activity of the DD-carboxypeptidase--endopeptidase system (40--50% at 0.5 microgram/ml). The results obtained differ from those of Presslitz and Ray [Antimicrob, Agents Chemother. 7, 578--581 (1975)] and show some resemblance to the effects of beta-lactams on the biosynthesis of Escherichia coli peptidoglycan.
研究了各种β-内酰胺类抗生素对铜绿假单胞菌X-48肽聚糖生物合成的内在影响。所测试的大多数头孢菌素和青霉素在0.5微克/毫升时就已强烈抑制：(a)新生肽聚糖掺入去污剂不溶性部分（大于75%），(b)肽交联的形成（大于60%），以及(c)DD-羧肽酶的活性，并部分抑制转肽酶的活性（分别约为90%和约40%）。另一组β-内酰胺类药物不抑制掺入十二烷基硫酸钠不溶性物质、肽交联的形成或转肽酶活性。它们仅部分抑制DD-羧肽酶-内肽酶系统的活性（0.5微克/毫升时为40-50%）。所获得的结果与Presslitz和Ray的结果[《抗菌剂与化疗》7, 578-581(1975)]不同，并且与β-内酰胺类对大肠杆菌肽聚糖生物合成的影响有一些相似之处。
