Tipper D J
Department of Microbiology, University of Massachusetts Medical School, Worcester 01604.
Rev Infect Dis. 1979 Jan-Feb;1(1):39-54. doi: 10.1093/clinids/1.1.39.
Biochemical investigations of the mode of action of beta-lactam antibiotics have focused on the interaction of these drugs with sensitive enzymes and penicillin-binding proteins in vitro and on the correlation of these data with physiological responses to the drugs. The classical response is inhibition of growth and cell death followed by lysis; however, the bacteriostatic response to penicillins, which is seen in certain bacterial species such as Streptococcus mutans and in mutants of species such as Streptococcus pneumoniae, is also described. The biochemical data remain consistent with the acyl-D-alanyl-D-alanine donor substrate analogue theory, but multiple targets with differential sensitivity to different beta-lactam antibiotics exist. The relationship of these targets to penicillin-binding proteins and their possible functions in cell growth and division are discussed.
β-内酰胺类抗生素作用模式的生化研究主要集中在这些药物与敏感酶及青霉素结合蛋白在体外的相互作用,以及这些数据与药物生理反应的相关性。经典反应是生长抑制、细胞死亡随后裂解;然而,也描述了某些细菌物种(如变形链球菌)以及肺炎链球菌等物种的突变体中对青霉素的抑菌反应。生化数据与酰基-D-丙氨酰-D-丙氨酸供体底物类似物理论仍然一致,但存在对不同β-内酰胺类抗生素敏感性不同的多个靶点。讨论了这些靶点与青霉素结合蛋白的关系及其在细胞生长和分裂中的可能功能。