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[细菌通过分子靶点改变或通透性降低获得抗生素耐药性]

[Acquisition of antibiotic-resistance in bacteria by alteration of molecular target, or by the decreased permeability].

作者信息

Hashimoto H

机构信息

Kitasato Institute.

出版信息

Nihon Rinsho. 1997 May;55(5):1167-72.

PMID:9155170
Abstract

The target of an antibiotic is any essential enzyme for bacterial growth and quantitative or qualitative alteration of the enzyme or its substrate may cause resistance to the drug. Thus, the alteration of DNA gyrase and/or topoisomerase IV may result in resistance to fluoloquinolones, and alteration of beta-subunit of RNA polymerase may cause rifampicin-resistance. The cell wall synthesizing enzymes which cross-bridge peptidoglycan units are called PBPs and their alteration cause resistance to beta-lactams, and the alteration of the substrate D ala-D ala to D ala-D lactate causes vancomycin-resistance. In other drug-resistances, various instances of alteration of enzymes are known. Drug-resistances are also brought about by decreased permeability of the drug. Some instances are described.

摘要

抗生素的作用靶点是细菌生长所必需的任何一种酶,酶或其底物的定量或定性改变可能导致对该药物产生耐药性。因此,DNA旋转酶和/或拓扑异构酶IV的改变可能导致对氟喹诺酮类药物耐药,RNA聚合酶β亚基的改变可能导致对利福平耐药。连接肽聚糖单位的细胞壁合成酶称为青霉素结合蛋白(PBPs),其改变会导致对β-内酰胺类药物耐药,底物D丙氨酰-D丙氨酸变为D丙氨酰-D乳酸会导致对万古霉素耐药。在其他耐药情况中,已知有多种酶改变的实例。耐药性也可由药物通透性降低引起。现描述一些实例。

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