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[微生物对抗生素耐药性的遗传和生化基础]

[Genetic and biochemical basis of microbial resistance to antibiotics].

作者信息

Popović M, Delić V

机构信息

Zavod za molekularnu biologiju.

出版信息

Lijec Vjesn. 1990 Jul-Aug;112(7-8):250-7.

PMID:2292900
Abstract

Antibiotics affect different structures or metabolic processes in a bacterial cell inhibiting its growth and reproduction what results in the destruction of microorganisms. Microorganisms have developed some resistance mechanisms in order to survive in the presence of antibiotics. Recent advances in molecular biology of microorganisms Recent advances in molecular biology of microorganisms and technique of recombinant DNA have helped us to understand more clearly the molecular aspects of resistance of microorganisms against antibiotics. Some of the mechanisms of drug resistance include: change of the binding site of the antibiotic due to the mutation of genes being responsible for the synthesis of the target sites of the antibiotic (aminoglycosides, chloramphenicol, beta-lactams); change of the binding site of the antibiotic by the activity of methylase (macrolides); diminished patency of the cell membrane for the antibiotic (tetracyclines, chloramphenicol, macrolides, aminoglycosides); active transport of the antibiotic outside the cell (tetracyclines); synthesis of specific enzymes modifying and thus inactivating the molecule of the antibiotic (aminoglycosides, chloramphenicol); tolerance of microorganisms to the activity of the antibiotic (beta-lactams); inactivation of the antibiotic molecule by the enzymes such as beta-lactamase for the beta-lactam antibiotic and by esterase for the antibiotic with a lactone ring (macrolides).

摘要

抗生素作用于细菌细胞内不同的结构或代谢过程,抑制其生长和繁殖,从而导致微生物的死亡。微生物为了在抗生素存在的情况下存活,已经进化出了一些耐药机制。微生物分子生物学的最新进展 微生物分子生物学和重组DNA技术的最新进展,帮助我们更清楚地了解微生物对抗生素耐药性的分子机制。一些耐药机制包括:由于负责抗生素靶位点合成的基因突变,导致抗生素结合位点改变(氨基糖苷类、氯霉素、β-内酰胺类);通过甲基化酶的作用改变抗生素结合位点(大环内酯类);细胞膜对抗生素的通透性降低(四环素类、氯霉素、大环内酯类、氨基糖苷类);抗生素主动转运出细胞(四环素类);合成特定酶修饰并使抗生素分子失活(氨基糖苷类、氯霉素);微生物对抗生素活性产生耐受性(β-内酰胺类);β-内酰胺酶使β-内酰胺类抗生素分子失活,酯酶使含内酯环的抗生素(大环内酯类)分子失活。

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