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[德尔卑沙门氏菌细胞对链霉素的耐药机制]

[Mechanisms of resistance of Salmonella derby cells to streptomycin].

作者信息

Ktsoian Zh A, Taisova A S, Sarkisian N N, Khanbekian L M, Karapetian V E

出版信息

Antibiot Khimioter. 1988 Oct;33(10):760-3.

PMID:3214210
Abstract

Mechanisms of high streptomycin resistance (8000 micrograms/ml) in S. derby cells carrying R plasmids were studied. The cells were isolated from clinical materials. The findings showed that the streptomycin resistance determinant in the S. derby cells was localized on the plasmid. In cell-free extracts of the strains, there was detected no inactivation of aminoglycosides by phosphorylation, adenylation and acetylation of the antibiotic molecules. The plasmid elimination from the cells of S. derby K89 by ethidium bromide resulted in loosing of streptomycin resistance by the cells. This indirectly excluded the mechanism associated with modification of the ribosomes. Streptomycin resistance in the strains studied must be due to decreased permeability of the S. derby K89 cell envelopes for streptomycin.

摘要

对携带R质粒的德尔卑沙门氏菌细胞中高链霉素抗性(8000微克/毫升)的机制进行了研究。这些细胞是从临床材料中分离出来的。研究结果表明,德尔卑沙门氏菌细胞中的链霉素抗性决定簇位于质粒上。在这些菌株的无细胞提取物中,未检测到抗生素分子通过磷酸化、腺苷化和乙酰化作用使氨基糖苷类失活。用溴化乙锭从德尔卑沙门氏菌K89细胞中消除质粒导致细胞失去链霉素抗性。这间接排除了与核糖体修饰相关的机制。所研究菌株中的链霉素抗性必定是由于德尔卑沙门氏菌K89细胞包膜对链霉素的通透性降低所致。

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