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1.
IJPR-Iranian Journal of Pharmaceutical Research. 2013; 12 (4): 925-930
en Inglés | IMEMR | ID: emr-139873

RESUMEN

Mar A activates two membrane dependent mechanisms of resistance to different antibiotics, such as ciprofloxacin and tetracycline, including promotion of outflux and inhibition of influx of antibiotics. Thus, MarA causes multiple antibiotic resistance phenotype. The activation of these mechanisms needs overexpression of mar A. This could happen through mutation in marR. Thus, the aim of this study was to measure mar A expression in ciprofloxacin resistant E. coli gyrA mutants and clones with or without marR mutation. For this purpose, real time PCR was used to measure relative expression ofmarA in above mutants and clones. Results showed that two clones, C14 and C17 overexpressed mar A. It is concluded that the level of mar A expression is important for activation of above mechanisms

2.
IJPR-Iranian Journal of Pharmaceutical Research. 2012; 11 (2): 595-600
en Inglés | IMEMR | ID: emr-131770

RESUMEN

Ciprofloxacin is one of the most widely used antibiotics for the treatment of several infections caused by Gram-negative bacteria, like E. coli. Changes in gyrA, encoding GyrA subunit of DNA gyrase, cause the resistance to ciprofloxacin. Some ciprofloxacin resistant gyrA mutants acquired constitutive expression of marRAB operon due to the gaining mutations in marR, a repressor of this operon. This leads to the expression of a multidrug resistance phenotype and high organic solvent tolerance. Thus, this study was aimed to provide more information on extra mechanisms of resistance in gyrA mutants with different ciprofloxacin MICs. For this purpose, the tolerance of organic solvent, resistance to tetracycline and presence of possible mutation in marOR were investigated in 10 gyrA mutants. Results showed that most of gyrA mutants behaved like MG1655, control strain, but 3 out of 10 were slightly more resistant to tetracycline than MG1655 and had better growth on hexane. Among three mutants, two possess a mutation in marOR. In conclusion, the generation of mutation in marOR is not enough by itself to produce the multidrug resistance phenotype and complete activation of AcrAB-TolC

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