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首页> 外文期刊>Antimicrobial agents and chemotherapy. >Reactive Oxygen Species Production Is a Major Factor Directing the Postantibiotic Effect of Fluoroquinolones in Streptococcus pneumoniae
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Reactive Oxygen Species Production Is a Major Factor Directing the Postantibiotic Effect of Fluoroquinolones in Streptococcus pneumoniae

机译：活性氧物种生产是指导氟喹诺酮类肺炎链球菌肺炎链球菌

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We studied the molecular mechanisms involved in the postantibiotic effect of the fluoroquinolones levofloxacin and moxifloxacin in Streptococcus pneumoniae Wild-type strain R6 had postantibiotic effects of 2.05 +/- 0.10 h (mean +/- standard deviation [SD]) and 3.23 +/- 0.45 h at 2.5x and 10x MIC of levofloxacin, respectively. Moxifloxacin exhibited lower effects of 0.87 +/- 0.1 and 2.41 +/- 0.29 h at 2.5x and 10x MIC, respectively. Fluoroquinolone-induced chromosome fragmentation was measured at equivalent postantibiotic effects for levofloxacin (2.5x MIC) and moxifloxacin (10x MIC). After 2 h of drug removal, reductions were approximately 7-fold for levofloxacin and 3-fold for moxifloxacin, without further decreases at later times. Variations in reactive oxygen species production were detected after 4 to 6 h of drug withdrawals, with decreases >= 400-fold for levofloxacin and >= 800-fold for moxifloxacin at 6 h. In accordance, after 4 to 6 h of drug withdrawal, the levofloxacin-induced upregulation of the fatCDEB operon, introducing iron in the bacteria, decreased up to 2- to 3-fold, and the moxifloxacin-induced upregulation of several genes involved in the production of pyruvate was reduced 3- to 7-fold. In accordance, lower postantibiotic effects (up to 1 h) were observed in strain R6 Delta spxB, lacking the main enzyme involved in oxygen peroxide production, than in R6. Although no change in the recovery of chromosome fragmentation was observed between R6 and R6 Delta spxB, 3.5 x 10(3)-fold lower reactive oxygen species production was observed in R6 Delta spxB, without changes after drug removal. These results show that reactive oxygen species are the main factors directing the postantibiotic effect of levofloxacin and moxifloxacin in S. pneumoniae.
机译：我们研究了氟喹啉酮左氧氟红酮和莫西沙星的分子机制，肺炎链球菌野生型菌株R6的野生型菌株r6为2.05 +/- 0.10小时（平均+/-标准偏差[SD]）和3.23 +/- 0.45小时，分别为左氧氟沙星的2.5倍和10倍。 Moxifloxacin分别表现出0.87 +/- 0.1和2.41 +/- 0.29 h的较低效果，分别为2.5倍和10倍麦克风。在左氧氟沙星（2.5x MIC）和Moxifloxacin（10x MIC）的当量季节性作用中测量氟喹诺酮诱导的染色体碎片。在药物去除2小时后，左氧氟沙星的减少约7倍，对于莫西沙星3倍，在后面的时间内没有进一步降低。在吸毒4至6小时后检测反应性氧物质产生的变化，减少> = 400倍的左氧氟沙星，6小时，Moxifloxacin的> = 800倍。根据4〜6小时的药物戒断，左氧氟沙星诱导的FATCDEB操纵子的上调，在细菌中引入铁，达到2至3倍，致莫西甲酰蛋白诱导的涉及涉及的几种基因的上调丙酮酸的生产减少了3至7倍。根据菌株R6 delta Spxb，缺乏参与氧化氧化的主要酶，缺乏氧化氧化酶，缺乏氧化酶，较低，缺乏氧化酶的产生。虽然在R6和R6δSpxb之间观察到染色体碎片的回收的变​​化，但在R6 delta SPxb中观察到3.5×10（3） - 在R6 delta Spxb中观察到较低的反应性氧物质生产，但除去药物除去后没有变化。这些结果表明，活性氧物种是指导左氧氟沙星和莫西沙星在S.肺炎的主要作用的主要因素。

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