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Quinolones are potent broad spectrum antibacterial drugs that target the bacterial type ii dna topoisomerases Quinolones inhibit dna replication by binding to bacterial type ii topoisomerase (dna gyrase), thereby preventing it from relaxing supercoiled chromosomal dna. Mechanisms contributing to quinolone resistance are mediated by chromosomal mutations and/or plasmid gene uptake that alter the topoisomerase targets, modify the quinolone, and/or reduce drug accumulation by either decreased uptake or increased efflux.
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Quinolones are some of the most broad spectrum and widely prescribed antibacterials in clinical use In this work, we demonstrate that norfloxacin, a model quinolone, converts escherichia colitopo iv into a poisonous adduct on dna as opposed to inhibiting topoisomerase. These antibacterials target bacterial type ii topoisomerases, stabilizing a cleaved dna intermediate that inhibits enzyme activity and can lead.
As is the case with other antibacterial agents, the rise in quinolone resistance threatens the clinical utility of this important drug class
Quinolones act by converting their targets, gyrase and topoisomerase iv, into toxic enzymes that fragment the bacterial chromosome. Topoisomerase iv (topo iv) is a mediator of quinolone toxicity in bacteria
