Description: Animation showing the mechanism of action of fluoroquinolones. The fluoroquinolones (norfloxacin, lomefloxacin, fleroxacin, ciprofloxacin, enoxacin, trovafloxacin, gatifloxacin, etc.) work by inhibiting one or more of a group of enzymes called topoisomerase, enzymes needed for supercoiling, replication and separation of circular bacterial DNA. For example, DNA gyrase is a topoisomerase that catalyzes the negative supercoiling of the circular DNA found in bacteria. Topoisomerase IV, on the other hand, is involved in the relaxation of the supercoiled circular DNA, enabling the separation of the interlinked daughter chromosomes at the end of bacterial DNA replication. In gram-positive bacteria, the main target for fluoroquinolones is DNA gyrase (topoisomerase II), an enzyme responsible for supercoiling of bacterial DNA during DNA replication; in gram-negative bacteria, the primary target is topoisomerase IV, an enzyme responsible for relaxation of supercoiled circular DNA and separation of the inter-linked daughter chromosomes.
When an antibiotic binds to a bacterial enzyme, it may alter the activate site of the enzyme and prevent it from reacting with its substrate

NOTE- The Enzyme here is TOPOISOMERASE and the Substrate is DNA
The fluoroquinolones (norfloxacin, lomefloxacin, fleroxacin, ciprofloxacin, enoxacin, trovafloxacin, gatifloxacin, etc.) work by inhibiting one or more of a group of enzymes called topoisomerase, enzymes needed for supercoiling, replication and separation of circular bacterial DNA. For example, DNA gyrase is a topoisomerase that catalyzes the negative supercoiling of the circular DNA found in bacteria. Topoisomerase IV, on the other hand, is involved in the relaxation of the supercoiled circular DNA, enabling the separation of the interlinked daughter chromosomes at the end of bacterial DNA replication. In gram-positive bacteria, the main target for fluoroquinolones is DNA gyrase (topoisomerase II), an enzyme responsible for supercoiling of bacterial DNA during DNA replication; in gram-negative bacteria, the primary target is topoisomerase IV, an enzyme responsible for relaxation of supercoiled circular DNA and separation of the inter-linked daughter chromosomes.
When an antibiotic binds to a bacterial enzyme, it may alter the activate site of the enzyme and prevent it from reacting with its substrate