Ciprofloxacin targets bacterial DNA replication. It achieves this by inhibiting two key enzymes: DNA gyrase and topoisomerase IV.
DNA gyrase is responsible for supercoiling bacterial DNA, allowing it to fit within the cell. Ciprofloxacin prevents this supercoiling. Topoisomerase IV is crucial for separating bacterial DNA strands during cell division. Ciprofloxacin disables this enzyme as well.
By inhibiting these enzymes, ciprofloxacin halts bacterial DNA replication and transcription, effectively killing the bacteria. This mechanism explains its broad-spectrum activity against a wide range of Gram-negative and some Gram-positive bacteria.
However, this powerful mechanism also presents potential risks. The interaction with bacterial DNA enzymes may indirectly affect human cells, although to a lesser extent. Individual susceptibility and pre-existing conditions can significantly modify this interaction. More research is needed to fully elucidate the complex interplay between ciprofloxacin’s mechanism of action and the development of neuropathy.
| DNA Gyrase | Supercoils bacterial DNA | Inhibition; prevents supercoiling |
| Topoisomerase IV | Separates DNA strands during replication | Inhibition; halts DNA separation and replication |
Understanding these mechanisms is crucial for clinicians to appropriately prescribe and monitor ciprofloxacin treatment, weighing the benefits against the potential for adverse effects like neuropathy.
