Ciprofloxacin, a fluoroquinolone antibiotic, disrupts bacterial DNA replication by inhibiting topoisomerases II (DNA gyrase) and IV. This action directly harms bacteria, but unfortunately, it can also affect human cells.
The primary mechanism of Ciprofloxacin toxicity stems from its interaction with human topoisomerases, albeit with less affinity than bacterial enzymes. This interaction can lead to DNA damage and subsequent cellular dysfunction. This effect is particularly pronounced in rapidly dividing cells, like those in the gastrointestinal tract, bone marrow, and cartilage.
Further, Ciprofloxacin can trigger oxidative stress, contributing to cellular damage. This involves the generation of reactive oxygen species (ROS), which can attack cellular components like lipids, proteins, and DNA. The resulting damage may manifest as various adverse effects.
Individual susceptibility to Ciprofloxacin toxicity varies depending on factors like genetics, age, and existing health conditions. For instance, patients with pre-existing mitochondrial dysfunction may experience more severe adverse effects due to Ciprofloxacin’s impact on mitochondrial DNA.
| Tendinitis/Tendon rupture | Inhibition of collagen synthesis, disruption of extracellular matrix |
| Peripheral neuropathy | Axonal damage, possibly due to oxidative stress |
| Gastrointestinal issues | Direct toxicity to rapidly dividing intestinal cells |
| Central nervous system effects | Unknown; possibly involving indirect effects through inflammation or oxidative stress |
Magnesium’s role in mitigating Ciprofloxacin toxicity is under investigation. Some studies suggest a potential protective effect, possibly by reducing oxidative stress or supporting cellular repair. However, more research is needed to fully elucidate this interaction.
