It is also noted in the FDA’s April 27, 2013 Pharmacovigilance Review, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure,” that the mechanism for action through which fluoroquinolones induce peripheral neuropathy is mitochondrial toxicity. The report says:
“Ciprofloxacin has been found to affect mammalian topoisomerase II, especially in mitochondria. In vitro studies in drug-treated mammalian cells found that nalidixic acid and ciprofloxacin cause a loss of motichondrial DNA (mtDNA), resulting in a decrease of mitochondrial respiration and an arrest in cell growth. Further analysis found protein-linked double-stranded DNA breaks in the mtDNA from ciprofloxacin-treated cells, suggesting that ciprofloxacin was targeting topoisomerase II activity in the mitochondria.”
I really do appreciate the research described in Feet First? Old Mitochondria Might Be Responsible For Neuropathy In The Extremities. Experiments, analysis and scientific documentation are needed. But synthesis of existing information is needed too.
Drugs that deplete mitochondrial DNA are leading to peripheral neuropathy. Perhaps the Johns Hopkins study is the piece of the puzzle that is missing from widespread recognition of this.