Fluoroquinolones are a class of antibiotics frequently and globally prescribed as a measure to cure bacterial infections in humans and animals. There is an extensive list of drugs in this class, but the most familiar are name brands Cipro, Levaquin (now off market), Avelox, and their generics  ciprofloxacin, levofloxacin, and moxifloxacin. These antibiotics have shown to inhibit DNA replication much like chemotherapy. Since May 12, 2016, the Food & Drug Administration (FDA) advises that fluoroquinolone antibiotics should be reserved for medical conditions only when no other options exist. In FDA and European Medicines Agency black box warnings over the last few years, they have indicated fluoroquinolones have been associated with disabling and potentially irreversible, serious adverse reactions within different body systems that can occur simultaneously to cause damage affecting:  central nervous system, musculoskeletal, visual and renal systems; tendon disorders and spontaneous ruptures; systemic peripheral neuropathy; psychosis; aortic aneurysm; diabetes/hypoglycemia; hepatotoxicity; cytochrome P450 (CYP450).

The following two studies provide compelling evidence that fluoroquinolones, including ciprofloxacin, can cause long-term or even permanent mitochondrial dysfunction. Mitochondrial impairment has been associated with a wide range of health conditions, from chronic fatigue and neuropathy to serious neurodegenerative and systemic diseases such as dementia, Parkinson’s disease, and cancer:

➡️  Ciprofloxacin disrupts mitochondrial DNA replication by inhibiting topoisomerase, an enzyme required to relieve DNA supercoiling during replication initiation. This effect occurs even at standard therapeutic doses and is amplified by fluoroquinolone accumulation in tissues, leading to stalled mtDNA replication, impaired mitochondrial biogenesis, reduced energy production, and long-term cellular dysfunction.[1]    

➡️  Fluoroquinolones cause mitochondrial toxicity by targeting key enzymes. Proteomic analysis reveals interactions with AIFM1, disrupting electron transport chain complexes I and IV, and with IDH2, impairing NADPH production and redox balance. These effects, seen even at therapeutic levels, trigger chronic oxidative stress, impaired bioenergetics, and long-term cellular dysfunction linked to Fluoroquinolone Associated Disability (FQAD).[2]