Fluoroquinolone drugs are 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 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).

Scientific work from Finland indicates the potential of permanent  mitochondria damage[1].  Mitochondrial dysfunction carries with it an extensive list of illnesses ranging from chronic fatigue to serious disease such as dementia, Parkinson's and cancers to name just a few. As noted in what we consider one of the most important fluoroquinolone studies ever done, the Finnish abstract states:

    "Maintenance of topological homeostasis is vital for gene expression and genome replication in all organisms. Similar to other circular genomes, also mitochondrial DNA (mtDNA) is known to exist in various different topological forms, although their functional significance remains unknown. We report here that both known type II topoisomerases Top2α and Top2β are present in mammalian mitochondria, with especially Top2β regulating the supercoiling state of mtDNA. Loss of Top2β or its inhibition by ciprofloxacin results in accumulation of positively supercoiled mtDNA, followed by cessation of mitochondrial transcription and replication initiation, causing depletion of mtDNA copy number. These mitochondrial effects block both cell proliferation and differentiation, possibly explaining some of the side effects associated with fluoroquinolone antibiotics. Our results show for the first time the importance of topology for maintenance of mtDNA homeostasis and provide novel insight into the mitochondrial effects of fluoroquinolones."