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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 8023935, 15 pages
Review Article

Treatment of the Fluoroquinolone-Associated Disability: The Pathobiochemical Implications

1Physics Faculty, Laboratory of Vision Science and Optometry, Adam Mickiewicz University in Poznań, Umultowska Street 85, 61-614 Poznań, Poland
2Nanobiomedical Center of Poznań, Umultowska Street 85, 61-614 Poznań, Poland
3Department of Biochemistry, Medical University of Lodz, Mazowiecka Street 6/8, 92-215 Łódź, Poland
4Outpatient Clinic, Polish Mother’s Memorial Hospital-Research Institute, Rzgowska Street 281/289, Łódź, Poland

Correspondence should be addressed to Aleksandra Sobolewska-Włodarczyk; lp.teno.atzcop@1akswelobosalo

Received 1 July 2017; Accepted 20 August 2017; Published 25 September 2017

Academic Editor: Jacek Kurzepa

Copyright © 2017 Krzysztof Michalak et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Long-term fluoroquinolone-associated disability (FQAD) after fluoroquinolone (FQ) antibiotic therapy appears in recent years as a significant medical and social problem, because patients suffer for many years after prescribed antimicrobial FQ treatment from tiredness, concentration problems, neuropathies, tendinopathies, and other symptoms. The knowledge about the molecular activity of FQs in the cells remains unclear in many details. The effective treatment of this chronic state remains difficult and not effective. The current paper reviews the pathobiochemical properties of FQs, hints the directions for further research, and reviews the research concerning the proposed treatment of patients. Based on the analysis of literature, the main directions of possible effective treatment of FQAD are proposed: (a) reduction of the oxidative stress, (b) restoring reduced mitochondrion potential ΔΨm, (c) supplementation of uni- and bivalent cations that are chelated by FQs and probably ineffectively transported to the cell (caution must be paid to Fe and Cu because they may generate Fenton reaction), (d) stimulating the mitochondrial proliferation, (e) removing FQs permanently accumulated in the cells (if this phenomenon takes place), and (f) regulating the disturbed gene expression and enzyme activity.