Fluoroquinolone antibiotics have been known to cause severe, multisystem adverse side effects, termed fluoroquinolone toxicity (FQT). This toxicity syndrome can present with adverse effects that vary from individual to individual, including effects on the musculoskeletal and nervous systems, among others. The mechanism behind FQT in mammals is not known, although various possibilities have been investigated. Among the hypothesized FQT mechanisms, those that could potentially explain multisystem toxicity include off-target mammalian topoisomerase interactions, increased production of reactive oxygen species, oxidative stress, and oxidative damage, as well as metal chelating properties of FQs. This review presents relevant information on fluoroquinolone antibiotics and FQT and explores the mechanisms that have been proposed. A fluoroquinolone-induced increase in reactive oxygen species and subsequent oxidative stress and damage presents the strongest evidence to explain this multisystem toxicity syndrome. Understanding the mechanism of FQT in mammals is important to aid in the prevention and treatment of this condition.
Affecting millions of Americans, depression is one of the leading causes of the Global Burden of Disease (GBD), followed by anxiety (Gibson-Smith et al., 2018). Communication that occurs between the human brain and the gut microbiome has been found to be a major contributor towards mental health. The human gut microbiome is comprised of many microbes that can communicate with the brain through the gut-brain axis. However, factors such as stress and diets can interfere with this process, especially after increasing the permeability of the intestine (Khoshbin et al., 2020). Perturbation of the gut-brain axis has been implicated across a wide scale of neurodegenerative disorders, with respect to psychopathology (Bonaz et al., 2018). The environment of the gut, along with which species reside there, can help determine the link between gut function and disease. Therefore, it may be possible to prevent the degradation of an individual’s immune function and well-being through alteration of the gut microbiome. (abstract)