Abstract
Ozone (O(3)) is a reactive oxygen species (ROS) that can interact with cellular components and cause oxidative stress. Following said logic, if O(3) induces such a stressful milieu, how does it exert antioxidant functions? This is mediated by controlled toxicity produced by low concentrations of O(3), which enhance the cell's suppliance of antioxidant properties without causing any further damage. Therapeutic concentrations vary extensively, although 50 µg/mL is commonly used in experimental and clinical procedures, given that augmented concentrations might work as germicides or cause endogenous damage. O(3) therapy has been shown to be effective when applied before or after traumatic renal procedures, whether caused by ischemia, xenobiotics, chronic damage, or other models. In this review, we focus on discussing the role of O(3) therapy in different models of kidney damage associated with fibrosis, apoptosis, oxidative stress, and inflammation. We integrate and report knowledge about O(3) in renal therapy, debunking skepticism towards unconventional medicine, explaining its proven therapeutic properties, and thus providing background for its use in further research as well as in clinical settings.