Protection of Mitochondria, Cells and Organs from Ischemia–Reperfusion Damage Through Preventive Redox Bioregulation by Ozone

Ischemia–reperfusion (I/R) damage remains a major problem in surgery, primarily based on high oxidative stress generated during the reperfusion process. Mitochondria are significantly affected, their metabolic and energetic processes are impaired, and the redox system is out of balance. Regulation and restoration of the redox balance by oxidative preconditioning with ozone is being investigated worldwide in cell and animal models. Selected preclinical trials and their results, with a focus on cardiological and neuronal I/R damage, are presented and discussed. We regularly find an upregulation of antioxidants, demonstrated in SOD (superoxide dismutase) and GSH (glutathione, reduced form, and a decrease in oxidative stress as a result, shown here using the typical stress parameters, MDA (malondialdehyde) and TBARS (thiobarbituric acid reactive substances). Mitochondrial biogenesis, comparable to moderate physical activity, is induced by ozone oxidative preconditioning in an I/R model in rats and reviewed in this paper.