Interdependence between mitochondrial dysfunctions and synthesis of the free radicals during the epileptogenesis is proved by number of publications. Xanthine Oxidase (XO) might serve as a source of hydrogen peroxide synthesis, which by its turn is able to disturb the process of ATP generation in mitochondria. Antioxidants, such as Skulachev’s cations, might be used as possible inhibitors of XO and prevent the formation of free radicals in mitochondria. In our current work, we found out that SkQ-1 might inhibit the activity of XO in homogenate as well as in the purified fraction in vitro. In vivo modeling of epilepsy with the utility of korazol showed that the quantity of XO final product – uric acid, is elevating, whereas addition of SkQ-1 might suppress that increase in mitochondria.