Archive 1995–2023

Oxidative stress plays an important role in the ischemic stroke pathomechanism. There has been a lot of experimental and clinical research devoted to the use of antioxidant activity compounds in the early phase of ischemic stroke. In spite of the fact that experimental studies on animals have been very successful, clinical research has fallen short of expectations. A great number of studies are still in the experimental phase. The main purpose of antioxidative treatment is to decrease oxidative stress, through inhibiting reactive oxygen species (ROS) formation and/or destroying the existing ones. Uric acid, allopurinol, oksypurinol, nimesulide, NS-398, edaravone can be included in the group of compounds whose mechanism is connected with inhibiting ROS generation, whereas glutathione, lipoic acid, N-acetylcysteine, melatonine, tirilazad, NXY-059 and STAZN belong to the group of compounds capable of removing the excessive ROS. The antioxidants which are supplemented are ascorbic acid and α-tocopherol. The compounds which act similarly to antioxidant enzymes such as ebselen, SOD:Tet451, PEG-SOD 1, PEG-CAT, EUK-8 and EUK-134 are also investigated. The attractiveness of antioxidative treatment of ischemic stroke hypothesis has inspired further research. However, in order to include antioxidant compounds in standard procedures, and make them part of the guidelines for treatment in the acute phase of ischemic stroke, we need further experimental and clinical trials, held in accordance with the STAIR (Stroke Therapy Academic Industry Roundtable) criteria.