[Oxidative stress in cerebral stroke].

Free radicals are molecules or ions containing non-paired electrons on the external orbit, which ensures their high chemical activity. In systemic homeostasis, free radicals are inactivated by endo- and exogenous antioxidants and do not have destructive effects. The human organism possesses protective mechanisms, i.e. enzymatic systems (peroxide dismutase, glutathione peroxidase, catalase) and non-enzymatic systems (vitamin C and E selenium, coenzyme Q, lipoid acid, bilirubin). Imbalance between continuous production of reactive oxygen forms and their elimination due to enzymatic and non-enzymatic neutralization reactions as well as effects of exogenous antioxidants is defined as oxidative stress. Recent studies demonstrated a significant role of inflammatory processes and oxidative stress in the pathomechanism of cerebral stroke. Increased production of free radicals was observed in both the ischaemic and haemorrhagic strokes and oxidative stress was shown to be one of the causative mechanisms of tissue damage in these diseases. This was confirmed by numerous studies assessing the concentration of oxidative stress biomarkers and levels of plasma antioxidants (enzymatic and non-enzymatic). At present, studies are being carried out about the use of antioxidative substances for the therapy of cerebral stroke. The present study reports current findings concerning oxidative stress issues in patients with stroke.