Oxidative stress and total antioxidant capacity in diabetic and nondiabetic acute ischemic stroke patients

Free radical formation is the pivotal mechanism of neuronal injury of ischemic and reperfused brain tissue. In healthy individuals, antioxidant activity counterbalances free radical production, but in the case of ischemia, the balance between reactive oxygen species and antioxidant activity is shifted toward free radicals, causing oxidative stress. The aim of this study is to assess total antioxidant capacity (TAC) and oxidative stress in diabetic and nondiabetic acute stroke patients with 2 different stroke subtypes: large and small vessel disease stroke. Sixty-five acute ischemic stroke patients (29 diabetic and 36 nondiabetic) and 20 age-matched healthy control subjects were recruited in the study. Plasma TAC and nitric oxide (NO) metabolite levels (nitrite and nitrate) were measured by enzyme-linked immunosorbent assay. The subtypes of stroke were defined according to Trial of Org 10172 in Acute Stroke Treatment criteria. The main findings of this study are that the TAC and NO levels were significantly higher in diabetic acute stroke patients than in nondiabetic patients and control cases (P < .001 and P < .001, respectively). The TAC and NO levels were higher also in nondiabetic stroke patients than in controls, but the difference did not reach any significance. No difference was found between NO and TAC levels in large and small vessel stroke subtypes of diabetic and nondiabetic patients. The authors conclude that oxidative stress and counterbalancing antioxidant capacity are more pronounced in diabetic acute stroke patients than in nondiabetic acute stroke patients.