Stroke is the third leading cause of death and the first leading cause of disability in industrially advanced countries [1]. The most frequent stroke type is the ischemic stroke which occurs after a blood clot blocks a brain blood vessel. In the ischemic stroke free radicals can play a crucial role because they can damage important molecules especially lipids. Significant nitrogen and oxygen radicals increase occurs in both, the ischaemic and reperfusion phases of ischemic stroke. If the antioxidant protection of the patient is not strong enough, the patients´ life is seriously endangered. There have not been developed any specific therapies against the acute ischemic stroke (AIS) so far.

In our combined cohort and case control study we have focussed on the evaluation of dynamic changes of oxidative stress markers (protein carbonyls, lipoperoxides) and oxidative stress protector (total antioxidant capacity (TAC)), in blood at three time intervals: 24h after AIS (group A, n = 81), 7-day (group B, n = 57) and 3-month (group C, n = 16) follow-ups. We have also compared plasma samples (group A) obtained from patients with control samples (n = 77), who did not experience any stroke attacks. Comparisons were done in the whole groups as well as between males (n = 45) and females (n = 36). Age influence was also taken into account.

Total antioxidant capacity was measured spectrophotometrically (UV-1800 Shimazu spectrophotometer) by the TEAC (Trolox Equivalent Antioxidant Capacity) assay [2]. Protein carbonyls in plasma were determined by the commercial OxiSelectTM protein carbonyl ELISA kit (Cell Biolabs, USA) according to manufacturer´s instructions. Lipoperoxides in plasma were determined spectrophotometrically (Epoch Microplate spectrophotometer (SN: 130-148) according to El-Saadani assay [3]. Statistical analyses were performed in statistical program StatsDirect 2.7.2.

We found a significant increase of TAC in AIS patients in group C compared to groups B (p < 0.05) and A (p < 0.05). Females after stroke were significantly older than males (p < 0.01) but their antioxidative status was similar to males after stroke at younger age. AIS patients (group A) had significantly higher concentrations of lipoperoxides compared to controls (p < 0.05) and males after stroke had marginally significantly higher TAC (p = 0.05) compared to controls (males). In logistic regression model we took age, gender, lipoperoxides, protein carbonyls and TAC into account. In the diagnostic test with sensitivity 71 % and specificity 64 % using cut-off point 0.5 higher oxidative stress was confirmed.

Our study confirms the national statistics that the males after stroke are significantly younger than females. Based on our results there are no significant gender differences in protein carbonyls, lipoperoxides and TAC in patients after stroke in spite of age differences. Higher lipid oxidation recorded in AIS patients is the evidence of elevated oxidative stress during the stroke attack. Increased antioxidant capacity in AIS patients 3 months after the attack may be the consequence of better lifestyle (diet rich in antioxidants) or a pharmacological treatment.