Antioxidant capacity after acute ischaemic stroke

Experimental studies have reported a rapid increase in the production of markers of oxidative damage following acute stroke due to the reperfusion event following ischaemia, and that endogenous antioxidant defences are rapidly depleted, permitting further tissue damage.

To measure changes in antioxidant capacity (individual and total) in stroke disease within a known time period post infarct.

Observational cohort study.

We studied 31 acute ischaemic stroke patients; 26 hospitalized non-stroke patients and 23 community-based healthy controls. Non-fasting venous blood was obtained within 24 h, at 48-72 h and at 7 days after stroke onset (after hospitalization for non-stroke patients) and at baseline for community controls. Vitamins E and C, total plasma glutathione, total antioxidant capacity (TAC), uric acid, thiobarbituric-acid-reactive substances (TBARS), serum albumin, transferrin and C-reactive protein (CRP) were measured.

Baseline glutathione concentrations were non-significantly lowest and TBARS significantly highest in ischaemic stroke patients compared with controls. Serum TAC strongly correlated with serum uric acid. Under multivariate analysis, serum uric acid explained most of the variance in TAC during the study period. Despite increased concentrations of uric acid, TAC was reduced in stroke patients compared with controls. Serum vitamin C concentrations deteriorated significantly in stroke patients, and differences between the cumulative changes between strokes and hospital controls were also statistically significant (p=0.013).

There was some evidence of reduction in TAC, despite increased uric acid concentrations, and deterioration in serum vitamin C levels in ischaemic stroke patients compared with controls.