Free radical production is increased in ischemic and
hemorrhagic stroke, leading to oxidative stress that contributes to brain damage. The measurement of oxidative stress in
stroke would be extremely important for a better understanding of its pathophysiology and for identifying subgroups of patients that might receive targeted therapeutic intervention. Since direct measurement of
free radicals and oxidized molecules in the brain is difficult in humans, several biological substances have been investigated as potential peripheral markers. Among lipid peroxidation products,
malondialdehyde, despite its relevant methodological limitations, is correlated with the size of
ischemic stroke and clinical outcome, while
F2-isoprostanes appear to be promising, but they have not been adequately evaluated. 8-Hydroxy-2-deoxyguanosine has been extensively investigated as markers of oxidative DNA damage but no study has been done in
stroke patients. Also enzymatic and nonenzymatic
antioxidants have been proposed as indirect markers. Among them
ascorbic acid,
alpha-tocopherol,
uric acid, and
superoxide dismutase are related to brain damage and clinical outcome. After a critical evaluation of the literature, we conclude that, while an ideal
biomarker is not yet available, the balance between
antioxidants and by-products of oxidative stress in the organism might be the best approach for the evaluation of oxidative stress in
stroke patients.