During the ischemia-reperfusion period, the hypoxanthine-xanthine oxidase system simultaneously generates superoxide (O2-). O2- has an extremely short half-life, as it rapidly undergoes Fenton-type reactions in the presence of iron and yields highly cytotoxic hydroxyl radicals (.OH). Oxygen-derived free radicals are induced as a contributing cause of cellular injury in several neurological disorders, including cerebral infarction and aging. Cerebral injury by ischemia-reperfusion following middle cerebral artery occlusion could be useful experimental model for studying cerebral injury induced by free radicals. Thiobarbituric acid reactants generally indicate lipid peroxidation associated with cellular damage caused by free radicals. Phosphatidylethanolamine hydroperoxide (PEOOH) is the primary peroxidative product of phosphatidylethanolamine, which is the most important functional lipid in the membrane. Plasma PEOOH levels appear to be a reliable indicator of cerebral damage caused by ischemia-reperfusion and other oxidative stress. Recently, an electron spin resonance (ESR) spectrometer was used in the detection of free radicals, in vivo and in vitro using 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO) as the radical-trapping reagent. Moreover, there are reports the electron spin resonance-computed tomography (ESR-CT) images of the cephalic region of rats for locating regions of pathological change are related to free radicals in the brain.