As oxidation of neural membranes by reactive oxygen species (ROS), especially hydroxyl radicals (・OH), is involved in the biochemical pathogenesis of post-traumatic epilepsy, post-traumatic epilepsy is thought to be prevented by treatment with ROS scavengers. In the present study, I first examined the effects of adenosine (Ado), 2-chloroadenosine (CI-Ado) and guanosine on ・OH and superoxide anion (O(-)(2)), generated by the Fenton reagent and the hypoxanthine-xanthine oxidase system, respectively, using electron spin resonance spectrometry. I also examined the effecta of Ado and Cl-Ado on the occurrence of epileptic discharges on the electrocorticogram (ECoG) induced by FeCl(3) injection (500nmol) into the sensorimotor cortex of rats, i.e., a model of an experimental post-traumatic epilepsy. Although O(-)(2) was not scavenged, ・OH were scavenged by Ado and Cl-Ado dose-dependently. The scavenging activity of Ado was 4 times stronger then thst of Cl-Ado. On the ECoG of rats given FeCl(3), sporadic spike discharges, polyspikes and/or ictal patterns started to be observed 15-90 min after the injection. Epileptic discharges did not appear or their occurrence was delayed by the intraperitioneal injection of Ado (5mg/kg) or Cl-Ado (1mg/kg) 30 min prior to the FeCl(3) injection, although Cl-Ado showed a chronotropic action. Thus Ado and Ci-Ado may be useful in the prevention and the attenuation of progression of post-traumatic epilepsy by scavenging ・OH and by their anticonvulsant effect.