Abstract
As oxidation of neural membranes by reactive oxygen species (ROS), especially hydroxyl radicals (·OH), is involved in the biochemical pathogenesis of post-traumatic epilepsy, posttraumatic 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 (Cl-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 effects of Ado and Cl-Ado on the occurrence of epileptic discharges on the electrocorticogram (ECoG) induced by FeCl3 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 than that of Cl-Ado. On the ECoG of rats given FeCl3, 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 intraperitoneal injection of Ado (5mg/kg) or Cl-Ado (1mg/kg) 30 min prior to the FeCl3 injection, although Cl-Ado showed a chronotropic action. Thus Ado and Cl-Ado may be useful in the prevention and the attenuation of progression of post-traumatic epilepsy by scavenging ·OH and by their anticonvulsant effect.
