arsenic and oxidative stress in pentylenetetrazole-induced seizures in mice

Background and objective: chronic arsenic toxicity is a widespread problem; the role of brain oxidative stress has been suggested in the genesis of epilepsy and in the post-seizure neuronal death. however, studies investigating the effects of arsenic on seizure and related mechanisms are limited. the purpose of this study was to examine the effect of prolonged exposure to sodium arsenite on oxidative damage in pentylenetetrazole (ptz)- induced seizures in mice. materials and methods: in this study, male nmri mice received sodium arsenite (0, 25, 50, and 100 ppm) in the drinking water for a period of 30 days. after exposure, all animals were injected ptz (ptz; 85 mg/kg, i.p.) to induce seizure, and the seizure parameters were evaluated for 30 minutes. then, the levels of malondialdehyde (mda) and reduced glutathione (gsh) were measured in the brain. results: the results of this study showed that sodium arsenite decreases the latency to the seizure onset and time of death (p<0.05). the greatest effect was observed at concentration of 50 ppm. the data indicated that exposure to sodium arsenite increases the levels of mda (p<0.05) and decreased the levels of gsh in brain (p<0.05). conclusion: our results suggest that ptz effects potentiated by arsenic and oxidative damage involved in exacerbation of arsenic convulsive effects. considering the role of arsenic in brain tissue damage following the seizure, it is recommended to control arsenic in drinking water.