In the present study, we found that mitochondrial UCP2 was significantly upregulated in the hippocampal CA3 region 12 to 48 h after the induction of experimental status epilepticus, at a time-point that lagged behind the increase in protein carbonylation and O2·- These results indicate that the endogenous activation of mitochondrial UCP2 in hippocampal CA3 neurons under prolonged epileptic seizures may be a consequence of the increase in ROS production. This evidence concerns the gene UCP2 and status epilepticus.