The existing data indicate that status epilepticus (SE) induced in immature animals is associated with oxidative stress and mitochondrial dysfunction. This has been demonstrated using two models of SE, induced by substances with a different mechanism of action (DL-homocysteic acid and 4-aminopyridine) which suggests that the findings are not model-dependent but they reflect more general phenomenon. Oxidative stress occurring in immature brain during and following seizures is apparently due to both the increased free radicals production and the limited antioxidant defense. Pronounced inhibition of mitochondrial complex I in immature brain was demonstrated not only during the acute phase of SE, but it persisted during long periods of survival, corresponding to the development of spontaneous seizures (epileptogenesis). The findings suggest that oxidative modification is most likely responsible for the sustained deficiency of complex I activity. It can be assumed that the substances with antioxidant properties combined with conventional therapies might provide a beneficial effect in treatment of epilepsy.