Fig. 7.

The relationship betweens seizures, mtDNA damage, mtBER expression and H₂O₂ production. Indices of the mitochondrial oxidative burden measured during this study illustrate how mitochondrial oxidative stress and mtDNA damage could play a role in the progression from acute seizure activity to chronic epilepsy. Acute seizure activity causes preferential oxidative damage to the mtDNA and the mtBER is induced to attempt to repair mtDNA lesions. However, there is a failure in the mtBER during the chronic phase of epilepsy, which may hinder the repair of mtDNA damage and contribute to increased mitochondrial oxidative stress. The increased mitochondrial oxidative stress burden and genomic instability may render the brain more susceptible to subsequent chronic epileptic seizures. The (X) represents the mean seizure score and the other data points represent the mean percentage change of mtDNA Damage, Ogg1, Pol γ and H₂O₂ production compared to controls.