Oxidative stress and mitochondrial dysfunction are implicated in the pathogenesis of many neurological disorders, including epilepsy.
Oxidative stress is traditionally defined as an imbalance between the production of reactive oxygen and/or nitrogen species (ROS and/or RNS) and antioxidant defense mechanisms. Our aim is to study the role of oxidative stress in immature brain during the acute phase of seizures and during epileptogenesis. We have demonstrated that oxidative stress occurs also in immature rats during seizures and it is apparently due to both the increased free radical production and the limited antioxidant defense. We have provided evidence of mitochondrial dysfunction in immature rat brain during seizures. Pronounced inhibition of mitochondrial complex I activity was evident not only during the acute phase of seizures, but it persists during periods of epileptogenesis. The findings suggest that oxidative modification of complex I is very likely responsible for the sustained deficiency of complex I activity. Our findings suggest that the substances with antioxidant properties combined with conventional therapies might provide a beneficial effect in treatment epilepsy.
Fluorescence of the oxidized products of hydroethidium (reflecting superoxide anion production) in CA3 region of the hippocampus following 60 min lasting seizures induced in immature rats by homocysteic acid (right panel – control, left panel – seizures).