Epilepsy is considered one of the most common
neurological disorders. The focus of this review is the acquired form of
epilepsy, with the development process consisting of three major phases, the acute injury phase, the latency epileptogenesis phase, and the phase of spontaneous recurrent
seizures. Nowadays, an increasing attention is paid to the possible interrelationship between oxidative stress resulting in disturbance of physiological signalling roles of
calcium and
free radicals in neuronal cells and
mitochondrial dysfunction, cell damage, and
epilepsy. The positive stimulation of mitochondrial
calcium signals by
reactive oxygen species and increased
reactive oxygen species generation resulting from increased mitochondrial
calcium can lead to a positive feedback loop. We propose that
calcium can pose both, physiological and pathological effects of mitochondrial function, which can lead in neuronal cell death and consequent epileptic
seizures. Various
antiepileptic drugs may impair the endogenous antioxidative ability to prevent oxidative stress. Therefore, some
antiepileptic drugs, especially from the older generation, may trigger
oxygen-dependent tissue injury. The prooxidative effects of these
antiepileptic drugs might lead to enhancement of seizure activity, resulting in loss of their efficacy or apparent functional tolerance and undesired adverse effects. Additionally, various reactive metabolites of
antiepileptic drugs are capable of covalent binding to macromolecules which may lead to deterioration of the epileptic
seizures and systemic toxicity. Since neuronal loss seems to be one of the major neurobiological abnormalities in the epileptic brain, the ability of
antioxidants to attenuate seizure generation and the accompanying changes in oxidative burden, further support an important role of
antioxidants as having a putative
antiepileptic potential.