Seizure-Induced Oxidative Stress in Temporal Lobe Epilepsy

Figure 3

Sequence of events during status epilepticus, latent period, and SRS. The damage to the specific areas of the brain during SE can initiate varying period of neurobiological changes that can lead to the development of SRS. The enzymes free radicals and the pathways involved in these disorders are common in all types of insult (SE, latent period, and SRS), as described in Figures 1 and 2, but with subtle differences. The concentration of antioxidant enzymes rises after an initial insult (imitating their protective role) such as glutamine synthetase in SE; later it reduces which may or may not recover after few days/weeks depending upon the severity of the insult. Latent period is generally characterized by a series of slow neurodegenerative changes in the brain leading to epileptogenesis. The concentration of GST falls during latency that affects glutamate metabolism. High levels of the glutamate in the extracellular and intracellular space can lead to neuronal excitability through activated calcium signaling, as described in Figure 2. Levels of H₂O₂ return to the basal levels with mtDNA repair and low GSH/GSSG and CoASH/CoASSG ratio. During latent period, nitrosylation of protein fragments and posttranslational modifications of ion channels and transporters will further lead to hyperexcitability of neurons [24, 48, 82, 83, 85, 86]. SRS: spontaneous recurrent seizures; GST: glutamine synthetase; mtDNA: mitochondrial DNA; X: reverse reaction does not occur; Li-Pilo: lithium- pilocarpine model.