Oxidative Stress and Epilepsy: Literature Review

Abstract

Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy. Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed. Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.

The effects of vagal nerve stimulation in focal cerebral ischemia and reperfusion model

“…In subcortical specimens, these levels were 12.83 ± 2.80, 2.94 ± 0.30, and 6.64 ± 0.59, respectively. There was a significant overall difference between three groups in terms of SOD activity levels in cortical and subcortical samples, F (2,18) 15, p<0.01, respectively. Post-hoc comparisons revealed significantly higher SOD activity level for the control group compared to I/R (p<0.05) and I/R+VNS groups (p<0.05) in cortical specimens.…”

“…The brain is particularly vulnerable to oxidative stress because of higher content of PUFA that are susceptible to lipid peroxidation (1). Under physiological conditions, free radicals are detoxified by endogenous antioxidant enzymes and molecules such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione (GSH), alpha-tocopherol, and ascorbate (1,2,35,46). However these defense systems are not sufficient in neutralizing the free radicals in pathological conditions including ischemia (2,46).…”

“…The SOD enzyme that is typically known for its antioxidant effects can also exert oxidant effects depending on other factors (2,15,40 might be a source of hydroxyl radicals (OH-), especially in case of insufficient catalase enzyme. OH-is known to be the most harmful of all reactive oxygen species (ROS) that causes cell injury through reacting with lipids, proteins, and nucleic acids.…”

Acute Administration of High Dose Trimetazidine Inhibits Pentylenetetrazol-Induced Seizures in Rats

“…Oxidative stress may also contribute to the pathophysiology of epilepsy. Moreover, free oxygen radicals are among the factors associated with resistant epilepsy patients [30][31][32][33] .…”

Antiepileptic effect of calcium channel blockers alone and in combination with phenytoin on MES induced epilepsy in rats

“…Experimental studies in animals have proved that neuroinflammation can lead increase in permeability of blood brain barrier and excitability of nervous tissue [6,7]. Role of oxidative stress in epileptogenesis process has been supported in various experimental studies [8]. Mitochondrial related oxidative stress plays an important role in the epileptogenesis in lithium-pilocarpine model of temporal lobe epilepsy in animals [9].…”