A Probable Causative Factor for an Old Problem: Selenium and Glutathione Peroxidase Appear to Play Important Roles in Epilepsy Pathogenesis

Abstract

Summary:Purpose: Only recently has it become known that oxidative stress and generation of reactive oxygen species are the cause and the consequence of epileptic seizures. Due to the protective role of selenium (Se) and selenoproteins against oxidative damage and the ability to promote neuronal cell survival, we compared serum selenium level and red blood cell Glutathione peroxidase activity (RBC GPx) between epileptic and healthy children.Methods: In a case control study, 53 epileptic children were compared with 57 healthy children in the same age and community of residence. Serum Se and RBC GPx activity were measured with an atomic absorption spectrophotometry and Cayman standard glutathione assay kit, respectively.Results: The mean (±standard deviation) of serum Se was 72.90 µg/L (±22.20) and 86.00 µg/L (±15.00) in patient and control groups, respectively. For RBC GPx activity the mean (±standard deviation) was 440.57 nmol/min/ml (±264.00) and 801.00 nmol/min/ml (±267.00) in patient and control groups, respectively. Statistical analysis showed a significant lower means of serum Se and RBC GPx activity in patient group compared to that of healthy control group (p < 0.001).Conclusion: Lower serum Se and RBC GPx activity in epileptic patients compared to healthy children may support the proposed crucial role of Se and GPx activity in the pathogenesis of epilepsy. However, RBC GPx activity in the case of selenium deficiency could not be a sensitive and specific indicator of Se status in serum that led us to supplant Se measurement with RBC GPx activity.

The effects of treadmill exercise on oxidative stress in Mongolian gerbils with penicillin-induced epilepsy

“…For all these reasons, the nervous system is very sensitive to the destructive effects of ROS [28,29]. Additionally, oxidative stress has been shown to induce neuronal degeneration in experimental models of epilepsy and many other neurodegenerative disorders including Alzheimer's disease and Parkinson's disease [7,[30][31][32][33]. In contrast, ROS is scavenged by defense mechanisms such as enzymatic antioxidants such as SOD and GPx, and thus reducing the deleterious effects of oxidative stress [8].…”

“…Oxidative stress, which can lead to irreversible cell damage, is the result of an imbalance between reactive oxygen species (ROS) and antioxidant defense mechanisms [6]. In addition, excessive ROS production also plays a role in the pathogenesis of many neurodegenerative disorders including the onset and progression of epilepsy, as well as Alzheimer's disease and Parkinson's disease [4,7]. However, ROS can be scavenged by enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) [8].…”

Redox Processes in Neurodegenerative Disease Involving Reactive Oxygen Species

“…Another report deals with the effect of SOD on seizures in an experimental model [12]. Only recently has it become known that OS and ROS generation are the cause and consequence of epileptic seizures [13]. Selenium and GSH peroxidase appear to play important roles in the pathogenesis in this context.…”

Plausible antioxidant biomechanics and anticonvulsant pharmacological activity of brain-targeted &beta;-carotene nanoparticles

“…9,12 Physiological levels of ROS are maintained by means of scavenging through enzymatic (eg, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and peroxiredoxins) and nonenzymatic reactions of antioxidants. 3,[14][15][16] Many biological experiments conducted by use of kainic acid, iron-salt, and electroshock induced seizures, as well as the kindling model by pentylenetetrazole (PTZ) have confirmed the relation of ROS and other species with convulsions. [17][18][19][20][21] PTZ, an epilepsy inducing agent, is a selective blocker of GABA A receptor-chloride ionophore complex, which induces convulsions by triggering the glutamatergic transmitter system.…”