A probable causative factor for an old problem: selenium and glutathione peroxidase appear to play important roles in epilepsy pathogenesis.
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OBJECTIVE
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 microg/L (+/-22.20) and 86.00 microg/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).
CONCLUSIONS
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.
