Evaluation of trace element levels, thiol-disulphide balance, intracellular oxidized and reduced glutathione levels in epileptic patients

In this study, we aimed to find the role of oxidative damage and trace elements in the epilepsy pathogenesis by evaluating the trace element levels, thiole disulphide balance and intracellular oxidized and reduced gluthation levels. 41 epilepsy patients and 43 healthy controls were included in the study. Serum copper, zinc and selenium levels were estimated using atomic absorption spectrometry. As a marker of oxidative stress serum thiol disulphide balance and intracellular oxidized and reduced glutathione levels were studied by spectrophotometric method. Serum copper levels were significantly higher (patient: 127.0 ± 31.2 (µg / dL), control: 102.9 ± 16.4 (µg / dL) p <0.001) while zinc levels were significantly lower in the patient group (patient: 90.9 ± 28.8 (µg / dL), control: 104.7 ± 29.5 (µg / dL), p: 0.0034). There was no significant difference in selenium levels (patient: 97.9 ± 25.0 (µg /L), control: 99.7 ± 21.0 (µg / L), p: 0.733). In our study, there was no significant difference in serum thiol disulfide balance in the patient group compared to the control group (p> 0.005). While intracellular oxidized glutathione levels were significantly higher in the patient group (patient: 113.7 ± 21.2 (µmol/L), control: 84.9 ± 27.3 (µmol/L), p <0.001), we found that the reduced glutathione levels were significantly lower (native GSH; patient: 584.4 ± 141.3 (µmol/L), control: 858.3 ± 243.9 (µmol/L), total GSH, patient: 818.8 ± 156.3 (µmol/L), control: 1028.2 ± 240.1 (µmol/L), p <0.001). In this study, we investigated for the first time the intracellular GSH / GSSG levels with serum trace element level and thiol-disulfide balance in epilepsy patients and found that the balance was significantly increased in favor of GSSG. We think that our data could be a guide to understand the pathogenesis of the disease. Keywords: Epilepsy, ıntracellular glutathion, thiole disulphide, trace elements