Blood Levels of Trace Elements, Electrolytes, and Oxidative Stress/Antioxidant Systems in Epileptic Patients

Abstract

Abstract. Epileptic patients exhibited variably altered status of trace elements, electrolytes, and free radical scavenging enzyme activities. We investigated the effect of epilepsy and long-term antiepileptic drug therapy on the serum level of some trace elements (zinc, selenium, and copper), electrolytes (calcium, magnesium, sodium, and potassium), and antioxidants (glutathione peroxidase, and uric acid) and plasma levels of lipid peroxidation index (malondialdehyde), total antioxidant capacity, and ceruloplasmin. Seventy epileptic patients and fourteen controls were recruited in this study. In the treated group (particularly with valproate), we reported increases in the levels of zinc, calcium, sodium, malondialdehyde, and glutathione peroxidase and decreases in the levels of copper, total antioxidant capacity, and ceruloplasmin with no difference in selenium, magnesium, and potassium. However among untreated epileptics, uric acid level was increased and total antioxidant capacity was markedly lowered. We conclude that the above parameters balance differs in epileptics comparable to controls and hence their correlation to seizures pathophysiology and their degree of control or resistance to antiepileptic drug therapy. Better regulation of the lipid peroxidation and antioxidants and fewer disturbances in mineral metabolism were observed in monotherapy versus polytherapy and with carbamazepine versus valproate therapy.

The Role of Reactive Species in Epileptogenesis and Influence of Antiepileptic Drug Therapy on Oxidative Stress

“…The role of valproic acid (VPA) in exacerbation of oxidative stress is supported by reduced total antioxidant capacity (TAC) [86, 90] and enhanced total oxidative status (TOS) [90], reported for patients treated with VPA. Erythrocyte GPX [91, 92], GR [93] and serum Se [94], uric acid and albumin [80], which are considered endogenous enzymatic and non-enzymatic antioxidant molecules, were found to be reduced in children and adults treated with VPA.…”

“…Erythrocyte GPX [91, 92], GR [93] and serum Se [94], uric acid and albumin [80], which are considered endogenous enzymatic and non-enzymatic antioxidant molecules, were found to be reduced in children and adults treated with VPA. Furthermore, in studies in patients with epilepsy, treated with VPA, increased levels of oxidative macromolecular damage markers, such as MDA [76, 86, 90, 91] and 15F-2t-isoP [95], which are markers of enhanced lipid peroxidation and increased levels of 8-OHdG [90, 96], which is a marker of nucleic acid damage, were observed. Similarly, enhanced lipid peroxidation [80] and decreased SOD and GPX [92] was seen in studies with phenobarbital.…”

“…The role of carbamazepine (CBZ) in generating free radicals and consequently causing neuronal damage is not so evident. CBZ enhanced plasma LP in adolescent and adult patients [86] and caused marked increase in serum total peroxide levels in children [80]. Lower TAC [86] and GSH [98] in plasma, and GPX and CAT in erythrocytes were also observed [92].…”

“…CBZ enhanced plasma LP in adolescent and adult patients [86] and caused marked increase in serum total peroxide levels in children [80]. Lower TAC [86] and GSH [98] in plasma, and GPX and CAT in erythrocytes were also observed [92]. In accordance with its pro-oxidative action, decreased SOD [92] and increased 8-OHdG [96] and nitrite/nitrate in erythrocytes were also observed.…”

“…In accordance with its pro-oxidative action, decreased SOD [92] and increased 8-OHdG [96] and nitrite/nitrate in erythrocytes were also observed. However, there are also studies which do not confirm CBZ pro-oxidative action [83, 86, 91, 95] and even studies with anti-oxidative action [88, 93, 99]. …”