Trace Elements and Electrolytes Homeostasis and Their Relation to Antioxidant Enzyme Activity in Brain Hyperexcitability of Epileptic Patients

Hamed, Sherifa A.; Abdellah, Moustafa M.

doi:10.1254/jphs.crj04004x

Cited by 62 publications

(54 citation statements)

References 92 publications

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“…Because epileptic seizures induce neurodegeneration in selected areas of brain it is suspected that metals may be involved in the pathogenesis and progress of epilepsy as well [5].…”

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confidence: 99%

The role of trace elements in the pathogenesis and progress of pilocarpine-induced epileptic seizures

et al. 2008

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Epilepsy, the third most common neurological disorder, is characterized by recurrent unprovoked seizures. Although the mechanisms of epileptic convulsions have been a subject of intensive investigations for many years in most cases the etiology of the disease is not known [1].Metallic elements participating in the processes like: oxidative stress, excitotoxicity, mitochondrial dysfunction or protein aggregation may lead to the atrophy and death of neurons in case of some neurodegenerative disorders [2][3][4]. Because epileptic seizures induce neurodegeneration in selected areas of brain it is suspected that metals may be involved in the pathogenesis and progress of epilepsy as well [5].Existing evidence suggests that epileptic seizures significantly change metabolism and distribution of trace elements in the nervous tissue [6][7][8]. From the other hand, content of metals determinates susceptibility to convulsions [9].In our experiment we used pilocarpine in order to induce epilepsy in rats. In order to find what elements are involved in the pathogenesis and progress of epileptic convulsions the comparison between pilocarpine treated and control rats was done. The samples of rat brain were cut using a cryomicrotome into 15 µm thick slices. Thin tissue sections were mounted on Ultralene foil and freeze-dried.X-ray fluorescence microscopy was employed for topographic and quantitative analysis of selected metals in the areas of brain tissue involved in epilepsy. The measurements were done on the bending magnet beamline L at HASYLAB. The multilayer monochromator was applied and the primary photon energy was set to 17 keV. The beam was focused with polycapillary optics for a final beam spot dimension of 15 µm x 15 µm. The characteristic X-ray lines were measured using the Vortex SDD detector from SII Nano Technology USA inc. and the time of spectra acquisition was equal to 6 s per pixel. Measurements of NIST standard reference materials (SRM 1833 and SRM 1832) were performed for spectrometer calibration.The elements such us P, S, Cl, K, Ca, Fe, Cu, Zn, Br, Rb and Sr were detected in rat brain sections. For each sample two-dimensional analysis of elemental distribution was performed for the area of hippocampus and brain cortex. The results of such analysis for selected control and epileptic sample were shown in Figures 1 and 2 respectively.For four regions of hippacampus formation (CA1 -Cornu Ammonis, CA3, DG -Dentate Gyrus and H -Hilus) and motor cortex the mean masses per unit area were evaluated. The areas taken into account in calculations were equal to 300 µm per 300 µm. The preliminary results showed that the level of Ca tends to be higher for CA1 region of hippocampus and cortex in case of animals with pilocarpine induced epilepsy. The opposite relation was observed for Zn level in the area of DG.1551

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“…Because epileptic seizures induce neurodegeneration in selected areas of brain it is suspected that metals may be involved in the pathogenesis and progress of epilepsy as well [5].…”

mentioning

confidence: 99%

The role of trace elements in the pathogenesis and progress of pilocarpine-induced epileptic seizures

et al. 2008

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“…Hyperuricemia has been recently reported among epileptics (untreated and treated) (7,26). Despite controversies regarding uric acid being a risk factor for vascular diseases, uric acid has been implicated in vascular endothelial cell dysfunction.…”

Section: C) Uric Acid Metabolism In Epilepticsmentioning

confidence: 99%

“…The tendency to have recurrent, unprovoked seizures occurs with a prevalence of about 0.5% and a cumulative lifetime prevalence of 3% (1). Many studies have demonstrated that prolonged treatment with antiepileptic drugs (AEDs) could have some undesirable metabolic side effects including elevated plasma concentration of homocysteine (Hcy) (2 -4) and altered serum levels of cholesterol, lipoproteins (5,6), and uric acid (7). These findings have important clinical relevance to vascular endothelial dysfunction and atherosclerosis-related diseases.…”

Section: Introductionmentioning

confidence: 99%

The High Atherosclerotic Risk Among Epileptics: the Atheroprotective Role of Multivitamins

Hamed

Nabeshima

2005

J Pharmacol Sci

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Abstract. Neurologists have little concern about the high atherosclerotic risk among epileptics. Recent evidences mount that chronic epilepsy and prolonged use of antiepileptic drugs (AEDs) are associated with multiple risk factors that are critically implicated in pathobiology and dysfunction of the vessel wall through complex molecular mechanisms that promote atherogenesis. This review is concerned with three metabolic alterations, which are attributed as major risk factors for atherosclerosis among epileptics: altered metabolism of a) homocysteine (Hcy), b) lipids and lipoproteins, and c) uric acid. Most conventional AEDs reduce folic acid levels, thereby raising Hcy levels. Hyperhomosysteinemia is recently believed to induce endothelial dysfunction and promote atherosclerosis through complex oxidative and excitatory neurotoxic molecular mechanisms. However, Hcy itself is a convulsing substance with increased seizure recurrence and intractability to antiepileptic medications. AEDs can disturb lipid metabolism with resultant hypercholestrolemia and dyslipidemia, common recognized risks for atherosclerosis. Altered uric acid metabolism is common among epileptics. Uric acid has been implicated in endothelial cell damage and decreased endothelial nitric oxide bioavailability. In the presence of atherosclerotic milieu, uric acid interacts with other substrate toxicities and increased reactive oxygen species, accelerating atherosclerosis. The above information forms the rationale for future routine screening and correction of such metabolic alterations in epileptics. A convincing argument now develops that routine polyvitamin supplementation (folic acid, vitamin B12, vitamin B6, vitamin C, vitamin E, and β-carotene) becomes increasingly important for women and men receiving AEDs at all ages. The atheroprotective effect of multivitamins is through their antioxidant and anti-inflammatory effects together with their lipid and Hcy lowering effects.

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“…In addition, epilepsy may be associated with neurodegeneration, presumably due to abnormal lipid peroxidation. 1,2 On the other hand, comorbid depression is common in patients with epilepsy. A review of available studies 3 suggested a high prevalence of mood (affective) disorders, especially major depression (8%-48%), followed by anxiety (5%-32%), in patients with epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Combination of valproate and paroxetine in mice exposed to picrotoxin

Kamal¹

2012

IJN

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Abstract:The frequent coexistence of depression in epileptic patients raises the issue of simultaneous use of antidepressants along with antiepileptic drugs in the management of such cases. However, it is necessary to evaluate the safety of these antiepileptic/antidepressant drug combinations. The present study investigates the effect of the antidepressant paroxetine (a selective serotonin reuptake inhibitor) administered alone or in combination with the antiepileptic drug sodium valproate on chemoconvulsions induced by picrotoxin (PTX). Seizure score was recorded in vivo, and the levels of thiobarbituric acid-reactive substances and gamma aminobutyric acid (GABA) were measured in the nucleus accumbens of the tested groups of mice. The results show enhancement of seizure severity with significant reduction in GABA levels upon PTX treatment that were reversed by its combination with sodium valproate. On the other hand, paroxetine administered in combination with sodium valproate provided significant protection against PTX-induced convulsions as well as a significant increase in GABA levels in selected brain areas. These results favor their application in management of epilepsy-depression comorbidities.

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Trace Elements and Electrolytes Homeostasis and Their Relation to Antioxidant Enzyme Activity in Brain Hyperexcitability of Epileptic Patients

Cited by 62 publications

References 92 publications

The role of trace elements in the pathogenesis and progress of pilocarpine-induced epileptic seizures

The role of trace elements in the pathogenesis and progress of pilocarpine-induced epileptic seizures

The High Atherosclerotic Risk Among Epileptics: the Atheroprotective Role of Multivitamins

Combination of valproate and paroxetine in mice exposed to picrotoxin

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