Erythrocyte Glutathione, Glutathione Peroxidase, Superoxide Dismutase and Serum Lipid Peroxidation in Epileptic Children With Valproate and Carbamazepine Monotherapy

Yüksel, Adnan; Cengiz, Müjgan; Seven, Mehmet; Ulutin, Turgut

doi:10.1515/jbcpp.2000.11.1.73

Cited by 69 publications

(82 citation statements)

References 20 publications

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“…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.…”

Section: Antiepileptic Drug Therapy and Oxidative Stressmentioning

confidence: 99%

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

Martinc

Grabnar²,

Vovk³

2012

Current Neuropharmacology

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Epilepsy is considered one of the most common neurological disorders. The focus of this review is the acquired form of epilepsy, with the development process consisting of three major phases, the acute injury phase, the latency epileptogenesis phase, and the phase of spontaneous recurrent seizures. Nowadays, an increasing attention is paid to the possible interrelationship between oxidative stress resulting in disturbance of physiological signalling roles of calcium and free radicals in neuronal cells and mitochondrial dysfunction, cell damage, and epilepsy. The positive stimulation of mitochondrial calcium signals by reactive oxygen species and increased reactive oxygen species generation resulting from increased mitochondrial calcium can lead to a positive feedback loop. We propose that calcium can pose both, physiological and pathological effects of mitochondrial function, which can lead in neuronal cell death and consequent epileptic seizures. Various antiepileptic drugs may impair the endogenous antioxidative ability to prevent oxidative stress. Therefore, some antiepileptic drugs, especially from the older generation, may trigger oxygen-dependent tissue injury. The prooxidative effects of these antiepileptic drugs might lead to enhancement of seizure activity, resulting in loss of their efficacy or apparent functional tolerance and undesired adverse effects. Additionally, various reactive metabolites of antiepileptic drugs are capable of covalent binding to macromolecules which may lead to deterioration of the epileptic seizures and systemic toxicity. Since neuronal loss seems to be one of the major neurobiological abnormalities in the epileptic brain, the ability of antioxidants to attenuate seizure generation and the accompanying changes in oxidative burden, further support an important role of antioxidants as having a putative antiepileptic potential.

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Section: Antiepileptic Drug Therapy and Oxidative Stressmentioning

confidence: 99%

“…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]. …”

Section: Antiepileptic Drug Therapy and Oxidative Stressmentioning

confidence: 99%

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

Martinc

Grabnar²,

Vovk³

2012

Current Neuropharmacology

View full text Add to dashboard Cite

show abstract

“…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.…”

Section: Influence Of Aeds On Antioxidants and Markers Of Oxidative Smentioning

confidence: 99%

“…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 prooxidative action [83,86,91,95] and even studies with antioxidative action [88,93,99].…”

Section: Influence Of Aeds On Antioxidants and Markers Of Oxidative Smentioning

confidence: 99%

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

Martinc¹,

Grabnar²,

Vovk³

2012

Current Neuropharmacology

View full text Add to dashboard Cite

Abstract:Epilepsy is considered one of the most common neurological disorders. The focus of this review is the acquired form of epilepsy, with the development process consisting of three major phases, the acute injury phase, the latency epileptogenesis phase, and the phase of spontaneous recurrent seizures. Nowadays, an increasing attention is paid to the possible interrelationship between oxidative stress resulting in disturbance of physiological signalling roles of calcium and free radicals in neuronal cells and mitochondrial dysfunction, cell damage, and epilepsy. The positive stimulation of mitochondrial calcium signals by reactive oxygen species and increased reactive oxygen species generation resulting from increased mitochondrial calcium can lead to a positive feedback loop. We propose that calcium can pose both, physiological and pathological effects of mitochondrial function, which can lead in neuronal cell death and consequent epileptic seizures. Various antiepileptic drugs may impair the endogenous antioxidative ability to prevent oxidative stress. Therefore, some antiepileptic drugs, especially from the older generation, may trigger oxygen-dependent tissue injury. The prooxidative effects of these antiepileptic drugs might lead to enhancement of seizure activity, resulting in loss of their efficacy or apparent functional tolerance and undesired adverse effects. Additionally, various reactive metabolites of antiepileptic drugs are capable of covalent binding to macromolecules which may lead to deterioration of the epileptic seizures and systemic toxicity. Since neuronal loss seems to be one of the major neurobiological abnormalities in the epileptic brain, the ability of antioxidants to attenuate seizure generation and the accompanying changes in oxidative burden, further support an important role of antioxidants as having a putative antiepileptic potential.

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“…Clinical data has shown that melatonin has an antioxidant activity in epileptic patients on carbamazepine (CBZ) (Gupta et al, 2004(Gupta et al, , 2006. Increased oxidative stress and disturbance of the endogenous antioxidant system can aggravate seizure activity (Yüksel et al, 2000). On the other hand, data has shown that the metabolites of several AEDs behave as pro-oxidant agents with toxic effects (Graf et al, 1998;Niketic et al, 1995;Yüksel et al, 2000).…”

Section: Melatonin and Epilepsymentioning

confidence: 99%

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

Tchekalarova

Moyanova

Fusco

et al. 2015

Brain Research Bulletin

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Abstract\ud \ud There is emerging evidence of the beneficial role of the melatonin system in a wide range of psychiatric and neurologic disorders, including anxiety, depression, and epilepsy. Although melatoninergic drugs have chronobiotic and antioxidant properties that positively influence circadian rhythm desynchronization and neuroprotection in neurodegenerative disorders, studies examining the use of melatonin for epilepsy's comorbid psychiatric and neurological symptomatology are still limited. Preclinical and clinical findings on the beneficial effects of the melatonin system on anxiety, depression, and epilepsy suggest that melatoninergic compounds might be effective in treating comorbid behavioral complications in epilepsy beyond regulation of a disturbed sleep-wake cycle

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Erythrocyte Glutathione, Glutathione Peroxidase, Superoxide Dismutase and Serum Lipid Peroxidation in Epileptic Children With Valproate and Carbamazepine Monotherapy

Cited by 69 publications

References 20 publications

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

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

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

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

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