Selenium and Intractable Epilepsy: Is There Any Correlation?

Ashrafi, Mahmoud Reza; Shabanian, Reza; Abbaskhanian, Ali; Nasirian, Abolfazl; Ghofrani, Mohammad; Mohammadi, Mohammad; Zamani, Gholamreza; Kayhanidoost, Zarrin; Ebrahimi, Sara Honarmand; Pourpak, Zahra

doi:10.1016/j.pediatrneurol.2006.09.001

Cited by 57 publications

(47 citation statements)

References 23 publications

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“…Oxidative stress and generation of ROS are strongly implicated in a number of neurological conditions including seizure disorders [39,40]. Increased oxidative stress has also been reported in rat cerebellum and cerebral cortex in a model of 3-mercaptopropionic acid-induced epilepsy [41].…”

Section: Oxidative Stress and Epilepsymentioning

confidence: 99%

“…If a strong antioxidant defense system is present in the cells, they will be protected from the damaging effects of ROS by the antioxidant. However, when the system is overused or chronically activated beyond its normal state, such as in the case of recurrent or intractable seizures, abnormal increases in byproducts can produce neuronal cell damage [39,40]. Recent evidence reported increased formation of protein nitrotyrosine as a marker of ONOO -accumulation during central nervous system hyperbaric oxygen exposure [42].…”

Section: Oxidative Stress and Epilepsymentioning

confidence: 99%

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Role of Selenium on Calcium Signaling and Oxidative Stress-induced Molecular Pathways in Epilepsy

2009

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Epilepsy is one of the oldest neurological conditions known to humankind. It is known that oxidative stress and generation of reactive oxygen species are a cause and consequence of epileptic seizures. Although recent years have seen tremendous progress in the molecular biology and metabolism of selenium, we still know little about the cell type-specific and temporal pattern of selenium and its derivatives in the brain of epileptic humans and experimental animals. It has been suggested that some antiepileptic drug therapies such as valproic acid, deplete the total body selenium level and selenium-dependent glutathione peroxidase (GSH-Px) activity although therapy with a new epileptic drug, topiramate, activated GSH-Px activity in epileptic animals and humans. An observation of lower blood or tissue selenium level and GSH-Px activity in epileptic patients and animals compared to controls in recent publications may support the proposed crucial role of selenium level and GSH-Px activity in the pathogenesis of epilepsy. Selenium is incorporated into an interesting class of molecules known as selenoproteins that contain the modified amino acid, selenocysteine. There are signs of selenium and selenoprotein deficiency in the pathogenesis of epilepsy. In conclusion, there is convincing evidence for the proposed crucial role of selenium and deficiency of GSH-Px enzyme activity in epilepsy pathogenesis. Blood GSH-Px activities could be a reliable indicator of selenium deficiency in patients with epilepsy.

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Section: Oxidative Stress and Epilepsymentioning

confidence: 99%

Section: Oxidative Stress and Epilepsymentioning

confidence: 99%

Role of Selenium on Calcium Signaling and Oxidative Stress-induced Molecular Pathways in Epilepsy

2009

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“…It has been found that epileptic patients, without medication, have lower blood and tissue levels of selenium in addition to lower levels of selenoproteins and lower levels of selenium-dependent redox enzymes. In particular, intractable epileptics have been shown to have significantly lower mean serum selenium levels compared to a control group (Ashrafi, Shabanian et al 2007). Animal models have shown that selenium can prevent the development of iron-induced epileptic symptoms due to selenium's ability to combat peroxidative injury (Rubin and Willmore 1980;Willmore and Rubin 1981).…”

Section: The Se-dependent Glutathione Peroxidasementioning

confidence: 99%

Epilepsy: Selenium and Aging

Rocourt¹,

Yu²,

Cheng³

2011

Clinical and Genetic Aspects of Epilepsy

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“…The resulting selenocysteyl-tRNA [Ser]Sec molecule is a provider of Sec into the growing polypeptide chain. The Sec residue can be incorporated in the N-terminal or C-terminal region [10]. [23].…”

Section: Introductionmentioning

confidence: 99%

Selenium in the therapy of neurological diseases. Where is it going?

Dominiak¹,

Wilkaniec²,

Wroczyński³

et al. 2015

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Selenium ( 34 Se), an antioxidant trace element, is an important regulator of brain function. These beneficial properties that Se possesses are attributed to its ability to be incorporated into selenoproteins as an amino acid. Several selenoproteins are expressed in the brain, in which some of them, e.g. glutathione peroxidases (GPxs), thioredoxin reductases (TrxRs) or selenoprotein P (SelP), are strongly involved in antioxidant defence and in maintaining intercellular reducing conditions. Since increased oxidative stress has been implicated in neurological disorders, including Parkinson's disease, Alzheimer's disease, stroke, epilepsy and others, a growing body of evidence suggests that Se depletion followed by decreased activity of Se-dependent enzymes may be important factors connected with those pathologies. Undoubtedly, the remarkable progress that has been made in understanding the biological function of Se in the brain has opened up new potential possibilities for the treatment of neurological diseases by using Se as a potential drug. However, further research in the search for optimal Se donors is necessary in order to achieve an effective and safe therapeutic income.

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Selenium and Intractable Epilepsy: Is There Any Correlation?

Cited by 57 publications

References 23 publications

Role of Selenium on Calcium Signaling and Oxidative Stress-induced Molecular Pathways in Epilepsy

Role of Selenium on Calcium Signaling and Oxidative Stress-induced Molecular Pathways in Epilepsy

Epilepsy: Selenium and Aging

Selenium in the therapy of neurological diseases. Where is it going?

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