Glutathione peroxidase deficiency and childhood seizures

Weber, Georg F.; Maertens, Paul; Meng, Xianzhong; Pippenger, C. E.

doi:10.1016/0140-6736(91)93130-2

Cited by 114 publications

(59 citation statements)

References 3 publications

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“…The possibility exists that several of these cases may be influenced by genetic differences in genes involved in selenium metabolism. Indeed, in some cases selenium supplementation has been reported to attenuate pediatric epilepsy (39,40). This uniquely parallels the finding that the neurological phenotype of Sepp1 Ϫ/Ϫ mice can be mitigated by selenium supplementation.…”

Section: Sepp1supporting

confidence: 60%

Mice Lacking Selenoprotein P and Selenocysteine Lyase Exhibit Severe Neurological Dysfunction, Neurodegeneration, and Audiogenic Seizures

Byrns¹,

Pitts²,

Gilman

et al. 2014

Journal of Biological Chemistry

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Section: Sepp1supporting

confidence: 60%

Mice Lacking Selenoprotein P and Selenocysteine Lyase Exhibit Severe Neurological Dysfunction, Neurodegeneration, and Audiogenic Seizures

Byrns¹,

Pitts²,

Gilman

et al. 2014

Journal of Biological Chemistry

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“…It has been suggested that, an increase in free radicals may cause neuronal degeneration through membrane lipid peroxidation and a decrease in GSH-Px level (21, 55). GSH-Px deficiency is suggested to be a cause of childhood seizures (56). In an experimental study, any increase in lipid peroxide levels in the epileptic focus was found to be prevented by antioxidant treatment in epileptic rats, thereby resulting in a decreased number of epileptic discharges (57,58).…”

Section: Relation Of Lipid Peroxidation and Antioxidant System To Neumentioning

confidence: 95%

“…Weber et al (56), described 4 children with intractable seizures, repeated infections, and intolerance to anticonvulsants with evidence of glutathione peroxidase deficiency. Two had low intracellular enzyme activity but normal blood selenium and high plasma GSH-Px concentrations.…”

Section: Relation Of Lipid Peroxidation and Antioxidant System To Neumentioning

confidence: 99%

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

Hamed

Abdellah

2004

J Pharmacol Sci

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Abstract. Epileptogenesis is a big challenge. Various experimental and human studies suggested that the homeostasis of trace elements, electrolytes, membrane lipid peroxidation, and antioxidants is crucial for brain function, and they were directly or indirectly implicated as taking part in the pathophysiology of neuronal excitability, neuronal excitotoxicity, and seizure recurrence and its resistance to treatment with antiepileptic drugs (AEDs). In addition, AEDs can also alter the homeostasis of trace elements, electrolytes, and seriously increase membrane lipid peroxidation at the expense of protective antioxidants, leading to an increase in seizure recurrence and an idiosyncratic drug effect. Differential effects were detected among different AEDs treatments in which carbamazepine (CBZ) was found to be better anticonvulsant for the control of free radical related seizures and the level of trace elements were better regulated with CBZ than with valproate (VPA) and phenytoin (PHT) therapies. It is concluded that adequate trace elements and antioxidants supply is important for brain functions and prevention of neurological diseases and further elucidation of the pathological actions of such substances in the brain should result in new therapeutic approaches. Trace elements and antioxidant might have neuroprotective biological targeted benefits when used in epileptic patients.

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“…There are a number of indications that Se is important to the brain:-during Se depletion the brain receives a priority supply; 36 the turnover rate of some neurotransmitters is altered in Se deficiency; 37 supplementation with Se reduced intractable epileptic seizures in children; 38,39 low plasma Se levels in the elderly were found to be significantly associated with senility and accelerated cognitive decline; 36,40 brain Se concentration in Alzheimer's patients was only 60% of that in controls. 36 Furthermore, the brain is deficient in catalase, 39 thus peroxidation products such as H 2 O 2 and primary peroxides must be removed by the antioxidant selenoenzymes.…”

Section: Moodmentioning

confidence: 99%