The antioxidant N-acetyl-l-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction associated with status epilepticus

H. J. Sleven; J. E. Gibbs; H. R. Cock

doi:10.1016/j.eplepsyres.2006.01.006

The antioxidant N-acetyl-l-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction associated with status epilepticus

H. J. Sleven, J. E. Gibbs, H. R. Cock

Research output: Contribution to journal › Article › peer-review

Abstract

Hippocampal reduced glutathione (GSH) levels diminish after status epilepticus (SE), which precedes damage to mitochondrial enzymes, which is associated with cell death. The rat perforant pathway stimulation model was used to assess whether intraperitoneal administration of the GSH precursor N-acetyl-l-cysteine (NAC) protected against these changes. NAC (300 mg/kg) treated animals exhibited the same GSH decrease post SE as vehicle treated. Furthermore, NAC treatment had no protective effects on mitochondrial dysfunction. © 2006 Elsevier B.V. All rights reserved.

Original language	English
Pages (from-to)	165-169
Number of pages	4
Journal	Epilepsy Research
Volume	69
Issue number	2
DOIs	https://doi.org/10.1016/j.eplepsyres.2006.01.006
Publication status	Published - May 2006

Keywords

Glutathione
In vivo
N-Acetyl-cysteine
Neuroprotection
Oxidative stress
Status epilepticus

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10.1016/j.eplepsyres.2006.01.006

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title = "The antioxidant N-acetyl-l-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction associated with status epilepticus",

abstract = "Hippocampal reduced glutathione (GSH) levels diminish after status epilepticus (SE), which precedes damage to mitochondrial enzymes, which is associated with cell death. The rat perforant pathway stimulation model was used to assess whether intraperitoneal administration of the GSH precursor N-acetyl-l-cysteine (NAC) protected against these changes. NAC (300 mg/kg) treated animals exhibited the same GSH decrease post SE as vehicle treated. Furthermore, NAC treatment had no protective effects on mitochondrial dysfunction. {\textcopyright} 2006 Elsevier B.V. All rights reserved.",

keywords = "Glutathione, In vivo, N-Acetyl-cysteine, Neuroprotection, Oxidative stress, Status epilepticus",

author = "Sleven, {H. J.} and Gibbs, {J. E.} and Cock, {H. R.}",

note = ", Wellcome Trust, United Kingdom",

year = "2006",

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AU - Gibbs, J. E.

AU - Cock, H. R.

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AB - Hippocampal reduced glutathione (GSH) levels diminish after status epilepticus (SE), which precedes damage to mitochondrial enzymes, which is associated with cell death. The rat perforant pathway stimulation model was used to assess whether intraperitoneal administration of the GSH precursor N-acetyl-l-cysteine (NAC) protected against these changes. NAC (300 mg/kg) treated animals exhibited the same GSH decrease post SE as vehicle treated. Furthermore, NAC treatment had no protective effects on mitochondrial dysfunction. © 2006 Elsevier B.V. All rights reserved.

KW - Glutathione

KW - In vivo

KW - N-Acetyl-cysteine

KW - Neuroprotection

KW - Oxidative stress

KW - Status epilepticus

U2 - 10.1016/j.eplepsyres.2006.01.006

DO - 10.1016/j.eplepsyres.2006.01.006

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SN - 0920-1211

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SP - 165

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JO - Epilepsy Research

JF - Epilepsy Research

IS - 2

ER -

The antioxidant N-acetyl-l-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction associated with status epilepticus

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Keywords

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