Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus (癲癇持續狀態) in the rat hippocampus [2006](IR91)

Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus (癲癇持續狀態) in the rat hippocampus [2006](IR91)

Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus (癲癇持續狀態) in the rat hippocampus [2006](IR91)

穀胱甘肽

Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic (邊緣的) status epilepticus (癲癇持續狀態) in the rat hippocampus (海馬（大腦中被認為是感情和記憶中心的部分)).

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(Memo Item created on November 4, 2009 04:12 PM)
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Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus in the rat hippocampus.

http://highwire.stanford.edu/cgi/medline/pmid;16290321?maxtoshow=&HITS=&hits=&RESULTFORMAT=1&andorexacttitle=and&fulltext=glutathione%2C+depletion%2C+epilepsy&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT

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Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus in the rat hippocampus.

H Sleven, JE Gibbs, S Heales, M Thom, and HR Cock
Neurochem Int, January 1, 2006; 48(2): 75-82.    

Abstract

Epilepsy Group, Centre for Clinical Neurosciences, St. George's, University of London, Cranmer Terrace, London SW17 0RE, UK.

The time course and critical determinants of mitochondrial dysfunction and oxidative stress following limbic status epilepticus (SE) were investigated in hippocampal sub-regions of an electrical stimulation model in rats, at time points 4-44h after status. Mitochondrial and cytosolic enzyme activities were measured spectrophotometrically, and reduced glutathione (穀胱甘肽) (GSH) concentrations by HPLC, and compared to results from sham controls. The earliest change in any sub-region was a fall in GSH, appearing as early as 4h in CA3 (-13%, p<0.05), and persisting at all time points. This was followed by a transient fall in complex I activity (CA3, 16h, -13%, p<0.05), and later changes in aconitase (CA1,-18% and CA3, -22% at 44h, p<0.05). The activity of the cytosolic enzyme glyceraldehyde-3-phosphate-dehydrogenase was unaffected at all time points. It is known that GSH levels are dependent both on redox status, and on the availability of the precursor cysteine, in turn dependent on the cysteine/glutamate antiporter, for which extracellular glutamate concentrations are rate limiting. Both mechanisms are likely to contribute indirectly to GSH Depletion (耗盡) following seizures. That a relative deficiency in GSH precedes later changes in the activities of complex I and aconitase in vulnerable hippocampal sub-regions, occurring within a clinically relevant therapeutic time window, suggests that strategies to boost GSH levels and/or otherwise reduce oxidative stress following seizures, deserve further study, both in terms of preventing the biochemical consequences of SE and the neuronal dysfunction and clinical consequences.

Publication Types:

Journal article
Research support, non-u.s. gov't
MeSH Terms:

Animals
Chromatography, High Pressure Liquid
Electric Stimulation
Electroencephalography
glutathione (穀胱甘肽)
Male
Mitochondria
Rats
Rats, Sprague-Dawley
Status Epilepticus
PMID: 16290321

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