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Updated: Aug 11, 2026

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
The antioxidant N-acetyl-L-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction
H J Sleven1, J E Gibbs, H R Cock
1Epilepsy Group, Centre for Clinical Neurosciences, St. Georges, University of London, Cranmer Terrace, Tooting, London SE1 0RE, UK.
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.
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