The antioxidant N-acetyl-L-cysteine does not prevent hippocampal glutathione loss or mitochondrial dysfunction associated with status epilepticus.
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.
Sleven
H J
HJ
Epilepsy Group, Centre for Clinical Neurosciences, St. Georges, University of London, Cranmer Terrace, Tooting, London SE1 0RE, UK.
Gibbs
J E
JE
Cock
H R
HR
D000111:Acetylcysteine / Q000627:therapeutic use*; D000704:Analysis of Variance; D000818:Animals; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000201:enzymology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000188:drug therapy* / Q000378:metabolism
D016166:Free Radical Scavengers; D005978:Glutathione; D000111:Acetylcysteine