Thiol redox state and lipid and protein oxidation in the mouse striatum after pentylenetetrazol-induced epileptic seizure.
OBJECTIVE
In the present study, we examined the effects of pentylenetetrazol (PTZ) administration on the thiol redox state (TRS), lipid peroxidation, and protein oxidation in the mouse striatum to (a) quantitate the major components of TRS and relate them to oxidative stress, and (b) investigate whether neuronal activation without synchronization, induced by subconvulsive doses of PTZ, can cause similar qualitative effects on TRS in this brain area. Specifically, we examined the TRS components glutathione (GSH), glutathione disulfide (GSSG), cysteine (CSH), protein thiols (PSH), and the protein (P) and nonprotein (NP/R) disulfides PSSR, NPSSR, NPSSC, and PSSP.


METHODS
TRS components were measured photometrically (GSSG enzymatically) as were lipid peroxidation and protein oxidation.


RESULTS
GSH, GSSG, and NPSSC levels are decreased by 45%, 38% and 26%, respectively, at 15 min after seizure; PSSP and PSSR levels and lipid peroxidation are increased by 47%, 200% and 22%, respectively, whereas CSH, NPSSR, PSH, PSSC, and protein carbonyl levels do not change. At 30 min after seizure, GSH, GSSG, CSH, NPSSC, and protein carbonyl levels are decreased by 26%, 62%, 25%, 40%, and 13%, respectively. PSSP and NPSSR levels are increased by 30% and 42%, respectively, whereas PSH, PSSC, PSSR, and lipid peroxidation remain unchanged. At 24 h after seizure, GSH, NPSSR, PSSR, and lipid-peroxidation levels return to normal; GSSG, CSH, NPSSC, and protein carbonyl levels are decreased by 44%, 22%, 30%, and 27%, respectively.


CONCLUSIONS
The significant decrease in GSH, GSSG, CSH, and NPSSC and the increase in PSSP, NPSSR, PSSR, and lipid peroxidation after PTZ-induced seizure strongly suggest increased oxidative stress in the mouse striatum.
Patsoukis
Nikolaos
N
Department of Biology, University of Patras, Patras, Greece.
Zervoudakis
George
G
Georgiou
Christos D
CD
Angelatou
Fevronia
F
Matsokis
Nikolaos A
NA
Panagopoulos
Nikolaos T
NT
D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism*; D003545:Cysteine / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004220:Disulfides / Q000378:metabolism; D004827:Epilepsy / Q000139:chemically induced*; D005978:Glutathione / Q000187:drug effects / Q000378:metabolism; D050356:Lipid Metabolism; D015227:Lipid Peroxidation; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010433:Pentylenetetrazole / Q000494:pharmacology; D013438:Sulfhydryl Compounds / Q000378:metabolism*; D013997:Time Factors
D004220:Disulfides; D009419:Nerve Tissue Proteins; D013438:Sulfhydryl Compounds; D005978:Glutathione; D003545:Cysteine; D010433:Pentylenetetrazole