Effect of pentylenetetrazol-induced epileptic seizure on thiol redox state in the mouse cerebral cortex

• Published in: Epilepsy research 2004-11, Vol.62 (1), p.65-74
• Main Authors: Patsoukis, Nikolaos, Zervoudakis, George, Georgiou, Christos D., Angelatou, Fevronia, Matsokis, Nikolaos A., Panagopoulos, Nikolaos T.
• Format: Article
• Language: English
• Subjects: Animals; Anticonvulsants. Antiepileptics. Antiparkinson agents; Biological and medical sciences; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Convulsants; Disulfides - metabolism; Epilepsy - chemically induced; Epilepsy - metabolism; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Investigative techniques, diagnostic techniques (general aspects); Left-right cerebral cortex; Lipid peroxidation; Lipid Peroxidation - drug effects; Male; Medical sciences; Mice; Mice, Inbred BALB C; Nerve Tissue Proteins - metabolism; Nervous system; Nervous system (semeiology, syndromes); Neurology; Neuropharmacology; Oxidation-Reduction; Oxidative stress; Pentylenetetrazol; Pentylenetetrazole; Pharmacology. Drug treatments; Protein oxidation; Radiodiagnosis. Nmr imagery. Nmr spectrometry; Sulfhydryl Compounds - metabolism; Thiol redox state
• ISSN: 0920-1211; 1872-6844
• DOI: 10.1016/j.eplepsyres.2004.08.005

In the present study we examined the effects of pentylenetetrazol (PTZ) administration on the thiol redox state (TRS), lipid peroxidation and protein oxidation in left and right mouse cerebral cortex in order (a) to quantitate the major components of the thiol redox state and relate them with oxidative stress and cortical laterality, and (b) to investigate whether neuronal activation without synchronization, induced by subconvulsive doses of PTZ, can cause similar qualitative effects on the thiol redox state. Specifically, we examined the TRS components [glutathione (GSH), glutathione disulfide (GSSG), cysteine (CSH), protein (P) thiols (PSH) and protein and non-protein (NP) mixed/symmetric disulfides (PSSR, NPSSR, NPSSC, PSSP)]. At 15 min after seizure, GSH, GSSG, CSH, NPSSC, PSSR and PSSC levels are decreased in left (14–50%) and right (11–53%) cortex while PSSP levels are increased in both left (1400%) and right (1600%) cortex. At 30 min after seizure, GSSG, CSH, NPSSC, PSSR and PSSC levels are decreased in left (14–51%) and right (18–56%) cortex while PSSP and protein carbonyl levels are increased in left (2300% and 20%, respectively) and right (2800% and 21%, respectively) cortex. At 24 h after seizure, the TRS components return to normal and protein carbonyl levels are decreased in left (16%) and right (20%) cortex. The significant decrease in GSH, GSSG, CSH, NPSSC, PSSR and PSSC, as well as the increase in protein carbonyl and the high increase in PSSP levels after PTZ-induced seizure indicate increased oxidative stress in cerebral cortex of mice, and of similar magnitude and TRS-component profiles between left and right cerebral cortex.