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Lithium-pilocarpine status epilepticus in rat: structure-related changes in the brain antioxidant enzyme activities and lipid peroxidation (CROSBI ID 536611)

Prilog sa skupa u časopisu | sažetak izlaganja sa skupa | domaća recenzija

Peternel, Sandra ; Blagaić, Ana ; Pilipović, Kristina ; Hrelja, Ana ; Mršić-Pelčić, Jasenka ; Vitezić, Dinko ; Župan, Gordana Lithium-pilocarpine status epilepticus in rat: structure-related changes in the brain antioxidant enzyme activities and lipid peroxidation // Neurologia Croatica / Ivkić, G ; Judaš, M ; Klarica, M et al. (ur.). 2007. str. 59-59

Podaci o odgovornosti

Peternel, Sandra ; Blagaić, Ana ; Pilipović, Kristina ; Hrelja, Ana ; Mršić-Pelčić, Jasenka ; Vitezić, Dinko ; Župan, Gordana

engleski

Lithium-pilocarpine status epilepticus in rat: structure-related changes in the brain antioxidant enzyme activities and lipid peroxidation

The lithium plus pilocarpine-induced status epilepticus (SE) triggers a cascade of events in the rat brain which leads to later development of spontaneous recurrent seizures resembling human temporal lobe epilepsy. The role of oxidative stress in seizure-induced neurodegeneration in this epilepsy model is not well characterized. Therefore, the aim of our study was to evaluate regional changes in the brain antioxidant enzyme activities as well as the level of lipid oxidative damage 24 hrs after induction of SE in rats. Experiments were performed on 80 to 90 days old male Wistar rats. SE was induced by administration of pilocarpine hydrochloride (30 mg/kg, i.p.) 22 hrs after LiCl (127 mg/kg, i.p) and 30 min after methylscopolamine nitrate (1 mg/kg, s.c.). SE was interrupted 2 hrs after its onset by an injection of diazepam (10 mg/kg, i.p.). Control animals received LiCl, saline and diazepam. Rats were sacrificed 24 hrs after the SE onset. Anterior olfactory nuclei, piriform/entorhinal cortex, temporal neocortex, thalamus and hippocampus were dissected and prepared for biochemical analyses. Regional brain antioxidant defense system was evaluated by spectrophotometric measurements of superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. Levels of the brain lipid peroxidation were determined by thiobarbituric acid reactive substances (TBARS) assay. Lithium plus pilocarpine-induced SE resulted in statistically significant increases of both SOD (20.3%) and GPX (15.7%) activities in thalamus and of GPX activity (29.7%) in piriform/entorhinal cortex. In other brain structures examined, with the exception of hippocampus, a tendency of increase in the activities of both enzymes was observed. The TBARS levels significantly increased in anterior olfactory nuclei (11.8%), piriform/entorhinal cortex (58.3%), temporal neocortex (28.8%) and thalamus (30.1%), but remained unchanged in hippocampus. Lithium-pilocarpine SE results in structure-related activation of the enzymatic antioxidant system and causes extensive oxidative damage of lipids in the rat brain 24 hrs after its onset. Piriform/entorhinal cortex and thalamus are the most vulnerable brain structures in our experimental conditions.

superoxide dismutase; glutathione peroxidase; lipid peroxidation; status epilepticus; rat

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Podaci o prilogu

59-59.

2007.

nije evidentirano

objavljeno

Podaci o matičnoj publikaciji

Neurologia Croatica

Ivkić, G ; Judaš, M ; Klarica, M ; Kostović, I ; Šimić, G, Petanjek, Z

Zagreb:

0353-8842

Podaci o skupu

Hrvatski kongres neuroznanosti (2 ; 2007)

poster

18.05.2007-19.05.2007

Zagreb, Hrvatska

Povezanost rada

Temeljne medicinske znanosti

Indeksiranost