Antioxidant enzymes in cerebral cortex of immature rats following experimentally-induced seizures: upregulation of mitochondrial MnSOD (SOD2)
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
23238024
DOI
10.1016/j.ijdevneu.2012.11.011
PII: S0736-5748(12)00602-8
Knihovny.cz E-zdroje
- MeSH
- antioxidancia metabolismus MeSH
- krysa rodu Rattus MeSH
- mozková kůra enzymologie MeSH
- oxidační stres MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku metabolismus MeSH
- stárnutí metabolismus MeSH
- superoxiddismutasa metabolismus MeSH
- tkáňová distribuce MeSH
- upregulace MeSH
- záchvaty enzymologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antioxidancia MeSH
- reaktivní formy kyslíku MeSH
- superoxiddismutasa MeSH
- superoxide dismutase 2 MeSH Prohlížeč
We have recently demonstrated the evidence of oxidative stress in brain of immature rats during seizures induced by DL-homocysteic acid (DL-HCA). The aim of the present study was to investigate the antioxidant defense mechanisms under these conditions. Seizures were induced in immature 12-day-old rats by bilateral icv infusion of DL-HCA (600 nmol/side), and the activities of the main antioxidant enzymes were examined in supernatants of the cerebral cortex during the acute phase of seizures and at several periods of survival, up to 5 weeks, following these seizures. In control animals individual antioxidant enzymes revealed different changes during the studied postnatal period (PD 12 till PD 47). Total superoxide dismutase (SOD), CuZn SOD (SOD1), Mn SOD (SOD2) and glutathione peroxidase (GPX) activities were increasing while, catalase activity decreased and the activity of glutathione reductase (GR) remained unchanged. In HCA-treated animals, the activity of total SOD, SOD1 and particularly SOD2 significantly increased at 20 h and 6 days of survival. Importantly, upregulation of SOD2 was also confirmed in mitochondria at the protein level by immunoblotting. The activities of other antioxidant enzymes including catalase and GPX did not significantly differ upon HCA treatment from the appropriate controls at any of the studied time intervals. The pronounced and selective upregulation of SOD2 points to enhanced ROS levels in the mitochondrial matrix. This may be associated with inhibition of respiratory chain complex I that we have demonstrated in our previous studies. The present findings suggest that oxidative stress occurring in the brain of immature rats during and following the seizures induced by DL-HCA is apparently due to both the increased free radical production and the limited antioxidant defense.
Citace poskytuje Crossref.org
Epilepsy Research in the Institute of Physiology of the Czech Academy of Sciences in Prague
