We examined the immunocytochemical distribution of mitochondrial Mn- superoxide dismutase (SOD-2) in the rat hippocampus after systemic injection of kainic acid (KA), in order to understand SOD-2-responsible antioxidant defense mechanism during the neurodegenerative process. SOD-2 immunostaining was more intense in CA3 pyramidal neurons than in CA1 neurons in the normal hippocampus. The immunoreactivity in region CA1 was reduced without significant neuronal losses within 12 h of KA injection. The CA1 and CA3 neurons lost their immunoreactivity, whereas SOD-2-positive glia-like cells proliferated, mainly throughout the CA1 sector, and had intense immunoreactivity 3 and 7 days after KA injection. This immunocytochemical distribution of SOD-2-positive non-neuronal elements was similar to that of glial fibrillary acidic protein (GFAP) and S-100 protein-positive cells. Activated microglial cells selectively marked with lectin occurred in the areas affected by the KA-induced lesion. Double-labeling immunocytochemistry showed the co-localization of SOD-2-positive non-neuronal cells and GFAP or S-100 protein-like immunoreactivity in the same cells. This suggests that astroglial cells mobilized to synthesize of SOD-2 protein in a response to KA toxicity designed to reduce the oxidative damage. (C) 2000 Elsevier Science Ireland Ltd.
Bibliographical noteFunding Information:
This study was supported by a grant (# HMP-98-N-2-0013) of the Good Health Research and Development Project (1998) of Ministry of Health and Welfare, Republic of Korea.
- Free radicals
- Kainic acid
- Mitochondrial Mn-superoxide dismutase
ASJC Scopus subject areas
- General Neuroscience