Changes of hippocampal Cu/Zn-superoxide dismutase after kainate treatment in the rat

Hyoung Chun Kim, Guoying Bing, Wang Kee Jhoo, Kwang Ho Ko, Won Ki Kim, Jeong Hye Suh, Seong Jin Kim, Kanefusa Kato, Jau Shyong Hong

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51 Citations (Scopus)


In order to evaluate the putative role of Cu,Zn-superoxide dismutase (SOD-1) in the antioxidant defense mechanism during the neurodegenerative process, we examined the level of mRNA, the specific activity and immunocytochemical distribution for SOD-1 in the rat hippocampus after systemic injection of kainic acid (KA). Hippocampal SOD-1 mRNA levels were significantly increased by the seizure intensity 3 and 7 days after KA. These enhanced mRNA levels for SOD-1 were consistent with the increased specific activities for SOD-1, suggesting that the superoxide radical generated in neurotoxic lesion, induced SOD-1 mRNA. The CA1 and CA3 neurons lost their SOD-1-like immunoreactivity, whereas SOD-1-positive glia-like cells mainly proliferated throughout the CA1 sector and had an intense immunoreactivity at 3 and 7 days after KA. This immunocytochemical distribution for SOD-1-positive non-neuronal elements was similar to that for glial fibrillary acidic protein (GFAP)-positive cells. Each immunoreactivity for SOD-1-positive non-neuronal cell or GFAP in the layers of CA1 and CA3 disappeared 3 and 7 days after a maximal stage 5 seizure. On the other hand, activated microglial cells as selectively marked with the lectin occurred in the areas affected by KA-induced lesion. Double-labeling immunocytochemical analysis demonstrated the co-localization of SOD-1-positive glia-like cells and reactive astrocytes as labeled by GFAP or S-100 protein immunoreactivity. This finding suggested that the mobilization of astroglial cells for the synthesis of SOD-1 protein is a response to the KA insult designed to decrease the neurotoxicity induced by oxygen-derived free radicals. Therefore, these alterations might reflect the regulatory role of SOD-1 against oxygen-derived free radical-induced neuronal degeneration after systemic KA administration. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)215-226
Number of pages12
JournalBrain Research
Issue number2
Publication statusPublished - 2000 Jan 24
Externally publishedYes

Bibliographical note

Funding 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.


  • Astrocyte
  • Cu,Zn-superoxide dismutase
  • Free radical
  • Hippocampus
  • Kainic acid
  • Microglia
  • Neurodegeneration
  • Superoxide

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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