Free radical generation during brief period of cerebral ischemia may trigger delayed neuronal death

K. Kitagawa, M. Matsumoto, T. Oda, M. Niinobe, Ryuji Hata, N. Handa, R. Fukunaga, Y. Isaka, K. Kimura, H. Maeda, K. Mikoshiba, T. Kamada

Research output: Contribution to journalArticle

191 Citations (Scopus)

Abstract

We investigated the pathogenic role of free radical formation in ischemic neuronal death using radical scavenger, Superoxide dismutase. Cerebral ischemia was produced in the gerbil by bilateral common carotid occlusion for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. The effects of free Superoxide dismutase and a derivatized Superoxide dismutase, pyran copolymer conjugated Superoxide dismutase, on early ischémie damages, detected sensitively by the immunohistochemical reaction for microtubule associated protein 2, and a subsequent delayed neuronal death after restoration of blood flow were investigated. Preischemic treatment by pyran conjugated Superoxide dismutase showed clear protective effects against both the neuronal damages detected by immunohistochemistry after 5 min ischemia and the delayed neuronal necrosis after one week of recovery, although no clear beneficial effects were observed when this drug was administered just before the recirculation or free Superoxide dismutase was used. These results strongly suggest that free radical generation during brief period of ischemia plays a pivotal role in triggering the ischémie neuronal damages causing delayed neuronal death at the selectively vulnerable areas of the brain.

Original languageEnglish
Pages (from-to)551-558
Number of pages8
JournalNeuroscience
Volume35
Issue number3
DOIs
Publication statusPublished - 01-01-1990

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Brain Ischemia
Superoxide Dismutase
Free Radicals
Pyran Copolymer
Ischemia
Pyrans
Microtubule-Associated Proteins
Gerbillinae
Hippocampus
Necrosis
Immunohistochemistry
Brain
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Kitagawa, K. ; Matsumoto, M. ; Oda, T. ; Niinobe, M. ; Hata, Ryuji ; Handa, N. ; Fukunaga, R. ; Isaka, Y. ; Kimura, K. ; Maeda, H. ; Mikoshiba, K. ; Kamada, T. / Free radical generation during brief period of cerebral ischemia may trigger delayed neuronal death. In: Neuroscience. 1990 ; Vol. 35, No. 3. pp. 551-558.
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abstract = "We investigated the pathogenic role of free radical formation in ischemic neuronal death using radical scavenger, Superoxide dismutase. Cerebral ischemia was produced in the gerbil by bilateral common carotid occlusion for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. The effects of free Superoxide dismutase and a derivatized Superoxide dismutase, pyran copolymer conjugated Superoxide dismutase, on early isch{\'e}mie damages, detected sensitively by the immunohistochemical reaction for microtubule associated protein 2, and a subsequent delayed neuronal death after restoration of blood flow were investigated. Preischemic treatment by pyran conjugated Superoxide dismutase showed clear protective effects against both the neuronal damages detected by immunohistochemistry after 5 min ischemia and the delayed neuronal necrosis after one week of recovery, although no clear beneficial effects were observed when this drug was administered just before the recirculation or free Superoxide dismutase was used. These results strongly suggest that free radical generation during brief period of ischemia plays a pivotal role in triggering the isch{\'e}mie neuronal damages causing delayed neuronal death at the selectively vulnerable areas of the brain.",
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Kitagawa, K, Matsumoto, M, Oda, T, Niinobe, M, Hata, R, Handa, N, Fukunaga, R, Isaka, Y, Kimura, K, Maeda, H, Mikoshiba, K & Kamada, T 1990, 'Free radical generation during brief period of cerebral ischemia may trigger delayed neuronal death', Neuroscience, vol. 35, no. 3, pp. 551-558. https://doi.org/10.1016/0306-4522(90)90328-2

Free radical generation during brief period of cerebral ischemia may trigger delayed neuronal death. / Kitagawa, K.; Matsumoto, M.; Oda, T.; Niinobe, M.; Hata, Ryuji; Handa, N.; Fukunaga, R.; Isaka, Y.; Kimura, K.; Maeda, H.; Mikoshiba, K.; Kamada, T.

In: Neuroscience, Vol. 35, No. 3, 01.01.1990, p. 551-558.

Research output: Contribution to journalArticle

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AU - Kitagawa, K.

AU - Matsumoto, M.

AU - Oda, T.

AU - Niinobe, M.

AU - Hata, Ryuji

AU - Handa, N.

AU - Fukunaga, R.

AU - Isaka, Y.

AU - Kimura, K.

AU - Maeda, H.

AU - Mikoshiba, K.

AU - Kamada, T.

PY - 1990/1/1

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N2 - We investigated the pathogenic role of free radical formation in ischemic neuronal death using radical scavenger, Superoxide dismutase. Cerebral ischemia was produced in the gerbil by bilateral common carotid occlusion for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. The effects of free Superoxide dismutase and a derivatized Superoxide dismutase, pyran copolymer conjugated Superoxide dismutase, on early ischémie damages, detected sensitively by the immunohistochemical reaction for microtubule associated protein 2, and a subsequent delayed neuronal death after restoration of blood flow were investigated. Preischemic treatment by pyran conjugated Superoxide dismutase showed clear protective effects against both the neuronal damages detected by immunohistochemistry after 5 min ischemia and the delayed neuronal necrosis after one week of recovery, although no clear beneficial effects were observed when this drug was administered just before the recirculation or free Superoxide dismutase was used. These results strongly suggest that free radical generation during brief period of ischemia plays a pivotal role in triggering the ischémie neuronal damages causing delayed neuronal death at the selectively vulnerable areas of the brain.

AB - We investigated the pathogenic role of free radical formation in ischemic neuronal death using radical scavenger, Superoxide dismutase. Cerebral ischemia was produced in the gerbil by bilateral common carotid occlusion for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. The effects of free Superoxide dismutase and a derivatized Superoxide dismutase, pyran copolymer conjugated Superoxide dismutase, on early ischémie damages, detected sensitively by the immunohistochemical reaction for microtubule associated protein 2, and a subsequent delayed neuronal death after restoration of blood flow were investigated. Preischemic treatment by pyran conjugated Superoxide dismutase showed clear protective effects against both the neuronal damages detected by immunohistochemistry after 5 min ischemia and the delayed neuronal necrosis after one week of recovery, although no clear beneficial effects were observed when this drug was administered just before the recirculation or free Superoxide dismutase was used. These results strongly suggest that free radical generation during brief period of ischemia plays a pivotal role in triggering the ischémie neuronal damages causing delayed neuronal death at the selectively vulnerable areas of the brain.

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