Ornithine decarboxylase activity in cerebral post-ischemic reperfusion damage: Effect of methionine sulfoximine

C. Di Giacomo, V. Sorrenti, R. Acquaviva, A. Campisi, G. Vanella, J. R. Perez-Polo, A. Vanella

    Research output: Contribution to journalArticle

    4 Scopus citations

    Abstract

    Excessive activation of glutamate receptors via the N-methyl-D-aspartate (NMDA) subtype appears to play a role in the sequence of cellular events which lead to irreversible ischemic damage to neurons. Furthermore, NMDA receptor activation induces a stimulation of omithine decarboxylase (ODC), the rate-limiting enzyme for polyamine (PA) biosynthesis. In order to better understand the role of PA we have measured ODC activity and the effect of methionine sulfoximine (MSO), a molecule able to stimulate ODC, on a model of transient cerebral ischemia. There was a significant increase in ODC activity in the rat cerebral cortex during post-ischemic reperfusion. The treatment with MSO induced a significant decrease in cerebral glutamine synthetase activity accompanied by a marked increase in ODC activity. In MSO-pretreated rats there was a significant decrease in the survival rate when compared to untreated ischemic rats.

    Original languageEnglish (US)
    Pages (from-to)1145-1150
    Number of pages6
    JournalNeurochemical Research
    Volume22
    Issue number9
    DOIs
    StatePublished - Aug 19 1997

    Keywords

    • Cerebral ischemia
    • GS
    • ODC
    • Polyamines
    • Reperfusion
    • Survival

    ASJC Scopus subject areas

    • Biochemistry
    • Cellular and Molecular Neuroscience

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  • Cite this

    Di Giacomo, C., Sorrenti, V., Acquaviva, R., Campisi, A., Vanella, G., Perez-Polo, J. R., & Vanella, A. (1997). Ornithine decarboxylase activity in cerebral post-ischemic reperfusion damage: Effect of methionine sulfoximine. Neurochemical Research, 22(9), 1145-1150. https://doi.org/10.1023/A:1027321420075