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. 1997 Sep;22(9):1145-50.
doi: 10.1023/a:1027321420075.

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

C Di Giacomo  1 , V Sorrenti, R Acquaviva, A Campisi, G Vanella, J R Perez-Polo, A Vanella
Affiliations

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

C Di Giacomo et al. Neurochem Res. 1997 Sep.

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 ornithine 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.

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