Ornithine decarboxylase activity in cerebral post-ischemic reperfusion damage: effect of methionine sulfoximine.
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.
Di Giacomo
C
C
Institute of Biochemistry, University of Catania, Italy.
Sorrenti
V
V
Acquaviva
R
R
Campisi
A
A
Vanella
G
G
Perez-Polo
J R
JR
Vanella
A
A
D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply / Q000187:drug effects*; D008297:Male; D008717:Methionine Sulfoximine / Q000494:pharmacology*; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000201:enzymology
D008717:Methionine Sulfoximine; D009955:Ornithine Decarboxylase