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

doi:10.1023/A:1027321420075

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 journal › Article › peer-review

5 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 language	English (US)
Pages (from-to)	1145-1150
Number of pages	6
Journal	Neurochemical Research
Volume	22
Issue number	9
DOIs	https://doi.org/10.1023/A:1027321420075
State	Published - 1997
Externally published	Yes

Keywords

Cerebral ischemia
GS
ODC
Polyamines
Reperfusion
Survival

ASJC Scopus subject areas

Biochemistry
Cellular and Molecular Neuroscience

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@article{165fa70c282f4791bd83eba7038f11e7,

title = "Ornithine decarboxylase activity in cerebral post-ischemic reperfusion damage: Effect of methionine sulfoximine",

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.",

keywords = "Cerebral ischemia, GS, ODC, Polyamines, Reperfusion, Survival",

author = "{Di Giacomo}, C. and V. Sorrenti and R. Acquaviva and A. Campisi and G. Vanella and Perez-Polo, {J. R.} and A. Vanella",

year = "1997",

doi = "10.1023/A:1027321420075",

language = "English (US)",

volume = "22",

pages = "1145--1150",

journal = "Neurochemical Research",

issn = "0364-3190",

publisher = "Springer",

number = "9",

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TY - JOUR

T1 - Ornithine decarboxylase activity in cerebral post-ischemic reperfusion damage

T2 - Effect of methionine sulfoximine

AU - Di Giacomo, C.

AU - Sorrenti, V.

AU - Acquaviva, R.

AU - Campisi, A.

AU - Vanella, G.

AU - Perez-Polo, J. R.

AU - Vanella, A.

PY - 1997

Y1 - 1997

N2 - 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.

AB - 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.

KW - Cerebral ischemia

KW - GS

KW - ODC

KW - Polyamines

KW - Reperfusion

KW - Survival

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JO - Neurochemical Research

JF - Neurochemical Research

IS - 9

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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