Abstract |
Oxidative stress has been involved in various neurological disorders and, in the central nervous system, astrocytes represent the cell type that contributes to neuroprotection via glutathione (GSH) metabolism, GSH-metabolizing enzymes like gamma-glutamyltransferase (GGT), and apoE secretion. In this study, using IL-1beta, a proinflammatory and prooxidant cytokine that is increased in numerous pathological situations, cells of astrocytoma cell line U373-MG were exposed to an oxidative stress, leading to c-Jun and c-Fos activation. IL-1beta decreased both GGT activity and intracellular GSH content and increased apoE secretion, initiating astroglial response to injury. We observed that antioxidants inhibit IL-1beta effects on c-Jun and c-Fos proteins, GGT activity and the GSH pool but not on apoE secretion. Our results allow us to conclude that neurological disorders associated with an IL-1beta-induced oxidative stress could be, at least experimentally, reversible in the presence of one antioxidant, N-acetylcysteine.
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Authors | C Malaplate-Armand, Y Gueguen, P Bertrand, L Ferrari, A M Batt |
Journal | Cell biology and toxicology
(Cell Biol Toxicol)
Vol. 16
Issue 3
Pg. 155-63
( 2000)
ISSN: 0742-2091 [Print] Switzerland |
PMID | 11032359
(Publication Type: Journal Article)
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Chemical References |
- Apolipoproteins E
- Free Radical Scavengers
- Interleukin-1
- Proto-Oncogene Proteins c-fos
- Proto-Oncogene Proteins c-jun
- Vitamin E
- gamma-Glutamyltransferase
- Glutathione
- Ascorbic Acid
- Acetylcysteine
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Topics |
- Acetylcysteine
(pharmacology)
- Apolipoproteins E
(metabolism)
- Ascorbic Acid
(pharmacology)
- Astrocytoma
- Blotting, Western
- Cell Survival
- Dose-Response Relationship, Drug
- Enzyme Activation
(drug effects)
- Free Radical Scavengers
(pharmacology)
- Glutathione
(metabolism)
- Humans
- Interleukin-1
(pharmacology)
- Oxidative Stress
(drug effects, physiology)
- Proto-Oncogene Proteins c-fos
(analysis)
- Proto-Oncogene Proteins c-jun
(analysis)
- Tumor Cells, Cultured
(drug effects, enzymology)
- Vitamin E
(pharmacology)
- gamma-Glutamyltransferase
(metabolism)
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