An optimal redox status for the survival of axotomized ganglion cells in the developing retina.

Détails

ID Serval
serval:BIB_F7B112BCCFB5
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
An optimal redox status for the survival of axotomized ganglion cells in the developing retina.
Périodique
Neuroscience
Auteur(s)
Castagné V., Lefèvre K., Natero R., Clarke P.G., Bedker D.A.
ISSN
0306-4522 (Print)
ISSN-L
0306-4522
Statut éditorial
Publié
Date de publication
1999
Volume
93
Numéro
1
Pages
313-320
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
The neuronal redox status influences the expression of genes involved in neuronal survival. We previously showed that antioxidants may reduce the number of dying ganglion cells following axotomy in chick embryos. In the present study, we show that various antioxidants, including the new spin trap azulenyl nitrone and 1,3-dimethyl-2-thiourea, protect axotomized ganglion cells, confirming that neuronal death involves an imbalance of the cellular redox status towards oxidation. However, high concentrations of antioxidants did not protect ganglion cells, suggesting that excessive reduction is detrimental for neurons. Simultaneous injections of two different antioxidants gave results only partly supporting this view. Combinations of azulenyl nitrone and N-acetyl cysteine in fact gave greater protection than either antioxidant alone, whereas N-acetyl cysteine lost its neuroprotective effects and diminished those of alpha-phenyl-N-tert-butyl nitrone when the two compounds were injected simultaneously. The results of the combined treatments suggest that azulenyl nitrone and alpha-phenyl-N-tert-butyl nitrone do not have the same chemical effects within the ganglion cells. Moreover, N-acetyl cysteine's own antioxidant properties enhance the spin trapping effects of azulenyl nitrone but potentiate the toxicity of alpha-phenyl-N-tert-butyl nitrone. Our main conclusion is that neuronal survival requires the maintenance of the redox status near an optimal set-point. "Reductive stress" may be as dangerous as oxidative stress.
Mots-clé
Acetylcysteine/pharmacokinetics, Acetylcysteine/pharmacology, Animals, Antioxidants/pharmacology, Axotomy, Azulenes, Cell Count, Cell Survival/drug effects, Cell Survival/physiology, Chick Embryo, Cyclic N-Oxides, Eye/metabolism, Neuroprotective Agents/pharmacokinetics, Neuroprotective Agents/pharmacology, Nitrogen Oxides/pharmacokinetics, Nitrogen Oxides/pharmacology, Oxidation-Reduction, Oxidative Stress/drug effects, Retina/cytology, Retina/drug effects, Retinal Degeneration/physiopathology, Retinal Degeneration/prevention & control, Retinal Ganglion Cells/drug effects, Retinal Ganglion Cells/physiology, Sesquiterpenes/pharmacokinetics, Sesquiterpenes/pharmacology, Thiourea/analogs & derivatives, Thiourea/pharmacokinetics
Pubmed
Web of science
Création de la notice
20/01/2008 18:49
Dernière modification de la notice
03/03/2018 22:50
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