Cooperation between glutathione depletion and protein synthesis inhibition against naturally occurring neuronal death.

Details

Serval ID
serval:BIB_A5EED109FA9B
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Cooperation between glutathione depletion and protein synthesis inhibition against naturally occurring neuronal death.
Journal
Neuroscience
Author(s)
Castagné V., Clarke P.G.H.
ISSN
0306-4522[print], 0306-4522[linking]
Publication state
Published
Issued date
1998
Volume
86
Number
3
Pages
895-902
Language
english
Abstract
It is generally agreed that naturally-occurring neuronal death in developing animals is dependent on the synthesis of proteins. Oxidative stress, as when intracellular concentrations of free radicals are raised or when cell constituents such as membrane lipids or protein thiols are oxidized, is also involved in various types of neuronal death. In the present report, we show that the number of naturally dying retinal cells in the chick embryo can be reduced by intraocular injections of cycloheximide, an inhibitor of protein synthesis. L-buthionine-[S,R]-sulfoximine, an inhibitor of glutathione synthesis, can either enhance or diminish the cell death, depending on the conditions of treatment. Moreover, when the two inhibitors are combined, L-buthionine-[S,R]-sulfoximine potentiates the neuroprotective effects of cycloheximide. Measurements of retinal glutathione concentration and protein synthesis show the specificity of the treatments: buthionine-sulfoximine diminishes glutathione concentrations but not protein synthesis whereas cycloheximide inhibits protein synthesis without decreasing glutathione concentrations. Naturally-occurring neuronal death thus seems to involve the synthesis of proteins, and is also influenced by oxidative phenomena. Our results extend previous data in tectal-lesioned embryos, and suggest that a moderate, non-lethal oxidative stress can enhance the resistance of ganglion cells that might otherwise have died (spontaneously or following axotomy) owing to insufficient retrograde trophic support.
Keywords
Animals, Buthionine Sulfoximine/pharmacology, Cell Division/drug effects, Chick Embryo, Cycloheximide/pharmacology, Glutathione/metabolism, Leucine/metabolism, Neurons/cytology, Neurons/drug effects, Protein Biosynthesis, Protein Synthesis Inhibitors/pharmacology, Retina/cytology, Retina/drug effects, Retinal Ganglion Cells/cytology, Retinal Ganglion Cells/drug effects
Pubmed
Web of science
Create date
20/01/2008 17:48
Last modification date
20/08/2019 15:11
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