A transient treatment of hippocampal neurons with alpha-tocopherol induces a long-lasting protection against oxidative damage via a genomic action

Autor: Michel Vignes, Nadine Crouzin, Janique Guiramand, Marie Celeste de Jesus Ferreira, Max Récasens, Catherine Cohen-Solal, Gérard Barbanel
Přispěvatelé: Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM), Plasticité cérébrale (PC), Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS)
Rok vydání: 2005
Předmět:
Antioxidant
MESH: Hippocampus
MESH: Rats
medicine.medical_treatment
Iron
alpha-Tocopherol
Excitotoxicity
MESH: Neurons
Oxidative phosphorylation
Cycloheximide
Pharmacology
medicine.disease_cause
Biochemistry
Neuroprotection
Hippocampus
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Physiology (medical)
medicine
Animals
MESH: Animals
MESH: Genome
MESH: Cycloheximide
Cells
Cultured

030304 developmental biology
MESH: Glutathione
Neurons
Protein Synthesis Inhibitors
0303 health sciences
MESH: Iron
MESH: Oxidative Stress
Genome
MESH: Protein Synthesis Inhibitors
Glutathione
Free Radical Scavengers
Rats
Oxidative Stress
chemistry
MESH: alpha-Tocopherol
MESH: Free Radical Scavengers
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
Trolox
030217 neurology & neurosurgery
Oxidative stress
MESH: Cells
Cultured
Zdroj: Free Radical Biology and Medicine
Free Radical Biology and Medicine, Elsevier, 2005, 39 (8), pp.1009-20. ⟨10.1016/j.freeradbiomed.2005.05.021⟩
ISSN: 0891-5849
DOI: 10.1016/j.freeradbiomed.2005.05.021⟩
Popis: International audience; Neuroprotection exerted by alpha-tocopherol against oxidative stress was investigated in cultured rat hippocampal neurons. In addition to its direct action as a radical scavenger revealed at concentrations above 10 microM, a transient application of 1 microM alpha-tocopherol phosphate (alpha-TP) to neurons induced a complete delayed long-lasting protection against oxidative insult elicited by exposure to Fe2+ ions, but not against excitotoxicity. A minimal 16-h application of alpha-TP was required to observe the protection against subsequent oxidative stress. This delayed protection could last up to a week after the application of alpha-TP, even when medium was changed after the alpha-TP treatment. Cycloheximide, added either 2 h before or together with alpha-TP, prevented the delayed neuroprotection, but not the acute. However, cycloheximide applied after the 16-h alpha-TP pretreatment did not alter the delayed neuroprotection. Neither Trolox, a cell-permeant analogue of alpha-tocopherol, nor other antioxidants, such as epigallocatechin-gallate and N-acetyl-L-cysteine, elicited a similar long-lasting protection. Only tert-butylhydroquinone could mimic the alpha-TP effect. Depletion of glutathione (GSH) by L-buthionine sulfoximine did not affect the delayed alpha-TP protection. Thus, in addition to its acute anti-radical action, alpha-TP induces a long-lasting protection of neurons against oxidative damage, via a genomic action on antioxidant defenses apparently unrelated to GSH biosynthesis.
Databáze: OpenAIRE