Alpha-tocopherol-mediated long-lasting protection against oxidative damage involves an attenuation of calcium entry through TRP-like channels in cultured hippocampal neurons
| Autor: | Rose-France Aimar, Michel Vignes, Nadine Crouzin, Marie-Céleste de Jesus Ferreira, Catherine Cohen-Solal, Janique Guiramand |
|---|---|
| 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) |
| Jazyk: | angličtina |
| Rok vydání: | 2007 |
| Předmět: |
inorganic chemicals
Ruthenium red MESH: Hippocampus MESH: Rats MESH: Biological Transport alpha-Tocopherol MESH: Neurons MESH: Rats Sprague-Dawley medicine.disease_cause Biochemistry Neuroprotection Hippocampus Rats Sprague-Dawley 03 medical and health sciences Transient receptor potential channel chemistry.chemical_compound 0302 clinical medicine TRPM Physiology (medical) medicine Animals MESH: Animals MESH: TRPC Cation Channels Cells Cultured 030304 developmental biology TRPC Cation Channels Neurons MESH: DNA Damage 0303 health sciences MESH: Oxidative Stress Chemistry Biological Transport Rats EGTA Oxidative Stress MESH: alpha-Tocopherol Metabotropic glutamate receptor MESH: Calcium Biophysics MESH: Calcium Channels NMDA receptor Calcium [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] Calcium Channels 030217 neurology & neurosurgery Oxidative stress DNA Damage MESH: Cells Cultured |
| Zdroj: | Free Radical Biology and Medicine Free Radical Biology and Medicine, Elsevier, 2007, 42 (9), pp.1326-37. ⟨10.1016/j.freeradbiomed.2007.01.032⟩ |
| ISSN: | 0891-5849 |
| DOI: | 10.1016/j.freeradbiomed.2007.01.032⟩ |
| Popis: | International audience; We have reported that a transient treatment of hippocampal neurons with alpha-tocopherol induced a long-lasting protection against oxidative damage mediated by Fe(2+) ions. This protection required protein synthesis. Here, we have studied whether this "hyposensitivity" to oxidative stress could be linked to an altered Ca(2+) homeostasis. Fe(2+) ions triggered a Ca(2+) entry which was required for Fe(2+) ion-induced toxicity. This influx was sensitive to blockers of TRP-like nonspecific Ca(2+) channels, including Ruthenium Red, La(3+), and Gd(3+) ions which also prevented the Fe(2+) ion-induced toxicity and oxidative stress as revealed by protein carbonylation status. The pretreatment with alpha-tocopherol resulted in a reduction of the Ca(2+) increase induced by Fe(2+) ions and masked the blocking effect of La(3+) ions. Moreover, such a pretreatment reduced the capacitive Ca(2+) entries (CCE) observed after metabotropic glutamate receptor stimulation, which are known to involve TRP-like channels. By contrast, in a model of "hypersensitivity" to oxidative stress obtained by chronic stimulation of glucocorticoid receptors, we observed an exacerbation of the various effects of Fe(2+) ions, i.e., cellular toxicity and Ca(2+) increase, and the glutamate-stimulated CCE. Therefore, we conclude that the long-lasting neuroprotection induced by alpha-tocopherol pretreatment likely results from an attenuation of Ca(2+) entries via TRP-like channels. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect