Trolox and 6,7-dinitroquinoxaline-2,3-dione prevent necrosis but not apoptosis in cultured neurons subjected to oxygen deprivation
| Autor: | Jean-Christophe Copin, Pak H. Chan, Yibing Li, Liza Reola |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Necrosis
Cell Survival Kainate receptor Apoptosis Biology Pharmacology medicine.disease_cause Antioxidants Lipid peroxidation chemistry.chemical_compound Mice Quinoxalines medicine DNQX Excitatory Amino Acid Agonists Animals Chromans Hypoxia Brain Molecular Biology Cells Cultured Neurons General Neuroscience DNA Flow Cytometry Oxidative Stress medicine.anatomical_structure Biochemistry chemistry Phosphopyruvate Hydratase Electrophoresis Polyacrylamide Gel Neurology (clinical) Trolox Neuron Lipid Peroxidation medicine.symptom Excitatory Amino Acid Antagonists Oxidative stress Developmental Biology |
| Zdroj: | Brain research. 784(1-2) |
| ISSN: | 0006-8993 |
| Popis: | There is a growing body of evidence suggesting that apoptosis is involved in ischemic brain injury. Recent studies suggest that a rapid necrosis masked a more subtle apoptotic death in neurons subjected to oxygen deprivation in culture. To test this hypothesis, we treated cultured neurons with potential antinecrotic drugs during and after oxygen deprivation. The results show that 6, 7-dinitroquinoxaline-2,3-dione (DNQX) and 6-hydroxy-2,5,7, 8-tetramethylchroman-2-carboxylic acid (Trolox), which interfered with kainate receptor activation and lipid peroxidation respectively, prevented necrosis but allowed neurons to undergo apoptosis. Flow cytometric analysis of DNA degradation and hydrogen peroxide generation, as well as fluorescent microscopy of nuclear fragmentation revealed that apoptotic activity was higher in 6, 7-dinitroquinoxaline-2,3-dione-treated cells than in Trolox-treated cells. This difference in occurrence of apoptosis may be due to the difference in oxidative stress generated from these two different agents. |
| Databáze: | OpenAIRE |
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