NADPH oxidase contributes to oxidative damage and mitochondrial impairment induced by acute ethanol treatment in rat hippocampal neurons
| Autor: | Francisco Canelo, María José Pérez, Rocío Loyola, Carola Tapia-Monsalves, Alejandra Aranguiz, Cesar Osorio-Fuentealba, Rodrigo A. Quintanilla |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cell Survival Primary Cell Culture Brain damage Mitochondrion Hippocampal formation medicine.disease_cause Hippocampus Rats Sprague-Dawley 03 medical and health sciences Cellular and Molecular Neuroscience chemistry.chemical_compound Adenosine Triphosphate 0302 clinical medicine Pregnancy medicine Animals Calcium Signaling Neurons Pharmacology chemistry.chemical_classification Reactive oxygen species NADPH oxidase Dose-Response Relationship Drug biology Chemistry Neurodegeneration NADPH Oxidases medicine.disease Mitochondria Rats Cell biology Oxidative Stress 030104 developmental biology Synapses Apocynin biology.protein Female Synaptic Vesicles medicine.symptom Reactive Oxygen Species Alcoholic Intoxication 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Neuropharmacology. 171:108100 |
| ISSN: | 0028-3908 |
| DOI: | 10.1016/j.neuropharm.2020.108100 |
| Popis: | Acute ethanol treatment induces neurodegeneration in cultured neurons and can lead to brain damage in animal models. Neuronal cells exposed to ethanol showed an increase in reactive oxygen species (ROS), oxidative damage and mitochondrial impairment contributing to synaptic failure. However, the underlying mechanisms of these events are not well understood. Here, we studied the contribution of NADPH oxidase, as a relevant source of ROS production in the brain, to mitochondrial impairment and oxidative stress induced by ethanol. We used primary hippocampal neurons subjected to an acute treatment of ethanol at increasing concentrations (25, 50, and 75 mM, 24 h), and we evaluated ROS production, mitochondrial function, and synaptic vesicle activity. Our studies showed that after ethanol administration, hippocampal neurons presented an increase in ROS levels, mitochondrial dysfunction, calcium handling defects, and synaptic impairment. Interestingly, treatment with the NADPH inhibitor, apocynin, significantly prevented oxidative stress, mitochondrial dysfunction, and the impairment of synaptic vesicle activity induced by ethanol treatment. These results indicate that NADPH oxidase could be a key participant in the molecular mechanism by which alcohol affects the brain. |
| Databáze: | OpenAIRE |
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