Glutathione depletion: Starting point of brain metabolic stress, neuroinflammation and cognitive impairment in rats
| Autor: | Lisette Blanco, Teresa Serrano, González-Fraguela Me, Jessica López Fernández, Caridad Ivette Fernández, Lourdes Lorigados |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Antioxidant medicine.medical_treatment Oxidative phosphorylation medicine.disease_cause Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound Random Allocation 0302 clinical medicine Internal medicine medicine Avoidance Learning Animals Buthionine sulfoximine Cognitive Dysfunction Maze Learning Cell damage Buthionine Sulfoximine Spatial Memory chemistry.chemical_classification Inflammation Reactive oxygen species Brain Diseases Tumor Necrosis Factor-alpha General Neuroscience Brain Glutathione medicine.disease Disease Models Animal Oxidative Stress 030104 developmental biology Endocrinology chemistry Synaptic signaling Psychology Reactive Oxygen Species Neuroscience 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Brain research bulletin. 137 |
| ISSN: | 1873-2747 |
| Popis: | Glutathione provides protection from oxidative stress-induced damage through the reduction of reactive oxygen species for the maintenance of oxidant homeostasis. Our purpose was to test the effects of depleting tissue GSH by buthionine sulfoximine on brain oxidative metabolism and cognitive performance in rats. Glutathione depletion induced a compensatory response on antioxidant enzymes and increase of cell damage indicators in all the examined cerebral areas at 24h. The effect of GSH depletion on spatial memory recorded at 24h post-surgery showed significant differences between experimental groups for the escape latency to the platform and percentage of total swim distance spending in the target quadrant. The acquisition of a new spatial condition 24h after GSH depletion revealed differences between experimental groups for latencies, swim distance, swim distance in the target quadrant and percentage of total swim distance spending in the target quadrant. The ability of BSO treated group to maintain a restraining behavior was significantly smaller compared with control group. We founded significant correlation among variables of the behavioral studies and oxidative stress indicators. In conclusion, our model shows how increased ROS production by transitory glutathione depletion constitutes the primary cause to neuronal metabolic stress with alterations in synaptic signaling and cognitive deficits. |
| Databáze: | OpenAIRE |
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