Time course of oxidative events in the hippocampus following intracerebroventricular infusion of quinolinic acid in mice
| Autor: | Deusa Vendite, Carina Rodrigues Boeck, Marcelo Ganzella, Fluvia Melina Alves Jardim |
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| Rok vydání: | 2006 |
| Předmět: |
Male
AIDS Dementia Complex Time Factors Antioxidant Free Radicals medicine.medical_treatment Excitotoxicity Oxidative phosphorylation Pharmacology medicine.disease_cause Hippocampus Antioxidants Mice chemistry.chemical_compound Seizures medicine Animals Cells Cultured Injections Intraventricular chemistry.chemical_classification Reactive oxygen species General Neuroscience Neurotoxicity Neurodegenerative Diseases General Medicine Quinolinic Acid medicine.disease Up-Regulation Disease Models Animal Oxidative Stress chemistry Biochemistry Nerve Degeneration Toxicity Encephalitis Reactive Oxygen Species Oxidative stress Quinolinic acid |
| Zdroj: | Neuroscience Research. 55:397-402 |
| ISSN: | 0168-0102 |
| DOI: | 10.1016/j.neures.2006.05.003 |
| Popis: | The excitotoxicity induced by QA has been related to its ability to increase free radical content and oxidative stress. In order to investigate the time course of toxicity and oxidative profile in the mice hippocampus following seizures induced by QA infusion (36.8 nM, i.c.v.), we evaluated the cellular damage (PI uptake assay), content of ROS formation (DCF assay) and the total radical antioxidant potential (TRAP) and reactivity (TAR) levels. The present results showed that a cellular damage occurred as early as 4 h after QA infusion coincident with an increase in the ROS contents, which returned to control levels after 24 h, while the cellular damage persisted for 72 h. There was a marked increased in the total antioxidant capacity at 8 h after QA infusion in both reactivity and potential levels. By 72 h post-treatment, the TRAP levels decreased, but the TAR levels remained augmented. Therefore, the delayed and persistent increase in the antioxidant capacity after QA insult may be a cellular adaptative response, probably contributing to decrease the ROS levels in order to prevent the spreading of the cellular damage. Therefore, the increase in the QA level in the brain ventricle may induce oxidative stress, which is followed by a persistent response in the antioxidant system in the hippocampus. The present study may, therefore, contribute to elucidate the mechanism of the brain dysfunction in patients with several neurological disorders involving elevation of QA in the CSF. |
| Databáze: | OpenAIRE |
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