Selenium (Se) is an essential mineral for mammals. It is a nutrient related to the complex metabolic and enzymatic functions. Although Se has important physiological functions in the cells, organic compounds of Se can be extremely toxic, and may affect the central nervous system. This study aims to investigate the effect of the chronic treatment with the vinyl chalcogenide 3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in the brain of rats. Animals received the vinyl chalcogenide (125, 250 or 500 μg/kg body weight) intraperitoneally once a day during 30 days. The cerebral cortex, the hippocampus, and the cerebellum were dissected and homogenized in KCl. Afterward, thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured in the brain. Results showed that the organoselenium enhanced TBARS in the cerebral cortex of rats but the compound was not able to change carbonyl levels. Furthermore, the organoselenium reduced thiol groups measured by the sulfhydryl assay in all tissues studied. The activity of the antioxidant enzyme CAT was increased by the organochalcogen in the cerebral cortex and in the cerebellum, and the activity of SOD was increased in the hippocampus. On the other hand, the activity of the antioxidant enzyme GPx was reduced in all brain structures. Our findings indicate that this organoselenium compound induces oxidative stress in different brain regions of rats, corroborating to the fact that this tissue is a potential target for organochalcogen action.
Rev Neurocienc 2012;20(2):294-301 revisão 294 RESUMO Introdução. Entre os mecanismos biológicos que originam o quadro hiperglicêmico a predominância é do diabetes melittus (DM). O DM representa um grupo de desordens metabólicas caracterizadas por hiperglicemia crônica que ocasiona severas alterações celulares e teciduais. Objetivo. O presente trabalho analisou através de revisão da literatura o comportamento de células gliais expostas a elevadas concentrações de glicose, similares às observadas no DM. Método. Foi realizada uma revisão literária através de artigos científicos das bases de dados Pubmed, Science Direct, Scopus e Scielo. Resultados. Foram selecionados artigos e livros entre 1988 e 2009 que discutiam hiperglicemia, sistema nervoso central e que relacionavam hiperglicemia e células gliais. Conclusão. A hiperglicemia crônica proporcionada pelo DM pode influenciar de maneira danosa o metabolismo cerebral exercendo ações sobre a atividade glial. Podendo afetar a sobrevivência neuronal através da excitotoxicidade glutamatérgica e da produção de espécies reativas de oxigênio (ERO) e de espécies reativas de nitrogênio (ERN) que geram como consequência o processo de neuroinflamação. Tal processo inflamatório pode resultar em dano e morte neural caracterizando um processo neurodegerativo. ABSTRACTIntroduction. Among the biological mechanisms that originate the hyperglycemic state the prevalence is the diabetes mellitus (DM). DM represents a group of metabolic disorders characterized by chronic hyperglycemia that causes severe cellular and tissue alterations. Objective. This study examined through literature review the actions of glial cells exposed to high glucose concentrations similar to those observed in DM. Method. We performed a literature review of scientific articles through Pubmed, Science Direct, Scopus and Scielo. Results. We selected articles and books between 1988 and 2009 that discussed hyperglycemia, central nervous system, and that related hyperglycemia and glial cells. Conclusion. The chronic hyperglycemia provided by DM may harmful influence brain metabolism exerting actions on the glial activity. It may affect neuronal survival by glutamatergic excitotoxicity and the production of reactive oxygen species (ROS) and nitrogen reactive species (RNS) that generates as a consequence the process of neuroinflammation. The inflammatory process can result in damage and death neural characterizing a neurodegenerative process.
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