作者: Fernando Dobrachinski , Luiza Lena Bastos , Jessika Cristina Bridi , Cristiane Lenz Dalla Corte , Daiana Silva de Ávila
DOI: 10.1007/S11064-012-0820-3
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摘要: Excessive formation of reactive oxygen species (ROS) and disruption glutamate uptake have been hypothesized as key mechanisms contributing to quinolinic acid (QA)-induced toxicity. Thus, here we investigate if the use diphenyl diselenide (PhSe)2, guanosine (GUO) MK-801, alone or in combination, could protect rat brain slices from QA-induced QA (1 mM) increased ROS formation, thiobarbituric substances (TBARS) decreased cell viability after 2 h exposure. (PhSe)2 μM) protected against this cortex striatum also prevented decreases induced by QA. (5 hippocampus. GUO (10 100 blocked increase caused MK-801 (20 abolished pro-oxidant effect When noneffective concentrations were used combination produced a decrease mainly + MK-801. These results demonstrate that be effective avoid toxic effects high Furthermore, data obtained cellular assays suggest different pathways amelioration toxicity present neurodegenerative process.