| Autor: |
da Silva Schmitz I; Curso de Biomedicina, Universidade Franciscana (UFN), Santa Maria, Rio Grande do Sul, Brazil., Schaffer LF; Curso de Biomedicina, Universidade Franciscana (UFN), Santa Maria, Rio Grande do Sul, Brazil., Busanello A; Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria (UFSM), Santa Maria, Rio Grande do Sul, Brazil., de Freitas CM; Programa de Pós-Graduação em Bioquímica Toxicológica, Universidade Federal de Santa Maria (UFSM), Santa Maria, Rio Grande do Sul, Brazil., Fachinetto R; Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria (UFSM), Santa Maria, Rio Grande do Sul, Brazil.; Programa de Pós-Graduação em Bioquímica Toxicológica, Universidade Federal de Santa Maria (UFSM), Santa Maria, Rio Grande do Sul, Brazil., Peroza LR; Mestrado em Ciências da Saúde e da Vida, Universidade Franciscana (UFN), Santa Maria, Rio Grande do Sul, 97010-032, Brazil. perozalr@gmail.com. |
| Abstrakt: |
Oxidative stress occurs due to an imbalance between antioxidant defenses and pro-oxidant agents in brain. This condition has been associated to the pathogenesis of several brain diseases; therefore, increasing the use of compounds that exert antioxidant activity. Thus, the objective of this study was to evaluate, in vitro, the effect of isoflavones in: (1) lipid peroxidation, catalase activity and thiol groups in the presence of pro-oxidants: sodium nitroprusside or Fe 2+ /EDTA complex in rat brain homogenates; (2) the activity of the enzyme monoamine oxidase (MAO). As a result, the isoflavones reduced lipid peroxidation in a manner dependent on the concentration and protected against the reduction of catalase activity as well as the induced thiol oxidation in brain tissue. In addition, isoflavones inhibited MAO activity (MAO-A and MAO-B). Taken together, our results showed that isoflavones avoided oxidative stress and decreased the MAO activity, suggesting a promissory use in the treatment of neurodegenerative diseases. |
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