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首页> 外文期刊>Brain research bulletin >Protective effect of S-allylcysteine on 3-nitropropionic acid-induced lipid peroxidation and mitochondrial dysfunction in rat brain synaptosomes.
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Protective effect of S-allylcysteine on 3-nitropropionic acid-induced lipid peroxidation and mitochondrial dysfunction in rat brain synaptosomes.

机译:S-烯丙基半胱氨酸对3-硝基丙酸诱导的大鼠脑突触体脂质过氧化和线粒体功能障碍的保护作用。

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摘要

3-Nitropropionic acid is a neurotoxin that irreversibly inhibits succinate dehydrogenase, a relevant enzyme constituting the complex II of the respiratory chain during mitochondrial electron transport. 3-Nitropropionic acid is known to produce oxidativeitrosative stress and evokes an experimental model of Huntington's disease. In this work we evaluated the effects of the antioxidant compound and major organosulfur garlic derivative, S-allylcysteine, on lipid peroxidation and mitochondrial dysfunction induced by 3-nitropropionic acid in synaptosomal fractions from rat brain. 3-Nitropropionic acid, at concentrations ranging 0.75-2.5 mM, produced enhanced levels of lipid peroxidation, while increasing concentrations of S-allylcysteine (0.1-2 mM) decreased the peroxidative action of 3-nitropropionic acid (1 mM) in synaptosomal fractions in a concentration-dependent manner. S-Allylcysteine (0.75 mM) also prevented the 3-nitropropionic acid (1mM)-induced mitochondrial dysfunction. These findings suggest that the protective actions that S-allylcysteine exert on the in vitro neurotoxicity induced by 3-nitropropionic acid are mediated by its antioxidant properties.
机译:3-硝基丙酸是一种神经毒素,它不可逆地抑制琥珀酸脱氢酶,琥珀酸脱氢酶是构成线粒体电子运输过程中呼吸链复合物II的相关酶。已知3-硝基丙酸会产生氧化/亚硝化应激,并引起亨廷顿舞蹈病的实验模型。在这项工作中,我们评估了抗氧化剂化合物和主要的有机硫大蒜衍生物S-烯丙基半胱氨酸对大鼠脑突触部分中3-硝基丙酸引起的脂质过氧化和线粒体功能障碍的影响。 3-硝基丙酸的浓度范围为0.75-2.5 mM,可提高脂质过氧化的水平,而增加浓度的S-烯丙基半胱氨酸(0.1-2 mM)则可降低滑膜中3-硝基丙酸(1 mM)的过氧化作用。浓度依赖性的方式。 S-烯丙基半胱氨酸(0.75 mM)还预防了3-硝基丙酸(1mM)引起的线粒体功能障碍。这些发现表明,S-烯丙基半胱氨酸对3-硝基丙酸诱导的体外神经毒性的保护作用是由其抗氧化特性介导的。

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