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首页> 外文期刊>Bulletin of experimental biology and medicine >Effect of Deprenyl on Free Radical Oxidation in Rat Brain during Immobilization Stress
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Effect of Deprenyl on Free Radical Oxidation in Rat Brain during Immobilization Stress

机译:异戊二烯对固定化应激过程中大鼠脑自由基氧化的影响

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摘要

Rarely repeated episodes of 1-h immobilization in rats were accompanied by an increase in the content of molecular products of lipid peroxidation and decrease in the amount of oxida-tively modified proteins. Monoamine oxidase B inhibitor deprenyl prevented the poststress activation of lipid peroxidation.Free radical oxidation is involved in the pathogenesis of vascular and neurodegenerative diseases and plays a role in the development of age-related injury to the central nervous system (CNS) [3,5,7]. Previous studies showed that monoamine oxidase B (MAO-B) inhibitor deprenyl reduces the severity of oxidative stress and produces a neuroprotective effect during Alzheimer's disease [12]. A relationship exists between the content of molecular products of lipid peroxidation (LPO) and activity of MAO-B in human CNS during postnatal ontogeny [5,6]. Published data show that similar variations are observed during rarely repeated episodes of 1-h immobilization (RRIM) [10]. These data suggest that activation of LPO in the brain is a MAO-B-depen-dent process. Here we tested this hypothesis.
机译:在大鼠中很少反复发生1-h固定化现象,伴有脂质过氧化分子产物含量的增加和氧化修饰蛋白的数量的减少。单胺氧化酶B抑制剂去异戊二烯阻止了脂质过氧化的后应激活化。自由基氧化参与血管和神经退行性疾病的发病机理,并在与年龄有关的中枢神经系统损伤(CNS)的发生中起作用[3,5 ,7]。先前的研究表明,单胺氧化酶B(MAO-B)抑制剂去异戊二烯降低了氧化应激的严重程度,并在阿尔茨海默氏病期间产生了神经保护作用[12]。出生后个体发育中人中枢神经系统脂质过氧化(LPO)分子产物的含量与MAO-B活性之间存在联系[5,6]。已发表的数据表明,在很少重复的1-h固定(RRIM)发作期间观察到类似的变化[10]。这些数据表明,大脑中LPO的激活是MAO-B依赖过程。在这里,我们检验了这一假设。

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