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Low dose (-)deprenyl is cytoprotective: It maintains mitochondrial membrane potential and eliminates oxygen radicals

机译:低剂量(-)异戊二烯基具有细胞保护作用:保持线粒体膜电位并消除氧自由基

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Hypoxia leads to a collapse in mitochondrial transmembrane potential (Delta phi(M)), a fall in the ATP/ADP ratio, and finally cell death. Since (-)deprenyl directly modulates Delta phi(M) and production of reactive oxygen species (ROS) by altering the respiratory function of initochondria, we were interested in the dose-response relations of these effects. The changes in JC-I red/green signal ratios {mitochondrial transmembrane potential), and the changes in the cerium staining (intracellular ROS) in hypoxic and normoxic PC 12 cell cultures were measured following I h of Argon hypoxia and 24 h of re-oxygenation in the absence and in the presence of various concentrations of (-)deprenyl. Aom shifted to lower values following hypoxia/re-oxygenation and all cells had decreased and uniform Delta phi(M) levels. The amount of ROS increased. Following 24 h of treatment with various concentrations of (-)deprenyl during the re-oxygenation period, survival increased, the Aom shift caused by oxygen deprivation was reversed and the peroxy radical levels decreased except for at 10(-3) M. (c) 2005 Elsevier Inc. All rights reserved.
机译:缺氧会导致线粒体跨膜电位(Delta phi(M))下降,ATP / ADP比率下降,并最终导致细胞死亡。由于(-)异戊二烯基直接通过改变线粒体的呼吸功能来直接调节Delta phi(M)和活性氧(ROS)的产生,因此我们对这些效应的剂量反应关系感兴趣。在缺氧1 h和再缺氧24 h后,测量缺氧和常氧PC 12细胞培养物中JC-1红/绿信号比(线粒体跨膜电位)的变化以及铈染色(细胞内ROS)的变化。在不存在和存在各种浓度的(-)异戊二烯基的情况下进行氧合。缺氧/复氧后,Aom移至更低的值,并且所有细胞均减少且均一的Delta phi(M)水平。 ROS的量增加。在补氧期间用各种浓度的(-)异戊烯基进行24小时处理后,存活率增加,除氧引起的Aom转变被逆转,过氧自由基水平降低,除了在10(-3)M时(c )2005 Elsevier Inc.保留所有权利。

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