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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Deficiency of ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1) leads to vulnerability to lipid peroxidation.
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Deficiency of ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1) leads to vulnerability to lipid peroxidation.

机译：泛素羧基末端水解酶-L1（UCH-L1）的缺乏导致对脂质过氧化的脆弱性。

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摘要

Lipid peroxidation has many deleterious effects on cells, and in the nervous system is considered to be involved in the pathogenesis of neurodegenerative diseases. To suppress lipid peroxidation, cells have various defense systems such as glutathione and thioredoxin, and defects in these defense systems will result in disturbance of normal cellular functions. Here we report that deficiency of ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1) leads to vulnerability to lipid peroxidation both in vivo and in vitro, through analyses of the UCH-L1-deficient mutant mouse gracile axonal dystrophy (gad). In the gracile fasciculus of gad mice, punctate deposits were observed to be immunoreactive for 4-hydroxy-2-nonenal, a by-product of lipid peroxidation. The motor deficits of gad mice were worsened by a diet deficient in vitamin E. When neurons from dorsal root ganglions (DRG) were cultured in the vitamin E-free medium, cell death was increased in the neurons of gad mice. These data suggest that UCH-L1 has a function in protecting DRG neurons from lipid peroxidation. Further, we describe newly identified properties: that UCH-L1 is localized on the inside of the plasma membrane of DRG neurons, and that UCH-L1 binds to phosphatidic acid according to the redox status and presence of mono-ubiquitin protein. These findings will provide clues for elucidating the physiological function of UCH-L1.
机译：脂质过氧化对细胞具有许多有害作用，并且在神经系统中被认为与神经退行性疾病的发病机理有关。为了抑制脂质过氧化，细胞具有各种防御系统，例如谷胱甘肽和硫氧还蛋白，并且这些防御系统中的缺陷将导致正常细胞功能的紊乱。在这里，我们通过对UCH-L1缺陷型突变型小鼠轴突营养不良（gad）的分析，报道了泛素羧基末端水解酶L1（UCH-L1）的缺乏导致体内和体外脂质过氧化的脆弱性。在性腺发育不良的小鼠的纤毛束中，观察到点状沉积物对脂质过氧化的副产物4-羟基-2-壬烯醛具有免疫反应性。缺乏维生素E的饮食会加剧gad小鼠的运动功能障碍。当在无维生素E的培养基中培养来自背根神经节（DRG）的神经元时，gad小鼠神经元的细胞死亡会增加。这些数据表明UCH-L1具有保护DRG神经元免于脂质过氧化的功能。此外，我们描述了新发现的特性：UCH-L1位于DRG神经元的质膜内部，并且UCH-L1根据氧化还原状态和单泛素蛋白的存在与磷脂酸结合。这些发现将为阐明UCH-L1的生理功能提供线索。

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