N-Acetylcysteine delays age-associated memory impairment in mice:: role in synaptic mitochondria
N-Acetylcysteine delays age-associated memory impairment in mice:: role in synaptic mitochondria
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DOI：
10.1016/s0006-8993(99)02349-5
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发表时间：
2000-02-07
期刊：
影响因子：
2.9
通讯作者：
Martínez, N
中科院分区：
文献类型：
--
作者：
Martínez, M;Hernández, AI;Martínez, N
线粒体氧化损伤与大脑老化和与年龄相关的神经退行性疾病有关。由于N-乙酰半胱氨酸(NAC)最近被证明可以防止衰老小鼠神经细胞的凋亡和保护突触线粒体蛋白免受氧化损伤，我们研究了饮食中给予这种硫代抗氧化剂是否延缓了与年龄相关的记忆丧失。48周龄时，对照组雌性-1小鼠饲喂标准饲料颗粒，另一组饲喂含0.3%(w/w)NAG的饲料颗粒。在这种饮食的23周后，NAC已经部分恢复了与衰老相关的小鼠记忆缺陷。此外，与年龄匹配的对照组相比，补充NAG的动物突触线粒体的脂质过氧化和蛋白质羰基含量显著降低。NAC的抗氧化特性和对突触终末线粒体生物能能力的可能作用至少部分解释了NAC的有益作用。(C)2000由爱思唯尔科学公司出版。保留所有权利。
Mitochondrial oxidative damage is implicated in brain aging and in age-related neurodegenerative diseases. Since N-acetylcysteine (NAC) has recently been shown to prevent apoptotic death in neuronal cells and protect synaptic mitochondria proteins from oxidative damage in aged mice, we have investigated whether dietary administration of this thiolic antioxidant retards age-related memory loss. At 48 weeks of age, a control female OF-1 mice group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of NAG. After 23 weeks of this diet, the NAC had partially restored the memory deficit associated with aging in mice. Moreover, the Lipid peroxide and protein carbonyl contents of the synaptic mitochondria were significantly decreased in the NAG-supplemented animals in comparison with their age-matched controls. The antioxidant properties and probable action on mitochondrial bioenergetic ability in the synaptic terminals may explain, at least partially, the beneficial action of NAC administration. (C) 2000 Published by Elsevier Science B.V. All rights reserved.