Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity.
Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity.
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DOI：
10.4137/jen.s39887
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发表时间：
2016
影响因子：
--
通讯作者：
De Pasquale R
中科院分区：
文献类型：
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作者：
Beckhauser TF;Francis-Oliveira J;De Pasquale R
在哺乳动物中枢神经系统中，活性氧(ROS)的产生被抗氧化剂防御所抵消。当ROS大量积累时，抗氧化机制变得不堪重负，可能会发生细胞氧化应激。因此，ROS的典型特征是毒性分子，氧化膜脂，改变蛋白质的构象，破坏核酸，导致突触可塑性缺陷。高ROS浓度与认知功能下降有关，如在一些神经退行性疾病中观察到的，以及与年龄相关的神经可塑性衰退。然而，受控的ROS产生为参与突触变化的转导通路的激活提供了最佳的氧化还原状态。由于ROS可能在调节神经元活动的同时引发负面影响，因此，有益和有害后果之间的区别尚不清楚。在这方面，本文对目前的研究进行了评价，描述了神经元中ROS的主要来源，明确了它们参与突触可塑性的过程，并区分了所涉及的生理和病理过程。
In the mammalian central nervous system, reactive oxygen species (ROS) generation is counterbalanced by antioxidant defenses. When large amounts of ROS accumulate, antioxidant mechanisms become overwhelmed and oxidative cellular stress may occur. Therefore, ROS are typically characterized as toxic molecules, oxidizing membrane lipids, changing the conformation of proteins, damaging nucleic acids, and causing deficits in synaptic plasticity. High ROS concentrations are associated with a decline in cognitive functions, as observed in some neurodegenerative disorders and age-dependent decay of neuroplasticity. Nevertheless, controlled ROS production provides the optimal redox state for the activation of transductional pathways involved in synaptic changes. Since ROS may regulate neuronal activity and elicit negative effects at the same time, the distinction between beneficial and deleterious consequences is unclear. In this regard, this review assesses current research and describes the main sources of ROS in neurons, specifying their involvement in synaptic plasticity and distinguishing between physiological and pathological processes implicated.