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首页> 外文期刊>Progress in Neurobiology: An International Review Journal >Relationships between neuronal death and the cellular redox status. Focus on the developing nervous system.
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Relationships between neuronal death and the cellular redox status. Focus on the developing nervous system.

机译：神经元死亡与细胞氧化还原状态之间的关系。专注于发展中的神经系统。

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摘要

During the development of the nervous system, a large number of neurons are eliminated through naturally occurring neuronal death. Many morphological and biochemical properties of such dying neurons are reminiscent of apoptosis, a type of death involving the action of genetically-programmed events but also epigenetic phenomena including oxidative stress. The following review contains three parts focusing respectively on basic knowledge of neuronal death and redox regulation, the mechanisms involved in neuronal death which are ordered in three sequential phases, and on the complex relations between neuronal fate and the redox status. Finally, we point out that oxidants are not always detrimental for neuronal survival. On the one hand, dying neurons often display signs of oxidative stress, including an elevation of their intracellular concentration of free radicals. Antioxidants may reduce the extent of neuronal death, suggesting a causal implication of free radicals in the death-process. On the other hand, at high concentrations antioxidants may lose their protective effects on developing neurons, and a non-lethal oxidative stress may potentiate the protective effects of other agents. These data suggest that free radicals, perhaps through their effects on cellular signalling pathways, may have positive effects on neuronal survival, provided that their intraneuronal concentrations are maintained at low levels. Much evidence suggests that the neuronal redox status must be maintained within a narrow range of values compatible with survival. Antioxidants may protect neurons subjected to an oxidative stress following axotomy or trophic factor-deprivation; but excessive reduction may become equally detrimental for neurons.
机译：在神经系统发育期间，通过自然发生的神经元死亡消除了大量神经元。这种垂死的神经元的许多形态和生化特性使人想起细胞凋亡，这是一种死亡，涉及基因编程事件的作用，也涉及表观遗传现象，包括氧化应激。下面的综述分为三个部分，分别集中在神经元死亡和氧化还原调节的基础知识，神经元死亡涉及的机制（按三个连续的阶段排列）以及神经元命运与氧化还原状态之间的复杂关系上。最后，我们指出氧化剂并不总是对神经元存活有害。一方面，垂死的神经元通常表现出氧化应激的迹象，包括其细胞内自由基浓度的升高。抗氧化剂可以减少神经元死亡的程度，表明自由基在死亡过程中具有因果关系。另一方面，在高浓度下，抗氧化剂可能会失去对发育中神经元的保护作用，而非致命的氧化应激可能会增强其他药物的保护作用。这些数据表明，自由基可能通过其对细胞信号传导途径的影响而对神经元存活产生积极影响，前提是它们的神经元内浓度保持在较低水平。许多证据表明，神经元氧化还原状态必须维持在与存活率相适应的狭窄范围内。抗氧化剂可以保护轴突切开术或营养因子剥夺后遭受氧化应激的神经元;但是过度减少可能对神经元同样有害。

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