Role of the proteasome in protein oxidation and neural viability following low-level oxidative stress
Role of the proteasome in protein oxidation and neural viability following low-level oxidative stress
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DOI：
10.1016/s0014-5793(03)00582-9
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发表时间：
2003-07-10
期刊：
影响因子：
3.5
通讯作者：
Keller, JN
中科院分区：
文献类型：
--
作者：
Ding, QX;Reinacker, K;Keller, JN
大量研究表明，蛋白酶体抑制可能在与氧化应激相关的条件下观察到的蛋白质氧化水平增加和神经元死亡中发挥因果作用。在目前的研究中，我们证明了给予无毒水平的氧化应激并不会导致20S/26S蛋白酶体活性的损害，而实际上是增加了特定蛋白酶体亚单位的表达。在存在蛋白酶体功能的情况下，观察到无毒水平的氧化应激可增加蛋白质的氧化量，这表明抑制蛋白酶体可能不会介导低水平氧化应激后蛋白质氧化的增加。根据蛋白酶体抑制剂治疗加剧氧化应激毒性的能力，维持基本的蛋白酶体功能似乎对于预防低水平氧化应激的神经毒性至关重要。综上所述，这些数据表明，维持神经蛋白酶体功能可能是预防神经毒性的关键，但不是低水平氧化应激后蛋白质氧化增加的关键。(C)2003年，埃尔塞维尔科学公司代表欧洲学会联合会出版。
Numerous studies suggest that proteasome inhibition may play a causal role in mediating the increased levels of protein oxidation and neuron death observed in conditions associated with oxidative stress. In the present study we demonstrate that administration of non-toxic levels of oxidative stress does not result in impairment of 20S/26S proteasome activity, and actually increases the expression of specific proteasome sub-units. Non-toxic levels of oxidative stress were observed to elevate the amount of protein oxidation in the presence of perserved proteasomal function, suggesting that proteasome inhibition may not mediate increases in protein oxidation following low-level oxidative stress. Perserving basal proteasome function appears to be critical to preventing the neurotoxicity of low-level oxidative stress, based on the ability of proteasome inhibitor treatment to exacerbate oxidative stress toxicity. Taken together, these data indicate that maintaining neural proteasome function may be critical to preventing neurotoxicity, but not the increase in protein oxidation, following low-level oxidative stress. (C) 2003 Published by Elsevier Science B.V. on behalf of the Federation of European Societies.