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首页> 外文期刊>Free Radical Biology and Medicine: The Official Journal of the Oxygen Society >Prooxidant activity of the superoxide dismutase (SOD)-mimetic EUK-8 in proliferating and growth-arrested Escherichia coli cells.
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Prooxidant activity of the superoxide dismutase (SOD)-mimetic EUK-8 in proliferating and growth-arrested Escherichia coli cells.

机译:模拟超氧化物歧化酶(SOD)EUK-8在增殖和生长受阻的大肠杆菌细胞中的抗氧化活性。

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摘要

Numerous studies have aimed to alleviate oxidative stress in a wide range of organisms by increasing superoxide dismutase (SOD) activity. However, experimental approaches have yielded contradictory evidence, and kinetics models have shown that increases in SOD activity may increase, decrease, or not change hydrogen peroxide (H2O2) production, depending on the balance of the various processes that produce and consume superoxide (O2-). In this study we tested whether administration of EUK-8, a synthetic mimetic of the SOD enzyme, can protect starving Escherichia coli cells against stasis-induced oxidative stress. Surprisingly, administration of EUK-8 to starving E. coli cells enhances the production of reactive oxygen species (ROS), resulting in a massive increase of oxidative damage and replicative death of the bacteria. Our results confirm that manipulation of ROS levels by increasing SOD activity does not necessarily result in a consequent decline of oxidative stress and can yield opposite results in a relatively simple model system such as starving E. coli cells.
机译:众多研究旨在通过增加超氧化物歧化酶(SOD)活性来减轻多种生物体的氧化应激。但是,实验方法得出了相互矛盾的证据,动力学模型表明,SOD活性的增加可能会增加,减少或不改变过氧化氢(H2O2)的产生,这取决于产生和消耗超氧化物(O2- )。在这项研究中,我们测试了EUK-8(一种SOD酶的合成模拟物)的施用是否可以保护饥饿的大肠杆菌细胞免受血瘀症引起的氧化应激。出乎意料的是,对饥饿的大肠杆菌细胞施用EUK-8可提高活性氧(ROS)的产生,从而导致细菌的氧化损伤和复制性死亡大量增加。我们的结果证实,通过提高SOD活性来控制ROS含量并不一定会导致氧化应激的下降,并且在相对简单的模型系统(如饥饿的大肠杆菌细胞)中可能产生相反的结果。

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