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首页> 外文期刊>Free Radical Biology and Medicine: The Official Journal of the Oxygen Society >Increasing extracellular H2O2 produces a bi-phasic response in intracellular H2O2, with peroxiredoxin hyperoxidation only triggered once the cellular H2O2-buffering capacity is overwhelmed
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Increasing extracellular H2O2 produces a bi-phasic response in intracellular H2O2, with peroxiredoxin hyperoxidation only triggered once the cellular H2O2-buffering capacity is overwhelmed

机译：细胞外H2O2的增加会在细胞内H2O2中产生两相反应，过氧化物酶毒素的过氧化仅在细胞H2O2的缓冲能力不堪重负时才触发

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Reactive oxygen species, such as H2O2, can damage cells but also promote fundamental processes, including growth, differentiation and migration. The mechanisms allowing cells to differentially respond to toxic or signaling H2O2 levels are poorly defined. Here we reveal that increasing external H2O2 produces a bi-phasic response in intracellular H2O2. Peroxiredoxins (Prx) are abundant peroxidases which protect against genome instability, ageing and cancer. We have developed a dynamic model simulating in vivo changes in Prx oxidation. Remarkably, we show that the thioredoxin peroxidase activity of Prx does not provide any significant protection against external rises in H2O2. Instead, our model and experimental data are consistent with low levels of extracellular H2O2 being efficiently buffered by other thioredoxindependent activities, including H2O2-reactive cysteines in the thiol-proteome. We show that when extracellular H2O2 levels overwhelm this buffering capacity, the consequent rise in intracellular H2O2 triggers hyperoxidation of Prx to thioredoxin-resistant, peroxidase-inactive form/s. Accordingly, Prx hyperoxidation signals that H2O2 defenses are breached, diverting thioredoxin to repair damage. (C) 2016 The Authors. Published by Elsevier Inc.
机译：活性氧，例如H2O2，可以破坏细胞，但也可以促进基本过程，包括生长，分化和迁移。尚不清楚使细胞对毒性或信号过氧化氢水平做出不同反应的机制。在这里，我们揭示了增加的外部H2O2在细胞内H2O2中产生了两相反应。过氧化物酶（Prx）是丰富的过氧化物酶，可防止基因组不稳定，衰老和癌症。我们已经开发了一个模拟体内Prx氧化变化的动力学模型。值得注意的是，我们表明Prx的硫氧还蛋白过氧化物酶活性不能提供任何有效的保护，以防止H2O2的外部升高。相反，我们的模型和实验数据与低水平的细胞外H2O2被其他硫氧还蛋白依赖性活性（包括巯基蛋白质组中的H2O2反应性半胱氨酸）有效缓冲的现象相一致。我们显示，当细胞外H2O2水平超过了这种缓冲能力时，细胞内H2O2的随之升高会触发Prx过度氧化成对硫氧还蛋白抗性，过氧化物酶无活性的形式。因此，Prx过氧化信号表明H2O2防御被破坏，使硫氧还蛋白转移以修复损伤。 （C）2016作者。由Elsevier Inc.发布

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