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本文引用的文献

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Oxygen and Oxygen Toxicity: The Birth of Concepts.氧气与氧中毒:概念的诞生
React Oxyg Species (Apex). 2016 Jan;1(1):1-8. doi: 10.20455/ros.2016.801.
2
Peroxiredoxin 6 phospholipid hydroperoxidase activity in the repair of peroxidized cell membranes.过氧化物酶 6 对过氧化细胞膜修复的磷脂氢过氧化物酶活性。
Redox Biol. 2018 Apr;14:41-46. doi: 10.1016/j.redox.2017.08.008. Epub 2017 Aug 12.
3
Peroxiredoxin 6 in the repair of peroxidized cell membranes and cell signaling.过氧化物酶体增殖物激活受体6在过氧化细胞膜修复及细胞信号传导中的作用
Arch Biochem Biophys. 2017 Mar 1;617:68-83. doi: 10.1016/j.abb.2016.12.003. Epub 2016 Dec 6.
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Astaxanthin supplementation attenuates immobilization-induced skeletal muscle fibrosis via suppression of oxidative stress.补充虾青素通过抑制氧化应激减轻固定诱导的骨骼肌纤维化。
J Physiol Sci. 2017 Sep;67(5):603-611. doi: 10.1007/s12576-016-0492-x. Epub 2016 Oct 6.
5
The analysis of antioxidant expression during muscle atrophy induced by hindlimb suspension in mice.小鼠后肢悬吊诱导肌肉萎缩过程中抗氧化剂表达的分析。
J Physiol Sci. 2017 Jan;67(1):121-129. doi: 10.1007/s12576-016-0444-5. Epub 2016 Mar 12.
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Moderate dependence of reactive oxygen species production on membrane potential in avian muscle mitochondria oxidizing glycerol 3-phosphate.在氧化磷酸甘油的禽类肌肉线粒体中,活性氧生成对膜电位的中度依赖性。
J Physiol Sci. 2015 Nov;65(6):555-9. doi: 10.1007/s12576-015-0395-2. Epub 2015 Sep 3.
7
Critical role of peroxiredoxin 6 in the repair of peroxidized cell membranes following oxidative stress.过氧化物酶体增殖物激活受体6在氧化应激后过氧化细胞膜修复中的关键作用。
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8
Solution structure of the reduced form of human peroxiredoxin-6 elucidated using zero-length chemical cross-linking and homology modelling.利用零长度化学交联和同源建模阐明人过氧化物还原酶-6还原形式的溶液结构。
Biochem J. 2015 May 15;468(1):87-98. doi: 10.1042/BJ20141463.
9
Inhibition of the phospholipase A2 activity of peroxiredoxin 6 prevents lung damage with exposure to hyperoxia.抑制过氧化物氧还蛋白6的磷脂酶A2活性可防止暴露于高氧环境时的肺损伤。
Redox Biol. 2015;4:321-7. doi: 10.1016/j.redox.2015.01.011. Epub 2015 Jan 16.
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A comparison of factors involved in the development of central nervous system and pulmonary oxygen toxicity in the rat.大鼠中枢神经系统和肺氧中毒发生过程中相关因素的比较。
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间歇性高压氧暴露动员过氧化物酶 6 以预防氧中毒。

Intermittent hyperbaric oxygen exposure mobilizing peroxiredoxin 6 to prevent oxygen toxicity.

机构信息

Department of Pharmacy, Shanghai Hospital of Traditional Chinese Medicine, Shanghai, China.

Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, 200433, China.

出版信息

J Physiol Sci. 2019 Sep;69(5):779-790. doi: 10.1007/s12576-019-00694-5. Epub 2019 Jul 8.

DOI:10.1007/s12576-019-00694-5
PMID:31286450
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10716995/
Abstract

Intermittent hyperbaric oxygen exposure (IE-HBO) can protect the body against oxygen toxicity, but the underlying mechanisms are not very clear. Peroxiredoxin 6 (Prdx6) is a special endogenous antioxidative protein. We explored if the protective effects of IE-HBO are related to Prdx6. Mice were exposed to 280 kPa O for 60 min, followed by 30-min exposure to 20% O/N mixture with equal pressure, repeated for six cycles. The Prdx6 protein level and non-selenium glutathione peroxidase (NSGPx) activity in the brain and lungs were then measured and the injury degree of lung and the oxidation level of brain and lung were evaluated. On this basis, the relationship between Prdx6 and IE-HBO's protection was explored. Generally, both IE-HBO and continuous exposure to HBO (CE-HBO) could increase the protein and mRNA levels of Prdx6, and such increases were more significant 24 h after cessation of exposure; moreover, the Prdx6 level of IE-HBO was higher than that of CE-HBO in both brain and lung, also more significantly 24 h after cessation of exposure. In addition, IE-HBO exposure could more effectively potentiate the activity of NSGPx and increase GSH content in brain and lung tissues. At the same time, it could reduce oxidation products in these tissues. IE-HBO could also provide protection for the lungs against injuries resulting from prolonged HBO exposure. These data showed that IE-HBO can potentiate the production and the activity of Prdx6 and consequently mitigate oxidative damages in brain and lungs. The influences of IE-HBO on Prdx6 may form an important basis for its protection against oxygen toxicity.

摘要

间歇性高压氧暴露(IE-HBO)可以保护机体免受氧毒性的影响,但具体的作用机制尚不清楚。过氧化物酶 6(Prdx6)是一种特殊的内源性抗氧化蛋白。本研究旨在探讨 IE-HBO 的保护作用是否与 Prdx6 有关。采用 280 kPa O2 60 min,随后以相同的压力 20% O2/ N2 混合物 30 min 的重复 6 个周期的方式对小鼠进行暴露。检测脑和肺组织中的 Prdx6 蛋白水平和非硒谷胱甘肽过氧化物酶(NSGPx)活性,并评估肺损伤程度和脑、肺组织的氧化水平。在此基础上,探讨了 Prdx6 与 IE-HBO 保护之间的关系。一般来说,IE-HBO 和持续高压氧暴露(CE-HBO)都可以增加 Prdx6 的蛋白和 mRNA 水平,并且在停止暴露 24 h 后增加更明显;此外,在脑和肺中,IE-HBO 的 Prdx6 水平高于 CE-HBO,在停止暴露 24 h 后更为明显。此外,IE-HBO 暴露可以更有效地增强 NSGPx 的活性,增加脑和肺组织中的 GSH 含量。同时,它可以减少这些组织中的氧化产物。IE-HBO 还可以为肺部提供针对长时间 HBO 暴露引起的损伤的保护。这些数据表明,IE-HBO 可以增强 Prdx6 的产生和活性,从而减轻脑和肺组织的氧化损伤。IE-HBO 对 Prdx6 的影响可能为其对抗氧毒性提供了重要的基础。