短期氧化预处理的辐射防护作用：锰超氧化物歧化酶的作用
Radioprotection by short-term oxidative preconditioning: role of manganese superoxide dismutase.
作者信息
Belikova Natalia A, Glumac Ashley, Rafikov Ruslan, Jiang Jianfei, Greenberger Joel S, Kagan Valerian E, Bayir Hülya
机构信息
Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15219, USA.
出版信息
FEBS Lett. 2009 Nov 3;583(21):3437-42. doi: 10.1016/j.febslet.2009.10.013. Epub 2009 Oct 12.
Abstract
Manganese superoxide dismutase (MnSOD) is vital to the protection of mitochondria and cells against oxidative stress. Earlier, we demonstrated that catalytically active homo-tetramer of MnSOD can be stabilized by oxidative cross-linking. Here we report that this effect may be translated into increased radioresistance of mouse embryonic cells (MECs) by pre-exposure to oxidative stress. Pre-treatment of MECs with antimycin A, rotenone or H(2)O(2) increased their survival after irradiation. Using MnSOD siRNA, we show that MECs with decreased MnSOD levels displayed a lowered ability to preconditioning. Thus oxidative preconditioning may be used for targeted regulation of MnSOD.
摘要
锰超氧化物歧化酶（MnSOD）对于保护线粒体和细胞免受氧化应激至关重要。此前，我们证明了MnSOD的催化活性同四聚体可通过氧化交联得到稳定。在此我们报告，这种效应可能通过预先暴露于氧化应激而转化为小鼠胚胎细胞（MECs）放射抗性的增加。用抗霉素A、鱼藤酮或H₂O₂预处理MECs可提高其辐照后的存活率。使用MnSOD siRNA，我们表明MnSOD水平降低的MECs预处理能力降低。因此，氧化预处理可用于对MnSOD进行靶向调控。
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2
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Neuropharmacology. 2008 Sep;55(3):334-44. doi: 10.1016/j.neuropharm.2008.02.017. Epub 2008 Mar 8.
3
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