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衰老过程中的超氧化物和一氧化氮

Superoxide and nitric oxide in senescence and aging.

作者信息

Afanas'ev Igor

机构信息

Vitamin Research Institute, Moscow, Russia.

出版信息

Front Biosci (Landmark Ed). 2009 Jan 1;14(10):3899-912. doi: 10.2741/3499.

Abstract

In this review some aspects of free radical theory of aging are discussed. Many new and interesting findings concerning the role of physiological free radicals superoxide and nitric oxide in senescence and aging development are considered and the mechanisms of processes mediated by these radicals are discussed. It has been known for a long time that being themselves mostly harmless species, superoxide and NO are precursors of really reactive species hydroxyl radicals and peroxynitrite, the initiators of aging and various pathologies. However, contemporary studies demonstrate the other maybe more important ways of damaging activity of physiological free radicals. Numerous studies show that lessening of NO production and its bioavailability could be a starting point of aging development. It results in a decrease in NO inhibition of mitochondrial cytochrome c oxidase and an increase in dioxygen consumption. That in its turn leads to an increase in the production of superoxide and the other reactive oxygen and nitrogen species and initiation of apoptosis, In conclusion the possibilities of pharmacological intervention with antioxidants and other antiradical procedures to suppress aging and senescence or even to expand the life span of animals are considered.

摘要

在这篇综述中,讨论了衰老自由基理论的一些方面。考虑了许多关于生理性自由基超氧化物和一氧化氮在衰老及衰老发展过程中作用的新的有趣发现,并讨论了由这些自由基介导的过程机制。长期以来人们都知道,超氧化物和一氧化氮本身大多是无害的物种,但它们是真正具有反应活性的物种羟基自由基和过氧亚硝酸盐的前体,而过氧亚硝酸盐是衰老和各种病理的引发剂。然而,当代研究表明了生理性自由基破坏活性的其他或许更重要的方式。大量研究表明,一氧化氮产生及其生物利用度的降低可能是衰老发展的起点。这会导致一氧化氮对线粒体细胞色素c氧化酶的抑制作用减弱以及耗氧量增加。进而导致超氧化物以及其他活性氧和氮物种的产生增加,并引发细胞凋亡。总之,还考虑了使用抗氧化剂和其他抗自由基程序进行药物干预以抑制衰老和延缓衰老甚至延长动物寿命的可能性。

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