Suppr超能文献

光合作用光胁迫的分子机制。

Molecular mechanisms of light stress of photosynthesis.

作者信息

Vass Imre, Cser Krisztián, Cheregi Otilia

机构信息

Institute of Plant Biology, Biological Research Center, Hungarian Academy of Sciences, 6726 Szeged, Temesvári krt. 62, Hungary.

出版信息

Ann N Y Acad Sci. 2007 Oct;1113:114-22. doi: 10.1196/annals.1391.017. Epub 2007 May 18.

Abstract

Photosynthesis is the basic energy conversion process on Earth, which makes possible the utilization of the energy of sunlight for living organisms. However, light is not only the basic driving force of photosynthesis, but also an important stress factor at the same time. Light-induced decline of photosynthetic activity, generally denoted as photoinhibition, is a general phenomenon in all oxygenic photosynthetic organism under conditions when the metabolic processes cannot keep up with the electron flow produced by the primary photoreactions. Although light-induced damage occurs in all pigmented photosynthetic complexes the primary site of photoinhibition is the photosystem II (PSII) complex, which performs light-driven oxidation of water to protons and oxygen. The main factors, which are responsible for the light sensitivity of photosystem II, are excited pigment molecules, oxygen, manganese, as well as electron donors with high-oxidizing potential. Photosystem II can be efficiently protected from photodamage by the combination of harmless dissipation of absorbed light energy, nonradiative charge recombination, and repair of damaged reaction center complexes, making possible the safe utilization of light, the highly energetic substrate of photosynthesis.

摘要

光合作用是地球上基本的能量转换过程,它使生物体能够利用太阳光的能量。然而,光不仅是光合作用的基本驱动力,同时也是一个重要的胁迫因素。光诱导的光合活性下降,通常称为光抑制,是所有光合放氧生物在代谢过程跟不上初级光反应产生的电子流的条件下普遍存在的现象。尽管光诱导的损伤发生在所有色素光合复合体中,但光抑制的主要位点是光系统II(PSII)复合体,它进行光驱动的水氧化为质子和氧气的过程。导致光系统II对光敏感的主要因素是激发的色素分子、氧气、锰以及具有高氧化电位的电子供体。通过吸收光能的无害耗散、非辐射电荷复合以及受损反应中心复合体的修复相结合,光系统II可以有效地免受光损伤,从而使光(光合作用的高能底物)得以安全利用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验