Molecular mechanisms of photodamage in the Photosystem II complex

被引:298
作者
Vass, Imre [1 ]
机构
[1] Biol Res Ctr, Inst Plant Biol, H-6701 Szeged, Hungary
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2012年 / 1817卷 / 01期
关键词
Photoinhibition; Photoprotection; Photosystem II; Charge recombination; UV-B RADIATION; SINGLET OXYGEN PRODUCTION; AMINO-ACID-RESIDUES; PHOTOSYNTHETIC ELECTRON-TRANSPORT; PHOTOINHIBITION IN-VIVO; FREE-RADICAL PRODUCTION; OXIDATIVE STRESS; THERMOSYNECHOCOCCUS-ELONGATUS; CRYSTAL-STRUCTURE; WATER-OXIDATION;
D O I
10.1016/j.bbabio.2011.04.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Light induced damage of the photosynthetic apparatus is an important and highly complex phenomenon, which affects primarily the Photosystem II complex. Here the author summarizes the current state of understanding of the molecular mechanisms, which are involved in the light induced inactivation of Photosystem II electron transport together with the relevant mechanisms of photoprotection. Short wavelength ultraviolet radiation impairs primarily the Mn4Ca catalytic site of the water oxidizing complex with additional effects on the quinone electron acceptors and tyrosine donors of PSII. The main mechanism of photodamage by visible light appears to be mediated by acceptor side modifications, which develop under conditions of excess excitation in which the capacity of light-independent photosynthetic processes limits the utilization of electrons produced in the initial photoreactions. This situation of excess excitation facilitates the reduction of intersystem electron carriers and Photosystem II acceptors, and thereby induces the formation of reactive oxygen species, especially singlet oxygen whose production is sensitized by triplet chlorophyll formation in the reaction center of Photosystem II. The highly reactive singlet oxygen and other reactive oxygen species, such as H2O2 and O-2(-), which can also be formed in Photosystem II initiate damage of electron transport components and protein structure. In parallel with the excess excitation dependent mechanism of photodamage inactivation of the Mn4Ca cluster by visible light may also occur, which impairs electron transfer through the Photosystem II complex and initiates further functional and structural damage of the reaction center via formation of highly oxidizing radicals, such as P680(+center dot) and Tyr-Z(+center dot). However, the available data do not support the hypothesis that the Mn-dependent mechanism would be the exclusive or dominating pathway of photodamage in the visible spectral range. This article is part of a Special Issue entitled: Photosystem II. (C) 2011 Elsevier By. All rights reserved.
引用
收藏
页码:209 / 217
页数:9
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