A2 Vertaisarvioitu katsausartikkeli tieteellisessä lehdessä
Photoinhibition of Photosystem II
Tekijät: Tyystjärvi E
Julkaisuvuosi: 2013
Journal: International Review of Cell and Molecular Biology
Tietokannassa oleva lehden nimi: INTENATIONAL REVIEW OF CELL AND MOLECULAR BIOLOGY, VOL 300
Lehden akronyymi: INT REV CEL MOL BIO
Vuosikerta: 300
Aloitussivu: 243
Lopetussivu: 303
Sivujen määrä: 61
ISBN: 978-0-12-405210-9
ISSN: 1937-6448
DOI: https://doi.org/10.1016/B978-0-12-405210-9.00007-2
Tiivistelmä
Photoinhibition of Photosystem II (PSII) is the light-induced loss of PSII electron-transfer activity. Although photoinhibition has been studied for a long time, there is no consensus about its mechanism. On one hand, production of singlet oxygen (O-1(2)) by PSII has promoted models in which this reactive oxygen species (ROS) is considered to act as the agent of photoinhibitory damage. These chemistry-based models have often not taken into account the photophysical features of photoinhibition-like light response and action spectrum. On the other hand, models that reproduce these basic photophysical features of the reaction have not considered the importance of data about ROS. In this chapter, it is shown that the evidence behind the chemistry-based models and the photophysically oriented models can be brought together to build a mechanism that confirms with all types of experimental data. A working hypothesis is proposed, starting with inhibition of the manganese complex by light. Inability of the manganese complex to reduce the primary donor promotes recombination between the oxidized primary donor and Q(A), the first stable quinone acceptor of PSII. O-1(2) production due to this recombination may inhibit protein synthesis or spread the photoinhibitory damage to another PSII center. The production of O-1(2) is transient because loss of activity of the oxygen-evolving complex induces an increase in the redox potential of Q(A), which lowers O-1(2) production.
Photoinhibition of Photosystem II (PSII) is the light-induced loss of PSII electron-transfer activity. Although photoinhibition has been studied for a long time, there is no consensus about its mechanism. On one hand, production of singlet oxygen (O-1(2)) by PSII has promoted models in which this reactive oxygen species (ROS) is considered to act as the agent of photoinhibitory damage. These chemistry-based models have often not taken into account the photophysical features of photoinhibition-like light response and action spectrum. On the other hand, models that reproduce these basic photophysical features of the reaction have not considered the importance of data about ROS. In this chapter, it is shown that the evidence behind the chemistry-based models and the photophysically oriented models can be brought together to build a mechanism that confirms with all types of experimental data. A working hypothesis is proposed, starting with inhibition of the manganese complex by light. Inability of the manganese complex to reduce the primary donor promotes recombination between the oxidized primary donor and Q(A), the first stable quinone acceptor of PSII. O-1(2) production due to this recombination may inhibit protein synthesis or spread the photoinhibitory damage to another PSII center. The production of O-1(2) is transient because loss of activity of the oxygen-evolving complex induces an increase in the redox potential of Q(A), which lowers O-1(2) production.
Turun yliopiston Tutkimustietojärjestelmän portaali