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Inhibition of Water Splitting Increases the Susceptibility of Photosystem II to Photoinhibition

机译:抑制水分解增加了光系统II对光抑制的敏感性

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摘要

Photosystem II (PSII)-enriched membrane particles were isolated from peas (Pisum sativum L.) and treated in several different ways to inhibit the water oxidation reactions, but not reaction center function itself, as judged by the light-induced rate of reduction of 2,6-dichlorophenol indophenol with and without the artificial electron donor, diphenyl carbazide. It was shown that such treatments increased the susceptibility of the PSII-enriched membranes to photoinhibition. This trend was further observed if 2,6-dichlorophenol indophenol was present during the illumination with photoinhibitory light. On the other hand, protection against the enhanced photoinhibition was found when the water-splitting activity was reconstituted or when the artificial electron donor diphenyl carbazide was present during the preillumination. The results indicate that irreversible photodamage occurred within the PSII reaction center as a consequence of illumination with strong light and that the rate of this damage was enhanced under conditions that are expected to give rise to a photoaccumulation of oxidizing species such as P680+ on the donor side of PSII. This mechanism of photoinhibitory damage occurred under both aerobic and anaerobic conditions.
机译:从豌豆(Pisum sativum L.)中分离出富含光系统II(PSII)的膜颗粒,并通过几种不同的方法对其进行处理,以抑制水氧化反应,但不能抑制反应中心本身的功能,这可以通过光诱导的Pb还原速率来判断有和没有人造电子供体的2,6-二氯苯酚吲哚酚,二苯卡巴肼。结果表明,这种处理增加了富含PSII的膜对光抑制的敏感性。如果在光抑制光照射期间存在2,6-二氯苯酚吲哚酚,则进一步观察到该趋势。另一方面,当重构水分解活性或在预照明期间存在人工电子给体二苯基咔嗪时,发现针对增强的光抑制的保护作用。结果表明,由于强光照射,PSII反应中心内发生了不可逆的光损伤,并且在预计会引起诸如P680 <+ 在PSII的捐助方。在有氧和厌氧条件下都发生了这种光抑制损伤的机理。

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