Molecular mechanisms of the response of photosynthesis to oxidative stress

光系统II（PSII）的光抑制是由于PSII的光损伤速率与受损PSII的修复速率之间的不平衡所致。光损伤是由光对放氧复合物的直接作用引发的，因此，PSII的光损伤是不可避免的。氧化应激对光损伤和随后的修复的影响的研究表明，活性氧（ROS）主要通过抑制光损伤的PSII的修复，而不是直接损伤PSII。因此，强光对PSII具有双重作用：它直接损伤PSII，并通过产生ROS抑制PSII的修复。ROS诱导的修复抑制的研究已经证明，ROS抑制PSII修复所需的蛋白质，如D1蛋白质的从头合成。此外，对多核糖体的分析已经确定ROS抑制的主要靶点是翻译的延伸步骤。在体外使用蓝藻翻译系统的调查表明，延伸因子G可能是主要的目标，在翻译机制，抑制活性氧。在这里，我们提出了一个新的范例的分子作用的ROS在光抑制。

Ph00otoinhibition of photosystem II (PSII) is due to the imbalance between the rate of photodamage to PSII and the rate of the repair of damaged PSII. Photodamage is initiated by the direct effects of light on the oxygen-evolving complex and, thus, photodamage to PSII is unavoidable. Studies of the effects of oxidative stress on photodamage and subsequent repair have revealed that reactive oxygen species (ROS) act primarily by inhibiting the repair of photodamaged PSII and not by damaging PSII directly. Thus, strong light has dual effects on PSII ; it damages PSII directly and it inhibits the repair of PSII via production of ROS. Investigations of the ROS-induced inhibition of repair have demonstrated that ROS suppress the synthesis de novo of proteins that are required for the repair of PSII, such as the D1 protein. Moreover, analysis of polysomes has determined that a primary target for inhibition by ROS is the elongation step of translation. Investigations using a cyanobacterial translation system in vitro have revealed that elongation factor G might be the primary target, within the translational machinery, of inhibition by ROS. Here we present a new paradigm for the molecular action of ROS in photoinhibition.