Michigan State University-Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, MI 48824.
Proc Natl Acad Sci U S A. 1984 Jul;81(13):4070-4. doi: 10.1073/pnas.81.13.4070.
A loss of electron transport capacity in chloroplast membranes was induced by high-light intensities (photoinhibition). The primary site of inhibition was at the reducing side of photosystem II (PSII) with little damage to the oxidizing side or to the reaction center core of PSII. Addition of herbicides (atrazine or diuron) partially protected the membrane from photoinhibition; these compounds displace the bound plastoquinone (designated as Q(B)), which functions as the secondary electron acceptor on the reducing side of PSII. Loss of function of the 32-kilodalton Q(B) apoprotein was demonstrated by a loss of binding sites for [(14)C]atrazine. We suggest that quinone anions, which may interact with molecular oxygen to produce an oxygen radical, selectively damage the apoprotein of the secondary acceptor of PSII, thus rendering it inactive and thereby blocking photosynthetic electron flow under conditions of high photon flux densities.
高光强会导致叶绿体膜中电子传递能力的丧失（光抑制）。抑制的主要部位是在光系统 II（PSII）的还原侧，对氧化侧或 PSII 的反应中心核心几乎没有损伤。除草剂（莠去津或敌草隆）的添加部分保护了膜免受光抑制；这些化合物取代了结合的质体醌（称为 Q(B)），质体醌在 PSII 的还原侧起次级电子受体的作用。通过失去与 [(14)C]莠去津结合的结合位点，证明了 32kDa 的 Q(B)脱辅基蛋白的功能丧失。我们认为，醌阴离子可能与分子氧相互作用产生氧自由基，选择性地破坏 PSII 的次级受体的脱辅基蛋白，从而使其失活，并在高光量子通量密度条件下阻断光合电子流。
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