Biggins J, Tanguay N A, Frank H A
Section of Biochemistry, Brown University, Providence, RI 02912.
FEBS Lett. 1989 Jul 3;250(2):271-4. doi: 10.1016/0014-5793(89)80736-7.
Photosystem I preparations were irradiated with UV to destroy vitamin K1 in situ. The depletion of vitamin K1 resulted in inactivation of NADP+ photoreduction and introduction of a approximately 220 ms component in the flash generated P700+ rereduction at room temperature. The photoreduction of the terminal FeS centers FA and FB in control and vitamin K1-depleted preparations at 7 K were comparable. The data confirm that vitamin K1 is functionally implicated in primary electron transfer reactions in PS I at physiological temperature, and that the anomalous results at cryogenic temperature may be explicable in terms of a by-pass of the vitamin K1 acceptor site or heterogeneity introduced into the photosystem by quinone removal.
用紫外线照射光系统I制剂以原位破坏维生素K1。维生素K1的消耗导致NADP+光还原失活，并在室温下的闪光产生的P700+再还原中引入了一个约220毫秒的成分。在7K下，对照制剂和维生素K1耗尽制剂中末端FeS中心FA和FB的光还原情况相当。数据证实，维生素K1在生理温度下在光系统I的初级电子转移反应中具有功能作用，并且低温下的异常结果可能可以通过维生素K1受体位点的旁路或醌去除引入光系统的异质性来解释。
