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水分解锰配合物控制光诱导的细胞色素 b559 在光系统 II 中的氧化还原变化。

Water-splitting manganese complex controls light-induced redox changes of cytochrome b559 in photosystem II.

机构信息

Department of Experimental Physics, Faculty of Science, Palacký University, Olomouc, Czech Republic.

出版信息

J Bioenerg Biomembr. 2010 Aug;42(4):337-44. doi: 10.1007/s10863-010-9299-2. Epub 2010 Jul 7.

Abstract

The effect of water-splitting Mn complex on light-induced redox changes of cytochrome b(559) (cyt b(559)) was studied in spinach photosystem II (PSII) membranes. Photoreduction of the heme iron in the intact PSII membranes was completely suppressed by DCMU, whereas photoreduction and photooxidation of the heme iron in the Mn-depleted PSII membranes were unaffected by DCMU. Interestingly, photoreduction and photooxidation of the heme iron in the Mn-depleted PSII membranes were completely diminished by exogenous superoxide dismutase (SOD), whereas no effect of SOD on photoreduction of the heme iron was observed in the intact PSII membranes. The current work shows that the light-induced redox changes of cyt b(559) proceed via a different mechanism in the both types of PSII membranes. In the intact PSII membranes, photoreduction of the heme iron is mediated by plastoquinol. However, in the Mn-depleted PSII membranes, photoreduction and photooxidation of the heme iron are mediated by superoxide anion radical formed in PSII.

摘要

在菠菜光系统 II(PSII)膜中研究了水分解 Mn 配合物对细胞色素 b(559)(cyt b(559))的光诱导氧化还原变化的影响。在 DCMU 存在下,完整 PSII 膜中血红素铁的光还原完全被抑制,而 Mn 耗尽 PSII 膜中血红素铁的光还原和光氧化不受 DCMU 影响。有趣的是,Mn 耗尽 PSII 膜中外源性超氧化物歧化酶(SOD)完全消除了血红素铁的光还原和光氧化,而在完整 PSII 膜中未观察到 SOD 对血红素铁光还原的影响。目前的工作表明,两种类型的 PSII 膜中 cyt b(559)的光诱导氧化还原变化通过不同的机制进行。在完整的 PSII 膜中,血红素铁的光还原由质体醌介导。然而,在 Mn 耗尽的 PSII 膜中,血红素铁的光还原和光氧化由 PSII 中形成的超氧阴离子自由基介导。

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