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二溴噻吩喹对细胞色素 b6f 抑制剂光系统 II 激发和电子传递的副作用再评价。

Re-evaluation of the side effects of cytochrome b6f inhibitor dibromothymoquinone on photosystem II excitation and electron transfer.

机构信息

Groupe de Recherche en Biologie Végétale, Département de Chimie-Biologie, Université du Québec à Trois-Rivières, C.P. 500, Trois-Rivières, QC, G9A 5H7, Canada.

出版信息

Photosynth Res. 2013 Nov;117(1-3):489-96. doi: 10.1007/s11120-013-9798-1. Epub 2013 Feb 2.

DOI:10.1007/s11120-013-9798-1
PMID:23377902
Abstract

Dibromothymoquinone (DBMIB) has been used as a specific inhibitor of plastoquinol oxidation at the Q0 binding site of the cytochrome b6f complex for 40 years. It is thought to suppress electron transfer between photosystem (PS) II and I, as well as cyclic electron transfer around PSI. However, DBMIB has also been reported to act as a quencher of chlorophyll excited states. In this study, we have re-evaluated the effects of DBMIB on chlorophyll excited states and PSII photochemistry. The results show that DBMIB significantly quenches the chlorophyll excited states of PSII antenna even at low concentration (from 0.1 μM), lowering the effective excitation rate of the actinic light. It also acts as a potent PSII electron acceptor retarding the reduction of the plastoquinone pool with almost maximal potency at 2 μM. Altogether, these results suggest that experiments using DBMIB can easily be misinterpreted and stress on the importance of taking into account all these side effects that occur in the same range of DBMIB concentration used for inhibition of plastoquinol oxidation (1 μM).

摘要

二溴代噻吩甲酰亚胺(DBMIB)作为质体醌氧化还原酶在细胞色素 b6f 复合物 Q0 结合部位的特异性抑制剂已经使用了 40 年。它被认为可以抑制光系统(PS)II 和 PSI 之间的电子传递,以及 PSI 周围的环式电子传递。然而,DBMIB 也被报道为叶绿素激发态的猝灭剂。在这项研究中,我们重新评估了 DBMIB 对叶绿素激发态和 PSII 光化学的影响。结果表明,DBMIB 即使在低浓度(从 0.1 μM)下也能显著猝灭 PSII 天线的叶绿素激发态,降低了激活光的有效激发率。它还作为一种有效的 PSII 电子受体,在 2 μM 时几乎最大程度地延迟质体醌库的还原。总之,这些结果表明,使用 DBMIB 的实验很容易被误解,因此强调了在使用与抑制质体醌醇氧化(1 μM)相同浓度的 DBMIB 时考虑所有这些副作用的重要性。

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