Packham N K, Barber J
Biochem J. 1984 Jul 15;221(2):513-20. doi: 10.1042/bj2210513.
The mechanism by which Ant2p [2-(3-chloro-4-trifluoromethyl)anilino-3, 5-dinitrothiophene] inhibits the oxygen evolution capacity of chloroplasts is thought to be due to a rapid reduction of the S2 and S3 oxidation states of the oxygen-evolving complex mediated by the oxidation of endogenous donors such as cytochrome b559. The results presented in this paper show that the degree of inhibition by Ant2p of the photosystem 2-supported electron transfer reactions, registered by the light-dependent rate of dichlorophenolindophenol reduction, varies according to the actinic light intensity. Moreover, a similar intensity-dependence can be detected in the extent of the Ant2p-induced cytochrome b559HP photo-oxidation. We show, however, that the dependence of the cytochrome oxidation is not due to the oxidation per se, but reflects changes in the high light-driven re-reduction reaction. The close correlation between the two Ant2p reactions is interpreted as indicating that the effect of Ant2p might be due to an inhibition of the S-state turnovers and not necessarily due to a deactivation process.
Ant2p [2-(3-氯-4-三氟甲基)苯胺基-3,5-二硝基噻吩]抑制叶绿体放氧能力的机制被认为是由于由细胞色素b559等内源性供体的氧化介导的放氧复合体的S2和S3氧化态的快速还原。本文给出的结果表明,通过二氯酚靛酚还原的光依赖速率记录的,Ant2p对光系统2支持的电子转移反应的抑制程度,会根据光化光强度而变化。此外,在Ant2p诱导的细胞色素b559HP光氧化程度中也能检测到类似的强度依赖性。然而,我们表明,细胞色素氧化的依赖性并非由于氧化本身,而是反映了高光驱动的再还原反应的变化。这两个Ant2p反应之间的密切相关性被解释为表明Ant2p的作用可能是由于对S态周转的抑制,而不一定是由于失活过程。