We have found that elevated copper concentrations, apart from the inhibition of oxygen evolution, changed the initial states distribution of the oxygen-evolving complex. Already at low concentrations, copper ions oxidized the low-potential form of cytochrome b559 and also its high-potential form at higher concentrations at which fluorescence quenching was observed. We suggest that the primary target sites in Photosystem II for copper is tyrosinez, both cytochrome b559 forms and chlorophyllz, and that these sites are the source of the copper-induced fluorescence quenching and oxygen evolution inhibition in Photosystem II.

Abbreviations used: Chl, chlorophyll; cyt b559, cytochrome b559; FCCP, carbonyl cyanide p-trifluoromethoxyphenylhydrazone; HP, high potential; LP, low potential; PSII, Photosystem II.

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