Abstract

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 b (559) 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 tyrosine(z), both cytochrome b (559) forms and chlorophyll(z), and that these sites are the source of the copper-induced fluorescence quenching and oxygen evolution inhibition in Photosystem II.

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