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Environmental and Stress Physiology

Copper Toxicity Affects Photosystem II Electron Transport at the Secondary Quinone Acceptor, Q_B¹

Institute of Plant Physiology, P. O. Box 521, H-6701, Szeged, Hungary, Biological Research Center of Hungarian Academy of Sciences, P. O. Box 521, H-6701, Szeged, Hungary

The nature of Cu²⁺ inhibition of photosystem II (PSII) photochemistry in pea (Pisum sativum L.) thylakoids was investigated monitoring Hill activity and light emission properties of photosystem II. In Cu²⁺-inhibited thylakoids, diphenyl carbazide addition does not relieve the loss of Hill activity. The maximum yield of fluorescence induction restored by hydroxylamine in Tris-inactivated thylakoids is markedly reduced by Cu²⁺. This suggests that Cu²⁺ does not act on the donor side of PSII but on the reaction center of PSII or on components beyond. Thermoluminescence and delayed luminescence studies show that charge recombination between the positively charged intermediate in water oxidation cycle (S₂) and negatively charged primary quinone acceptor of pSII (Q_A^–) is largely unaffected by Cu²⁺. The S₂Q_B^– charge recombination, however, is drastically inhibited which parallels the loss of Hill activity. This indicates that Cu²⁺ inhibits photosystem II photochemistry primarily affecting the function of the secondary quinone electron acceptor, Q_B. We suggest that Cu²⁺ does not block electron flow between the primary and secondary quinone acceptor but modifies the Q_B site in such a way that it becomes unsuitable for further photosystem II photochemistry.

¹ This work was supported by the Research Funds of the Hungarian Academy of Sciences AKA(219/86) and OKKFT (TT 310/86).

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