Abstract

Abstract The effects of potassium-(picrate)-(18-crown-6) on the electron transport of photosystem II was investigated in isolated pea thylakoids. Low concentrations of the compound inhibited the fast decay of fluorescence yield associated with electron transfer between the primary (QA) and secondary (QB) quinone electron acceptor and increased the intermediary level of fluorescence to the Fmax level. The decay half-time of fluorescence yield measured in the presence of DCMU(S2QA - charge recombination) decreased from about 1.8 s to about 0.3 s in thylakoids treated with potassium-(picrate)-(18-crown-6). While the inhibition of electron transport by DCMU gave rise to the appearance of a thermoluminescence band at about + 10°C (S2QA - charge recombination) addition of potassium-(picrate)-(18-crown-6) resulted in a thermoluminescence band at about -10°C. Increasing concentrations of potassium-(picrate)-(18-crown-6) diminished the fluorescence yield and the -10°C TL band and abolished the Signal IIS and Signal IIf EPR signals of the tyrosine-D and tyrosine-Z electron donors, respectively. The phenolic-type inhibitor, potassium picrate had the same effect on thermoluminescence and on the tyrosine EPR signals. It is concluded that potassium-(picrate)-(18-crown-6) is a phenolic type inhibitor owing to its picrate constituent. At low concentrations picrate and potassium-(picrate)-18-crown) not only block the electron transport between QA and QB but they probably decrease the midpoint redox potential of QA, as well. At high concentrations they also inhibit the light-induced oxidation of the tyrosine-D and tyrosine-Z donors.

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