EFFECTS OF POTASSIUM-(PICRATE)-(18-CROWN-6) ON THE PHOTOSYNTHETIC ELECTRON-TRANSPORT

The effects of potassium-(picrate)-(18-crown-6) on the electron transp ort of photosystem II was investigated in isolated pea thylakoids. Low concentrations of the compound inhibited the fast decay of fluorescen ce yield associated with electron transfer between the primary (Q(A)) and secondary (Q(B)) quinone electron acceptor and increased the inter mediary level of fluorescence to the F-max level. The decay half-time of fluorescence yield measured in the presence of DCMU (S(2)Q(A)(-) ch arge recombination) decreased from about 1.8 s to about 0.3 s in thyla koids treated with potassium-(picrate)-(18-crown-6). While the inhibit ion of electron transport by DCMU gave rise to the appearance of a the rmoluminescence band at about +10 degrees C (S(2)Q(A)(-)charge recombi nation) addition of potassium-(picrate)-(18-crown-6) resulted in a the rmoluminescence band at about -10 degrees C. Increasing concentrations of potassium-(picrate)-(18-crown-6) diminished the fluorescence yield and the -10 degrees C TL band and abolished the Signal IIs and Signal IIf EPR signals of the tyrosine-D and tyrosine-Z electron donors, res pectively. The phenolic-type inhibitor, potassium picrate had the same effect on thermoluminescence and on the tyrosine EPR signals. It is c oncluded that potassium-(picrate)-(18-crown-6) is a phenolic type inhi bitor owing to its picrate constituent. At low concentrations picrate and potassium-(picrate)-18-crown) not only block the electron transpor t between Q(A), and Q(B) but they probably decrease the midpoint redox potential of Q(A), as well. At high concentrations they also inhibit the light-induced oxidation of the tyrosine-D and tyrosine-Z donors.