DCMU (3-(3,4-dichlorophenyl)-1,1-dimethylurea) at concentrations higher than 10 μM suppresses the second time range delayed fluorescence (DF) of pea chloroplasts, due to inhibition of the oxidizing side of photosystem II (PS II). The inhibition of the reducing side of PS II resulting in the suppression of millisecond DF takes place at much lower (∼0.01 μM) DCMU concentrations. The variation in the herbicide-affinities of the reducing and oxidizing sides of PS II is not the same for DCMU and phenol-type herbicides. The DCMU-affinity of the oxidizing side considerably increases and approximates that of the reducing side upon mild treatment of chloroplasts with oleic acid. Probably this is a result of some changes in the environment of the binding site at the oxidizing side. At DCMU concentrations higher than 1 mM, the chaotropic action of DCMU leads to the generation of millisecond luminescence which is not related to the functioning of the reaction centres.
Intensity of 2 s delayed fluorescence (DF) as a function of steady-state actinic light intensity was investigated in pea chloroplasts in the presence of 10 μM DCMU. The light saturation curve of DF was approximated by a sum of two hyperbolic components which differ by an order of magnitude in the half-saturating incident light intensity. The relative contribution of the amplitudes of the components was practically independent of cation (Na(+) and Mg(2+)) concentration and a short-term heating of the chloroplasts at 45°C. The component saturating at low incident light intensity was selectively suppressed by 100 μM DCMU or by 1 μmol μg(-1) Chl oleic acid. DF intensity following excitation by a single saturating 15 μs flash was equal to the intensity of the component saturating at a low incident light intensity. Upon flash excitation, the maximum steady-state DF level was found to be attained only after a series of saturating flashes. It is concluded that the two components of the DF light saturation curves are related to PS II centres heterogeneity in quantum yield of stabilization of the reduced primary quinone acceptor.
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