Influence of herbicide binding on the redox potential of the quinone acceptor in photosystem - II. Relevance to photodamage and phytotoxicity

Here we show that herbicide binding influences the redox potential (Em) of the plastoquinone Q(A)/Q(A)(-) redox couple in Photosystem II (PSII). Pheno lic herbicides lower the Em by approximately 45 mV, while DCMU raises the E m by 50 mV, These shifts are reflected in changes in the peak temperature o f thermoluminescence bands arising from the recombination of charge pairs i nvolving Q(A)(-). The herbicide-induced changes in the Em of Q(A)/Q(A)(-) c orrelate with earlier work showing that phenolic herbicides increase the se nsitivity of PSII to light, while DCMU protects against photodamage. This c orrelation is explained in terms of the following hypothesis which is based on reactions occurring in the bacterial reaction center. The back-reaction pathway for P(680)(+)Q(A)(-) is assumed to be modulated by the free-energy gap between the P(680)(+)Q(A)(-) and the P680+Ph- radical pairs. When this gap is small (i,e., when the Em of Q(A)/Q(A)(-) is lowered), a true back-r eaction is favored in which P680+Ph- is formed, a state which decays formin g a significant yield of P-680 triplet, This triplet state of chlorophyll r eacts with oxygen, forming singlet oxygen, a species likely to be responsib le for photodamage. When the free-energy gap is increased (i,e., when the E m of Q(A)/Q(A)(-) is raised), the yield of the P680+Ph- is diminished and a greater proportion of the P(680)(+)Q(A)(-) radical pair decays by an alter native, less damaging, route. We propose that at least some of the phytotox ic properties of phenolic herbicides may be explained by the fact that they render PSII ultrasensitive to light due to this mechanism.