Influence of herbicide binding on the yield of singlet oxygen production in photosystem II and on charge recombination kinetics in the T4 mutant of Rhodopseudomonas viridis

Abstract

Herbicide binding influences the redox potential (Em) of the QA/QA- redox couple. Phenolic herbicides lower the Em by 45 mV, while DCMU raises it by 50 mV. Earlier work shows that phenolics increase photodamage, while DCMU protects against it. This is explained by the following hypothesis, based on reactions occurring in the bacterial reaction centre. The P680+QA- recombination pathway is assumed to be modulated by the free energy between the P680+QA- and P680+Ph- radical pairs. When this gap is small (i.e., when the Em of QA/QA- is lowered), a true back-reaction is favoured via P680+Ph-, a state which decays forming a significant yield of 3P680. 3Chl reacts with O2, forming 1O2, a species likely to be responsible for photodamage. When the free energy gap is increased, the yield of P680+Ph- is diminished and a greater proportion of the P680QA- radical pair decays by an alternative, less damaging, route. We measured the yield of 1O2 formation in the presence of herbicides by EPR spectroscopy, using 2,2,6,6-Tetramethyl-piperidine as a spin trap. Furthermore we measured the temperature dependence of P+QA- recombination kinetics by flash-induced absorption spectroscopy using the PSII herbicide-sensitive T4 mutant of Rhodopseudomonas viridis. In the presence of phenolics the yield of 1O2 formation is higher, the reduction P+ is faster and the activation energy needed for recombination is smaller compared with urea type herbicides. Some of the phytotoxic properties of phenolics may be explained by the fact that they render PSII ultrasensitive to light due to this mechanism.