Changes in [14C]Atrazine Binding Associated with the Oxidation-Reduction State of the Secondary Quinone Acceptor of Photosystem II

Abstract

One hypothesis of triazine-type herbicide action in photosynthetic material is that the herbicide molecule competes with a secondary quinone acceptor, B, for a binding site at the reaction center of photosystem II. The binding affinity of B was suggested to change with its level of reduction, being most strongly bound in its semiquinone form. To test this hypothesis, [14C]atrazine binding studies have been carried out under different photochemically induced levels of B reduction in Pisum sativum. Herbicide binding is reduced in continuously illuminated samples compared to dark-adapted samples. Decreased binding of atrazine corresponds to an increase in the semiquinone form of B. With flash excitation, the herbicide binding oscillates with a cycle of 2, being low on odd-numbered flashes when the amount of semiquinone form of B is greatest. Treatment with NH2OH significantly decreased the strength of herbicide binding in the dark as well as stop the ability of p-benzoquinone to oxidize the semiquinone form of B. The mode of action of NH2OH is disruption of quinones or their environment on both the oxidizing and reducing sides of photosystem II. Herbicide binding was unaltered under conditions when p-benzosemiquinone oxidation of the reduced primary acceptor, Q-, is herbicide insensitive; weak herbicide binding cannot explain this herbicide insensitivity. The quinone-herbicide competition theory of herbicide action is correct. Also, since quinones are lipophilic the importance of the lipid composition of the thylakoid membrane in herbicide interactions is stressed.