Characterization of the Inhibition of Photosynthetic Electron Transport in Pea Chloroplasts by the Herbicide 4,6-Dinitro-o-cresol by Comparative Studies with 3-(3,4-Dichlorophenyl)-1,1- dimethylurea

Abstract

An attempt to characterize the mechanism of inhibition of photosynthetic electron transport in isolated pea chloroplasts by the herbicide 4,6-dinitro-o-cresol (DNOC) by a comparison with the effects of 3-(3,4-dichlorophenyl)-1.1-dimethylurea (DCMU) revealed the following: 1.The percent inhibition of oxygen evolution by a given herbicide concentration is the same at various light intensities except at very low intensities where the percent inhibition becomes larger. The same results are obtained with the herbicide DCMU. 2.The concentration of DCMU causing 50% inhibition of oxygen evolution decreases with de­creasing chloroplast (and thus of chlorophyll) concentration. With DNOC, the relative decrease is much less than with DCMU. At the inhibited molecule, there appears to be a cooperative binding of DCMU with two binding sites and a noncooperative binding of DNOC with only one binding site. 3.The chlorophyll a fluorescence induction is influenced by DNOC in the same characteristic way as it is by DCMU: both herbicides cause a faster rise in fluorescence yield than in control chloroplasts, although a higher concentration of the former is required for the same effect. 4.The chlorophyll fluorescence emission spectra at 77 CK show a slight decrease in the bands at 685 and 735 nm, and no or only a very slight decrease at 695 nm upon addition of high con­centrations of either DCMU or DNOC before the onset of illumination. 5.The degree of polarization of chlorophyll a fluorescence is lower after addition of DCMU or DNOC upon excitation by 460 or 660 nm light. It is concluded that, although the chemical structure of DNOC is completely different from that of DCMU, its site and mechanism of inhibition is similar to that of DCMU. Both herbicides inhibit electron transport between the primary electron acceptor of photosystem II and the plastoquinone pool. This causes a closing of the reaction centers of photosystem II. However, the interaction with the inhibited molecule is different for the two herbicides.