Summary:
The mechanism whereby Iinuron changes the functional and structural characteristics of chloroplast membranes was studied. The primary effect of the herbicide, the inhibition of phoiosynihetic electron transport results in an immuediatecessa‐tion of carbon dioxide fixation and alterations in the membrane energization. These are accompanied by secondary processes contributing to phytotoxicity. The fundamental action in its phytotoxicity, as shown in a model system of isolated chloro‐plasts, is the peroxidaiive breakdown of the polyunsaturated membrane lipids. This leads to destruction of the pigments, changes in the energy transfer, disorganization of the chloro‐plast membranes, and accumulation of toxic organic peroxides.
Summary
The herbicide safener N‐dichloroacetyl‐1‐oxa‐4‐aza‐spiro‐4,5‐decane (AD‐67) is of similar efficiency as the extensively used N.N‐diallyl‐2,2‐dichloroacetamide (R‐25788) and the structurally related 3‐(dichloroacetyl)‐2,2‐dimethyl‐1,3‐oxa‐zolidine (AD‐2) in reducing EPTC [S‐ethyl‐N,N‐dipropyl (thiocarhamate)] injury to maize (Zea mays L. cv. KSC 360). EPTC treatment produces growth retardation and deformities and inhibits CO2 fixation. It does not reduce epicuticular lipids appreciably but affects wax arrangement on the leaf surface. When EPTC is applied together with one of these safeners, these injuries are not observed. All three safeners act similarly. Each prevents the herbicide‐induced aggregation of epicuticular wax of maize, thereby protecting the plants against the formation of areas where the underlying cuticle layers are exposed and increase in transpiration.
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