The role of light in bentazon toxicity to cocklebur: Physiology and ultrastructure

Leaves from intact 10 to 14-day-old common cocklebur (Xanthium pensylvanicum Wallr.) plants were treated with 0.01 to 1 kg/ha of 3-isopropyl-1H-2,1,3-benzothiadiazin-(4)3H-one 2,2-dioxide (bentazon), and exposed to 21 to 86 klux. At intervals from 30 min to 38 hr, primary leaves were fixed for electron microscopic examination. Also, immediately after application of the herbicide, treated plants were placed in an assimilation chamber and net CO₂ exchange was measured.Light was required for necrosis to develop in bentazon-treated leaves; the higher the illuminance, the faster necrosis developed. At low levels of illuminance (21 to 36 klux), the chloroplasts became spherical and aggregated in the cells before the occurrence of general membrane rupture and the subsequent development of necrosis. However, at 86 klux, chloroplast shape and distribution did not change before membrane rupture. In both control and treated leaves that were placed in darkness, chloroplasts became spherical and aggregated. Therefore, the changes in shape and distribution of chloroplasts were not considered a toxic response.In all cases, cessation of photosynthesis preceded cytological changes. Photosynthesis was arrested more rapidly as the dose of bentazon increased. Regardless of the length of time required to stop photosynthesis, necrosis developed about 7 hr after photosynthesis was arrested when plants were grown under 86 klux. These data are consistent with the hypothesis that photo-induced toxic by-products result from stopping photosynthesis.