The foliar uptake of the AOPPs is very rapid, and studies using radiolabelled herbicides have shown that almost all of the applied dose remains at the site of application, and so contact damage is commonly observed at the treated leaf (Figure 8.5; Carr et al., 1986). De-esterification occurs in the leaf tissues, and the phytotoxic acid accumulates at the apical meristem, which becomes necrotic. Active plant growth and warm temperatures encourage active transport within the phloem and passive movement in the xylem, so that the acid accumulates in all meristematic zones. However, most herbicidal injury is noted in the apical meristem due to the limited translocation of these herbicides, with far fewer symptoms noted in the root meristem. Interference with lipid biosynthesis causes an irreversible disruption in membrane synthesis, so that normal plastid development is not observed and metabolism is drastically altered. Leaf elongation ceases within two days and plastid disruption is most marked in young leaves, which appear chlorotic. The main site of action is the apical meristem where large levels of de novo fatty acid biosynthesis are taking place to support growth. Within two to four days new tissue at the meristem can be easily detached from the rest of the plant. Grass death follows within two to three weeks after application. Grasses treated with the alaninopropionates and the CHDs show similar symptoms to those described above, although the CHDs have slower rates of penetration into the treated leaf.
Pre-planting or pre-emergent treatments with the thiocarbamates and chloroaceta-mides effectively provides a chemical barrier for the growth of grass seedlings. These compounds penetrate the mesocotyl of germinating weeds to inhibit lipid biosynthesis in these young tissues. Consequently, any tissues that emerge are chlorotic and short-lived. Indeed, seedling death will occur when seed reserves of fatty acids are exhausted.
apical meristem 0.64%
Figure 8.5 Percentage 14C-activity recovered from plants of Setaria viridis 72 h after treatment with radiolabelled fluazifop-butyl (modified from Carr et al., 1986).
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