Lesson Media Objects
Metabolism of Herbicides or Xenobiotics in Plants
Metabolism of Herbicides or Xenobiotics in Plants - Field Considerations
Field considerations of Herbicide Metabolism
Corn root-worm insecticides and sulfonylureas - The root-worm insecticide, terbufos (an organophosphate insecticide), is applied as an in-furrow treatment with corn seeds. This treatment enhances the activity of primsulfuron and thus, corn injury. Crop safety is lost because terbufos binds to cytochrome P450 enzymes in corn, so the crop is less able to detoxify the herbicide. To avoid this problem, growers were advised not to use an in-furrow type treatment or to use a new formulation of Counter called Counter CR (Controlled Release). Now growers can also use BT-resistant crops.
Antagonists (also known as safeners, antidotes or crop protectants) - Safeners selectively protect crop plants from herbicide injury without protecting weeds. Many safeners are structurally similar to the herbicides that they antagonize.
Soil-applied safeners - These safeners are applied with the seed prior to planting or applied to the soil or crop together with the herbicides. They protect large-seeded grass crops (corn, sorghum, rice) against pre-plant incorporated or pre-emergence applications of thiocarbamate and chloroacetanilide herbicides. Most of the evidence suggests that these safeners protect the crop from injury by inducing enzymes that metabolize the herbicide, rather than by affecting herbicide absorption and translocation or its site of action. For example, these safeners increase the level of glutathione conjugation of chloracetanilide and thiocarbamate herbicides by inducing glutathione-S-transferases. As a result they may also increase the level of glutathione in the plant tissue.
In some cases, the biological activity of certain herbicides is increased via metabolism. A classic example is the bioactivation of the phenoxybutyric acids (e.g. 2,4-DB). These herbicides are not toxic until two carbons are removed enzymatically from butyric acid via ß-oxidation (Figure 36). This selectivity mechanism protects legumes from herbicidal injury as they do not catalyze this reaction; broadleaf weeds cleaving off the two carbons convert the phenoxybutyric acid into the herbicidal phenoxyacetic acid, such as 2,4-D.
Mechanisms of herbicide resistance are often based on changes in site of action; single point mutations in the genetic code alter the gene product such that it no longer binds the herbicide. There are several instances where the mechanism of herbicide resistance is metabolism based. In these cases, the resistant plant is able to metabolize the herbicide to a non-toxic form. Examples of enzymes expressed in resistant weeds that detoxify the herbicide include cytochrome-P450 monooxygenases, acyl arylamidases, and glutathione-S-transferases. An example of metabolism-based selectivity is Liberty Link crop technology. Crop resistance to Liberty (glufosinate) is based on the ability to metabolize the herbicide. Herbicide Resistance Lesson for more detail.
Other examples where herbicide metabolism may affect selectivity:
The formulated product, Distinct® is a combination of the auxinic herbicide, dicamba and the auxin transport inhibitor, diflufenzopyr. Diflufenzopyr enhances dicamba activity on broadleaf weeds because it blocks the transporters that would normally move auxin from cell to cell; because broadleaf weeds are less able to metabolize dicamba, the trapped herbicide is phytotoxic. If this formulation is applied when corn plants are too young, there is risk of crop injury. The younger corn tissue is apparently unable to handle dicamba accumulation. Is it possible they are not able to metabolize dicamba at a fast enough rate?
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