Field considerations of Herbicide Metabolism
Differential metabolism of herbicides between crops and weeds has long been the basis for successful weed management. Selectivity can be altered by a variety of factors that can increase or decrease herbicide activity, including interaction with soil-applied insecticides, use of safeners, or the development of resistance in weeds. Bioactivation is also an example of selectivity. This section provides some examples of how important herbicide metabolism is in crop protection.
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.
Insecticides and propanil - Propanil activity on rice weeds can be increased with the addition of malathion (an organophosphate insecticide). Organophosphate insecticides can inhibit acyl arylamidase, the enzyme responsible for propanil metabolism. This approach also increases the likelihood of crop injury if too much enzyme inhibition occurs in the crop as well.
Metribuzin and PABA - Metribuzin activity on ivyleaf morning glory (Ipomoea hederacea) can be increased when the synergist PABA (picolinic acid t-butylamide or MZH 2091) is included in the spray solution. Normally, ivyleaf morningglory is able to metabolize metribuzin via deamination followed by conjugation. However, in the presence of PABA, deamination is slowed and thus, ivyleaf morningglory is more susceptible to metribuzin.
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.
Foliar-applied safeners - These safeners enhance the activity of cytochrome P450 monooxygenases and glucosyltransferases to protect grass crops from aryloxyphenoypropionate, sulfonylurea or imidazolinone herbicide injury. An example is the safener, fenchlorazole-ethyl used to protect grass crops (i.e. wheat, rye, barley) from fenoxyprop-ethyl injury. Normally, this class of herbicides controls grasses, but not broadleaf plants. These crop species possess higher levels of glutathione than grassy weeds and the safener enhances these levels further in the crop species, protecting them from herbicide damage.
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.
Another example of bioactivation is the photochemical reduction of paraquat (Figure 37). This reaction is nonenzymatic as an electron from the electron transport system in the chloroplast during the light reactions of photosynthesis reduces paraquat, creating a free radical (see the Reduction Reactions section for further explanation).
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?
Crop injury can increase under cool, wet conditions (Figure 38) - is it possible that the herbicide is taken up and translocated in these plants, but mechanisms of herbicide metabolism are compromised?