Metabolism based resistance

Nandula and Messersmith (2001) found that a wild oat accession with metabolism-based resistance to imazameth-abenz, an ALS inhibitor, was cross-resistant to flucarbazone-sodium (BAY MKH 6562). 

In certain situations it is possible to overcome herbicide metabolism-based resistance by adding an ingredient that will block detoxification of the herbicide in the resistant weed. One example is with propanil-resistant Echinochloa colona in rice in Latin America. The addition of piperophos, an organophosphate insecticide that inhibits the aryl acylamidase activity that confers resistance on the weed biotype [11]. This combination, based on an undo standing of the resistance mechanism, has beat approved for use on resistant... 

Two other Lolium ri dum biotypes from Australia (WLR2 and VLR69) developed metabolism-based resistance to PSII inhibitors. WLR2 came from a field with selection pressure by atrazine and amitrole, but never by phenylureas, and VLR69 from a field with selection pressure by diuron and atrazine. Both biotypes were resistant to triazines, and, despite the field selection by atrazine, resistance was more pronounced to the structurally related simazine. Furthermore, both biotypes were resistant to chlorotoluron, though only VLR69 was previously exposed to phenylureas. Analytical work revealed that in both resistant biotypes... 

Studies on the mode of inheritance of metabolic herbicide resistance in Mope-curus myosuroides did not result in a uniform picture. It was reported that a single gene was responsible for metabolism-based resistance in a biotype resistant to fenoxaprop and flupyrsulfuron [72], while in another biotype resistance to chloroto-luron was attributed to more than one gene [73]. 

Mechanisms of resistance to ACC-inhibiting herbicides can be divided into two categories ACC-related and metabolism-based. Metabolism-based resistance is well described and reviewed in the literature [35, 36]. In most cases, resistance is due to alteration of the target enzyme, making it less sensitive to inhibition, as reviewed by Devine [37] and by Delye [38] the latter gives an overview on homomeric plastidic ACC isoforms with altered sensitivities to AOPPs and CHDs or both [38]. Furthermore, the identification of mutations involved in altered sensitivity was achieved recently (Table 9.2) [38]. 

Perhaps plans have not heen formulated in several cases, or results disseminated. The avenues of research that the identification of a natural product may open are many, so that in the true sense these compounds may be considered allelochemic (J )as opposed to strictly allelopathic. For example, the discovery of a novel biologically active natural product logically presupposes that the metabolic pathway will eventually he elucidated, that possible synthesis, or partial synthesis may be attempted, that homologs and analogs will be described and that other areas may be considered for eventual employment of these materials, not only in more obvious uses such as pesticides, hut also medicinal and non-biological areas. An example of a non-biological use is that of orlandin ( ) which is denatured in acetone to produce an acid and base resistant product which is ceramic-like and is not soluble in organic solvents. 

The imidazolinone herbicides (Table 2.3.1) are a family of six compounds that were discovered and developed by American Cyanamid Corporation. Readers may obtain comprehensive and detailed information in The Imidazolinone Herbicides [1], a book authored by the researchers who discovered and developed the herbicides. The herbicides as a class are broad spectrum and are active both pre-and postemergence. Imidazolinones are absorbed and moved through both xylem and phloem, eventually accumulating in the meristematic tissue. Activity is characterized by rapid cessation of growth followed by plant death days or weeks after treatment. Selectivity is based most often on metabolic inactivation except for selection-developed target site based resistance. 

ACC-based resistance is expressed in pollen, whereas metabolism based is not [53, 54]. 

Because the MET-I acariddes share the same mode of action, a reasonable expectation would be that target site resistance may play a role in some of the cases where cross-resistance between MET-I acaricides has been observed. Perhaps, however, due to the complexity of the MET-I site with its many components originating from both mitochondrial and nuclear sources, target site-based resistance does not yet appear to be a primary resistance mechanism. Available information suggests that other resistance mechanisms such as metabolism predominate. As noted above, the MET-I acaricides are primarily metabolized by monooxygenases. 

Metabolically-based cross-resistance among the MET-I insecticides/acaricides should not be surprising. Despite the rather different chemistries involved, the MET-I compounds share similar molecular features, can assume a similar molecular shape [20], and the substituents on the tail region typically include a t-butyl or alkyl moiety. As noted in the above section on metabolism (Section 28.3.4), the t-butyl tail is also a common site for metabolism. Thus, any strain developing an enhanced metabolism to one of these compounds could reasonably be expected to exhibit some level of enhanced metabolism to the other members of this group, which is, in general, what has been observed. 

Resistance mechanisms associated with changes in toxicokinetics are predominately cases of enhanced metabolic detoxication. With readily biodegradable insecticides such as pyrethroids and carbamates, enhanced detoxication by P450-based monooxygenase is a common resistance mechanism (see Table 4.3). 

Resistance to DDT has been developed in many insect species. Although there are some cases of metabolic resistance (e.g., strains high in DDT dehydrochlorinase activity), particular interest has been focused on kdr and super kdr mechanisms based upon aberrant forms of the sodium channel—the principal target for DDT. There are many examples of insects developing resistance to dieldrin. The best-known mechanism is the production of mutant forms of the target site (GABA receptor), which are insensitive to the insecticide. 

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