Detoxication resistance mechanisms

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). 

Another common resistance mechanism is enhanced detoxication in plants. Atrazine has an electrophilic carbon that may be attacked by glutathione, and biotypes of various weeds may have glutathione transferases that have a better ability to catalyze this reaction ... 

The other major mechanism of pyrethroid resistance found in some field strains of Heliothis virescens was enhanced detoxication due to a high rate of oxidative detoxication, mediated by a form of cytochrome P450 (McCaffery 1998). Some strains, such as PEG 87, which was subjected to a high level of field and laboratory selection, possessed both mechanisms. Other example of pyrethroid resistance due to enhanced detoxication may be found in the literature on pesticides. 

Figure 2. Detoxicative mechanisms imparting organo-phosphorus-resistance (e.g. to methyl parathion)...

The conjugation of xenobiotics with glutathione (GSH) in higher plants was first demtxistrated to be a major enzymatic detoxication mechanism with the atrazine herbicide in sorghum, corn, and other atrazine resistant species (77-80) (Equation 15). Since this... 

Our current understanding of insecticide resistance phenomena in insects and other arthropods is based upon genetic and biochemical evidence, which implicates a number of different mechanisms (1). These include metabolic mechanisms, which result in enhanced rates of insecticide detoxication or sequestration of insecticide, and also mechanisms involving reduced... 

Besides detoxication, another pharmacokinetic mechanism of resistance, retarded penetration, has been identified and mapped to linkage group III of the house fly where it is known as Pen (1) or tin (2). This gene imparts low resistance however, its combination with other mechanisms can be synergistic in producing higher than expected resistance. Because the biochemical basis of this mechanism is unknown, it will not be discussed further in this paper. 

During the 1950s, an era when biochemical knowledge developed very fast, there was a very strong belief that by finding the biochemical mechanism for resistance, it should be easy to find some substance that counteracted it, for instance, inhibitors of enzymes that detoxicate the pesticide or a new pesticide that shows higher activity toward the resistant insects. 

The biochemical and physiological mechanisms may be many, but resistance is often due to an insensitive target for the pesticide or to increased detoxication. 

The feasibility of using these antinutritive plant systems as multiple-factor/multiple-mechanism resistance against noctuid larvae remains to be determined. It is possible that such a multiple onslaught against nutrient acquisition is redundant. In other words, perhaps merely the use of PPO and chlorogenic acid is sufficient. It also remains to be determined whether this proposed multiple-factor/multiple-mechanism of resistance renders the insects detoxicative systems more susceptible to traditional control tactics, and whether the evolution of resistance to such multiple antinutritive factors is more difficult than to insecticides. 

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