Insecticides mechanisms

Mode of Action. All of the insecticidal carbamates are cholinergic, and poisoned insects and mammals exhibit violent convulsions and other neuromuscular disturbances. The insecticides are strong carbamylating inhibitors of acetylcholinesterase and may also have a direct action on the acetylcholine receptors because of their pronounced stmctural resemblance to acetylcholine. The overall mechanism for carbamate interaction with acetylcholinesterase is analogous to the normal three-step hydrolysis of acetylcholine however, is much slower than with the acetylated enzyme. 

Chambers JE, Carr RE. 1995. Biochemical mechanisms contributing to species differences in insecticidal toxicity. Toxicology 105 291-304. 

Truhaut R, Gak JC, Graillot C. 1974. [Organochlorine insecticides Research work on their toxic action, its modalities and mechanisms. Part 1 Comparative study of the acute toxicity on the hamster and the rat.] Eur J Toxicol Environ Hyg 7 159-166. (French)... 

Many pesticides are not as novel as they may seem. Some, such as the pyre-throid and neonicotinoid insecticides, are modeled on natural insecticides. Synthetic pyrethroids are related to the natural pyrethrins (see Chapter 12), whereas the neo-nicotinoids share structural features with nicotine. In both cases, the synthetic compounds have the same mode of action as the natural products they resemble. Also, the synthetic pyrethroids are subject to similar mechanisms of metabolic detoxication as natural pyrethrins (Chapter 12). More widely, many detoxication mechanisms are relatively nonspecific, operating against a wide range of compounds that... 

Mechanism of action can be an important factor determining selectivity. In the extreme case, one group of organisms has a site of action that is not present in another group. Thus, most of the insecticides that are neurotoxic have very little phytotoxicity indeed, some of them (e.g., the OPs dimethoate, disyston, and demeton-5 -methyl) are good systemic insecticides. Most herbicides that act upon photosynthesis (e.g., triaz-ines and substituted ureas) have very low toxicity to animals (Table 2.7). The resistance of certain strains of insects to insecticides is due to their possessing a mutant form of the site of action, which is insensitive to the pesticide. Examples include certain strains of housefly with knockdown resistance (mutant form of Na+ channel that is insensitive to DDT and pyrethroids) and strains of several species of insects that are resistant to OPs because they have mutant forms of acetylcholinesterase. These... 

Hodgson, E. and Kuhr, R.J. (1990). A multiauthor work with a wealth of information on the mechanism of action of insecticides. 

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). 

In some resistant strains, both types of resistance mechanism have been shown to operate against the same insecticide. Thus, the PEG87 strain of the tobacco bud worm (Heliothis virescens) is resistant to pyrethroids on account of both a highly active form of cytochrome P450 and an insensitive form of the sodium channel (Table 4.3 and McCaffery 1998). 

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. 

There have been many reports of insect pest species developing resistance to OP insecticides, to the extent that control of the pest has been lost. A detailed account of resistance lies ontside the scope of the present book, and readers are referred to specialized texts by Georghion and Saito (1983), Brown (1971), and Otto and Weber (1992). A few examples will now be considered that illustrate the mechanisms by which insects become resistant to OP insecticides. 

Apart from the importance of OP resistance in pest control, ecotoxicologists have become interested in the development of resistance as an indication of the environmental impact of insecticides. Thus, the development of esteratic resistance mechanisms by aquatic invertebrates may provide a measure of the enviromnental impact of OPs in freshwater (Parker and Callaghan 1997). 

Eldefrawi, M.E. and Eldefrawi, A.T. (1991). Nervous-System-Based Insecticides—Describes the mechanisms of action of a wide range of neurotoxic compounds, both human-made and naturally occurring. 

Brooks, G.T. (1992). Progress in structure-activity smdies on cage convnlsants and related GABA receptor chloride ionophore antagonists. In D. Otto and B. Weber (Eds.) Insecticides Mechanism of Action and Resistance. Newcastle npon Tyne, UK Intercept Press, 237-242. 

Pilling, E.D., Bromley-ChaUenor, K.A.C., and Walker, C.H. et al. (1995). Mechanism of synergism between the pyrethroid insecticide lambda cyhalothrin and the imidazole fungicide prochloraz in the honeybee. Pesticide Biochemistry and Physiology 51, 1-11. 

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