The unique toxicology of insects provides the safety mechanisms for the major insecticides. The selectivity of insecticidal nerve poisons is attributable to structural differences in binding subsites (acetylcholinesterase and nicotinic receptor) or receptor subunit interfaces (γ-aminobutyric acid receptor) or transmembrane regions (voltage-sensitive sodium channel) supplemented by metabolic activation and detoxification. Slow action limits the use of the remarkably selective insecticides acting at juvenile hormone and ecdysone receptors and inhibiting chitin biosynthesis. The δ-endotoxin of Bacillus thuringiensis induces midgut lysis and death in insects by a mechanism not applicable in mammals. Future pest management will rely on continuing advances in insect toxicology.
2004 Pesticide Science Society of Japan