Abstract: Insecticide resistance is “the development of an ability in a strain of some organisms to tolerate doses of a toxicant which would prove lethal to a majority of individuals in a normal population of the same species". Mechanisms of resistance, such as behavioral change, physiological modification or metabolic detoxification, decrease the effective dose available at the target site. Behavioral resistance is defined as any behavior that reduces an insect's exposure to toxic compounds or that allows an insect to survive in an environment that is harmful and/or fatal to the majority of insects. Physiological modification mechanisms permit insects to survive lethal doses of a toxicant through decreased penetration of insecticides, increased sequestration/storage of insecticides, and accelerated excretion of insecticides. Metabolic detoxification is conferred by cytochrome P450 monooxygenases (cytochrome P450s), hydrolases, and glutathione transferases (GSTs). Cytochrome P450s constitute the largest gene superfamily and are critical for the detoxification and/or activation of xenobiotics and the metabolism of endogenous compounds. Increased P450-mediated detoxification has been found in many insect species, resulting in enhanced insecticide resistance. Glutathione transferases (GSTs) are soluble dimeric proteins involved in the metabolism, detoxification, and excretion of a large number of endogenous and exogenous compounds. Elevated GST activities have been implicated in resistance in many insect species. Hydrolases or esterases, a group of heterogeneous enzymes, have been identified as the active agents promoting hydrolase-mediated resistance that protect insects by either binding and sequestering insecticides through overproduction of proteins, or enhancing the metabolism of insecticides through increased enzyme activities.

Key words: Insecticide resistance, behavioral change, physiological modification, metabolic detoxification, glutathione S-transferases, cytochrome P450