In 1958 A. W. A. Brown's landmark publication, Insecticide Resistance in Arthropods, established the principle that insects as well as other related invertebrates are capable of developing resistance to insecticides through natural selection. The probability of the development of resistance largely depends on (1) the frequency of the resistance-conferring gene in the given population, (2) the level of selection pressure, (3) the degree to which resistant gene density is diluted by susceptible genes through influx of individuals from untreated areas, and (4) the stability of the resistance gene in the given population. In some cases, once established, resistance genes may persist in the same locality for many years. A good example may be the pyrethroid resistance of the moth Helicoverpa armígera, in Australia.
How insects develop resistance to insecticides is a topic that has fascinated many entomologists. Basically, there are two major ways through which insect pests acquire resistance: increased detoxification capabilities and alteration of the insecticide target sites (target sensitivity). The first type of resistance occurs more frequently than the second type, as well as all others. Detoxification of toxic insecticidal chemicals is carried out by specialized enzymes designed to handle all chemicals toxic to insects, not just insecticides. Insects, particularly those feeding on plants that produce naturally large amounts of toxic chemicals, have well-developed detoxification enzymes. There are three major types of detoxification enzymes: (1) broad-spectrum oxidases such as mixed function oxidases catalyzed by cytochrome P450, (2) hydrolases that break up esters, ethers, and epoxides, and (3) conjugation systems such as glutathione S-transferase, which are mediated to cover up the reactive part of the toxic chemical and further facilitate its removal. Every type of detoxification enzyme has been documented to play a role in the development of some form of resistance against various classes of insecticides.
In determining which type of detoxification enzymes will become the key player in the development of resistance, the most important factor for consideration is the chemical properties of the insecticide. For instance, carbamates and pyrethrins are readily detoxified by mixed function oxidases; therefore, if resistance is reported against these insecticides, one must first look for increased activities of mixed function oxidases in the resistant insects. If higher activity levels are found, the resistance spectrum (i.e., cross-resistance of carbamate-resistant insects to other types of insecticide) is usually wide because mixed function oxidases are capable of detoxifying chemicals of many different types. In contrast, organophosphorus and pyrethroid insecticides are mainly degraded by hydrolases. Thus, the involvement of an increased hydrolytic enzyme activity may be suspected when insects develop resistance against these chemicals.
A good example of this is malathion resistance. Malathion molecules contain two extra carboxylic acid ethyl ester parts. Malathion-resistant insects always show increased car-boxylesterase activity. Esterases of these types are not broad-spectrum enzymes, and therefore malathion resistance is usually specific (i.e., usually the insects resistant to malathion are not resistant to other insecticides). Insecticides with labile halogens, epoxides, methoxy unsaturation, and some aliphatic unsaturation may be degraded through these glutathione-mediated detoxification systems, and hence their elevated presence could be suspected to cause resistance. This scheme is, however, merely a rough guess about the possible mechanism of development of metabolic resistance. Indeed, unexpected and unique resistance mechanisms have been reported to occur in some combinations of insecticides and insects (e.g., DDT resistance in Drosophila). The recommended method of identification of the metabolic cause is to co-treat insects with the insecticide and specific inhibitors for each type of metabolic detoxification system, such as piperonyl butoxide for mixed function oxidase and DEF for esterases.
In studies of mechanisms for target insensitivity resistance, mutations occurring in the sodium channel, the GABA receptor, and acetylcholinesterase have been found in insects resistant to DDT/pyrethroids, cyclodiene insecticides, and organophosphorus and carbamate insecticides, respectively. Those resistances are characterized by their specificity (low degrees of cross-resistance) and the general stability of resistance among insect populations in given localities.
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