Enzyme Induction as Detoxification Mechanism

The importance of the cytochrome P450 monooxygenases, glutathione S-transferases, car-boxylesterases, and epoxide hydrolases in insecticide metabolism and detoxification, as well as in insecticide resistance, is well documented. It is, therefore, logical to expect that an increase in these enzyme activities resulting from induction by xenobiotics would decrease the toxicity of an insecticide because of enhanced metabolism (see review by Yu, 1986a). 

Dietary a-pinene causes southern armyworm larvae to become more tolerant to the botanical insecticide, nicotine. Enhanced tolerance to synthetic insecticides also has been demonstrated in phytophagous insects fed plants capable of inducing microsomal monooxygenase activity. Variegated cutworm larvae fed peppermint leaves are more tolerant of the insecticides carbaryl, acephate, methomyl, and malathion than larvae fed snap bean leaves. Increased tolerance for carbaryl and methomyl also has been observed in larvae of the cabbage looper and alfalfa looper (Autographa califomica) fed peppermint plants instead of their favored host plants, broccoli and alfalfa. 

Further studies reveal that corn leaves, a potent inducer of microsomal monooxygenases, cause fall armyworm larvae to become less susceptible to the insecticides methomyl, acephate, methamidophos, diazinon, trichlorfon, monocrotophos, permethrin, and cypermethrin than soybean-fed larvae. 

Induction of glutathione S-transferases by phenobarbital in houseflies provides some protection against the toxicity of methyl parathion, methyl paraoxon, azinphosmethyl, and methidathion. Similarly, induction of glutathione S-transferase by host plants in fall armyworm larvae protects the larvae against organophosphate insecticides. Larvae fed 

Induction of carboxylesterases and epoxide hydroloases would also affect the toxicity of insecticides. For example, host plant induction of 1-naphthyl acetate esterase would decrease the toxicity of certain insecticides containing an ester linkage such as organo-phosphates, pyrethroids, and some juvenile hormone analogs and, possibly, carbamates. 

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