| Abstract: | This study was conducted to evaluate genetic and biochemical aspects of metabolic resistance to insecticides. The temporal and dose effects of Arochlor₁₂₅₄ on diazinon tolerance and glutathione S-transferase activities were evaluated in one susceptible and two resistant house fly strains to determine the time and dose dependency of induction. Induction of diazinon tolerance and of glutathione S-transferase activity was observed in both susceptible and resistant strains of house flies. Resistant strains responded faster and to lower doses of Arochlor₁₂₅₄ than did the susceptible strain. This hypersensitivity to the xenobiotic was correlated to resistance and to the inheritance of chromosomes II and V from the resistant parent. The effects of chromosome II were of higher magnitude than that of chromosome V. Chromosome III also contributed to the changes in glutathione S-transferase activity after prolonged exposure to Arochlor₁₂₅₄. The presence of high-affinity juvenile hormone I (JHI)-binding proteins was established in both susceptible and resistant strains of house flies. JH-binding characteristics were correlated with resistance, with resistant strains showing higher K[subscript d] (lower affinity for JHI) and B[subscript max] (higher number of JH-binding sites) than the susceptible strain. K[subscript d] values ranged from 5.24 nM in the susceptible strain to 10.70 nM in the resistant strain. B[subscript max] values ranged from 1-3 pmol/mg of fractionated house fly proteins. The inheritance of JH-binding characteristics was followed using flies from the susceptible X resistant strain backcross. High K[subscript d] and B[subscript max] values correlated primarily with the inheritance of chromosomes II and V from the resistant parent. For K[subscript d] values, effects of chromosome V from the resistant parent were of higher magnitude than the effects of chromosome II. For B[subscript max] values the effects of chromosome II were found to be more than twice the effect of chromosome V. A number of xenobiotics were able to bind to JH-binding sites in house fly proteins. Methoprene, myrcene, Arochlor₁₂₅₄, DDT, diazinon, cypermethrin and methomyl showed measurable binding with JH-specific sites in house fly proteins. Phenobarbital and 3-methylcholanthrene failed to show any binding in JH-specific sites. Low but statistically significant differences in xenobiotic binding patterns were observed between susceptible and resistant strains. This study showed that the induction of detoxifying enzymes is a significant; component of metabolic resistance. Furthermore, the results also indicated that high-affinity JH-binding proteins, whose binding characteristics correlated with resistance and the inheritance of resistance chromosomes, are capable of binding xenobiotics. Through an unknown mechanism, these proteins are probably involved in the expression of metabolic resistance. |
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