Abstract

Pyrethroid resistance in AustralianHelicoverpa armigerafield populations is primarily a consequence of the overproduction of esterase isoenzymes which metabolise and possibly sequester pyrethroid insecticides. Biochemical studies show that pyrethroid resistance-associated esterases inH. armigeraare inhibited by organophosphorous compounds, such as ethion, chlorpyrifos and its oxon, profenofos, and acephate. The organophosphates bind to the active site of the enzyme, thus preventing pyrethroid detoxification. Esterase inhibition by organophosphates does not occur immediately after dosage, but occurs rapidly, with maximum enzyme inhibition from 2 to 24 h after dosage, depending on the inhibitor used. These enzyme inhibition studies are supported by bioassay data using nontoxic doses of organophosphate as synergists for pyrethroids. The data show excellent levels of pyrethroid synergism against resistantH. armigera.One hundred percent mortality could be achieved whenH. armigerawere pretreated with some organophosphates and then dosed with pyrethroid, during the time of maximum enzyme inhibition. However, even when synergists and pyrethroids were applied together, up to 90;pc mortality was observed with more effective pyrethroids. Use of organophosphate synergists in the field may have the potential to restore some pyrethroid susceptibility in AustralianH. armigera.

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