Rachel R Rix1, G Christopher Cutler1. 1. Department of Plant, Food and Environmental Sciences, Faculty of Agriculture, Dalhousie University, Truro, Nova Scotia, Canada.
Abstract
BACKGROUND: Hormetic preconditioning, whereby exposure to mild stress primes an organism to better tolerate subsequent stress, is well documented. It is unknown if exposure to hormetic concentrations of insecticide can trans-generationally prime insects to better tolerate insecticide exposure, or whether exposure to hormetic concentrations of insecticide can induce mutations in genes responsible for insecticide resistance. Using the aphid Myzus persicae (Sulzer) and the insecticide imidacloprid as a model, we examined if exposure to mildly toxic and hormetic concentrations of imidacloprid reduced aphid susceptibility to insecticides across four generations, and whether such exposures induced mutations in the imidacloprid binding site in post-synaptic nicotinic acetylcholine receptors. RESULTS: Chronic, multigenerational exposure of aphids to hormetic concentrations of imidacloprid primed offspring to better survive exposure to certain concentrations of imidacloprid, but not exposure to spirotetramat, an insecticide with a different mode of action. Exposure to hormetic and mildly toxic concentrations of imidacloprid did not result in mutations in any of the examined nicotinic acetylcholine receptor subunits. CONCLUSION: Our findings demonstrate that exposure to hormetic concentrations of insecticide can prime insects to better withstand subsequent chemical stress, but this is dependent upon the insecticide exposure scenario, and may be subtle over generations.
BACKGROUND: Hormetic preconditioning, whereby exposure to mild stress primes an organism to better tolerate subsequent stress, is well documented. It is unknown if exposure to hormetic concentrations of insecticide can trans-generationally prime insects to better tolerate insecticide exposure, or whether exposure to hormetic concentrations of insecticide can induce mutations in genes responsible for insecticide resistance. Using the aphid Myzus persicae (Sulzer) and the insecticide imidacloprid as a model, we examined if exposure to mildly toxic and hormetic concentrations of imidacloprid reduced aphid susceptibility to insecticides across four generations, and whether such exposures induced mutations in the imidacloprid binding site in post-synaptic nicotinic acetylcholine receptors. RESULTS: Chronic, multigenerational exposure of aphids to hormetic concentrations of imidacloprid primed offspring to better survive exposure to certain concentrations of imidacloprid, but not exposure to spirotetramat, an insecticide with a different mode of action. Exposure to hormetic and mildly toxic concentrations of imidacloprid did not result in mutations in any of the examined nicotinic acetylcholine receptor subunits. CONCLUSION: Our findings demonstrate that exposure to hormetic concentrations of insecticide can prime insects to better withstand subsequent chemical stress, but this is dependent upon the insecticide exposure scenario, and may be subtle over generations.