Neonicotinoid insecticides have posed a great threat to non-target organisms, yet the mechanisms underlying their toxicity are not well characterized. Major modes of action (MoAs) of imidacloprid were analyzed in an aquatic insect Chironomus dilutus. Lethal and sublethal outcomes were assessed in the midges after 96-h exposure to imidacloprid. Global transcriptomic profiles were determined using de novo RNA-sequencing to more holistically identify toxicity pathways. Transcriptional 10% biological potency values derived from ranked KEGG pathways and GO terms were 0.02 (0.01-0.08) (mean (95% confidence interval) and 0.05 (0.04-0.06) μg L-1, respectively, which were more sensitive than those from phenotypic traits (10% lethal concentration: 0.44 (0.23-0.79) μg L-1; 10% burrowing behavior concentration: 0.30 (0.22-0.43) μg L-1). Major MoAs of imidacloprid in aquatic species were identified as follows: the activation of nicotinic acetylcholine receptors (nAChRs) induced by imidacloprid impaired organisms' nerve system through calcium ion homeostasis imbalance and mitochondrial dysfunction, which posed oxidative stress and DNA damage and eventually caused death of organisms. The current investigation highlighted that imidacloprid affected C. dilutus at environmentally relevant concentrations, and elucidated toxicity pathways derived from gene alteration to individual outcomes, calling for more attention to toxicity of neonicotinoids to aquatic organisms.
Keywords: Biological potency distribution curve; Mitochondrial dysfunction; Neonicotinoid insecticides; Oxidative stress; Sensitive pathway.
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