Neonicotinoid insecticides imidacloprid and clothianidin affect differently neural Kenyon cell death in the cockroach Periplaneta americana

The intracellular toxicity of the neonicotinoid insecticides imidacloprid and clothianidin was studied on cockroach Periplaneta americana Kenyon cells using the trypan blue exclusion test and the adenylate kinase (AK) detection reagent. To evaluate cytotoxicity, Kenyon cells were exposed to different concentrations (1, 5, 10, 50 and 100 μM) of both imidacloprid and clothianidin at different delays (1, 3, 5, 8 and 24 h). Our data show that both imidacloprid and clothianidin decreased cell viability, with a more pronounced effect following imidacloprid exposure. Indeed, a significant decrease of cell viability was observed for 50 and 100 μM imidacloprid at 8 and 24 h, with trypan blue exclusion test. Study of the AK activity revealed that 50 and 100 μM imidacloprid induced an increase of AK activity, except for 50 μM at 24 h whereas at the same concentrations, clothianidin induced a transient effect at 5 and 8 h. According to previous studies showing that imidacloprid was a partial agonist and clothianidin a full agonist of insect nicotinic acetylcholine receptors, we demonstrated that both imidacloprid and clothianidin were also able to induce distinct intracellular toxic effects.

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► We study the toxic effect of imidacloprid and clothianidin on Kenyon cell death.
► Both imidacloprid and clothianidin induced cell death at higher concentrations.
► Imidacloprid induces a persistent adenylate kinase activity while clothianidin induced a transient effect.
► We suggested that imidacloprid and clothianidin activate distinct intracellular mechanisms.