Avaliação da exposição ao imidacloprida sobre o modelo de transtorno neurodesenvolvimental em Drosophila melanogaster

Abstract

Neurodevelopmental disorders have as main constituents Autism Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD). Imidacloprid is an insecticide belonging to the neonicotinoid family, which act as potent acetylcholine receptor agonists, having the ability to promote behavioral changes in Drosophila melanogaster, which are similar to the human phenotypes TEA and ADHD. The aim of the present study was to corroborate the action of imidacloprid as a chemical model of neurological development disorders at the behavioral level, together with the investigation of neurochemical changes induced by exposure to imidacloprid, which are related to the symptoms of these disorders in the Drosophila melanogaster model. Virgin flies and 3-day-old cheeks were used, divided into four groups and exposed to a standard diet (control) or diet containing imidacloprid (200, 400 or 600 pM) for 7 days. After the progeny hatched, the flies were subjected to in vivo activities (negative geotaxis, open field, social interaction, aggression, light/dark and grooming) and ex vivo [food consumption, dopamine levels, acetylcholinesterase activity (AChE), oxidative stress indicators (superoxide dismutase, SOD; catalase, CAT; glutathione S-transferase, GST; reactive oxygen species, ROS; substances reactive to thiobarbituric acid, TBARS; and protein and non-protein assays, PSH and NPSH) and assays cell viability (resazurin)]. The progeny of flies exposed to imidacloprid showed increased hyperactivity (geotaxis and open field task), aggressiveness, anxiety and repetitive movements, together with a decrease in social interaction. In addition, the progeny of flies exposed to imidacloprid showed decreased levels of dopamine and cell viability and increased oxidative stress (ROS and TBARS), however, the activity of AChE, CAT and GST and PSH and NPSH remained unchanged. Our results suggest the involvement of dopamine and oxidative stress as a possible mechanism of action for behavioral damage similar to TEA and ADHD induced by imidacloprid in Drosophila melanogaster.