Imidacloprid Impacts on Neurobehavioral Performance, Oxidative Stress, and Apoptotic Events in the Brain of Adolescent and Adult Rats.

Currently, imidacloprid (IMI) is the first insecticide and the second agrochemical highly applied all over the world. Here, we report on the impacts of IMI on neurobehavioral performance, oxidative stress, and apoptotic changes in the brain in either adult or adolescent rats. Forty male rats (adult and adolescent) were allocated to four groups. IMI groups were orally given 1 mg IMI/kg b.wt. dissolved in corn oil, whereas the controls were orally administered corn oil daily for 60 days. The obtained results demonstrated that IMI exposure resulted in less exploratory activity, deficit sensorimotor functions, and high depression. Levels of neurotransmitter including serotonin, gamma-aminobutyric acid, and dopamine were significantly reduced. Oxidative damage of brain tissues was evident following IMI exposure represented by the high levels of protein carbonyl, 8-hydroxyguanosine, and malondialdehyde, but total antioxidant capacity was reduced. Histopathological investigations of the brain tissues of IMI treated group revealed varying degrees of degeneration of the neuron. The immunohistochemical evaluation revealed a strong presence of glial fibrillary acidic protein (GFAP) and Bax positive cells, but a low expression of Bcl-2. These injurious impacts of IMI were very prominent in the adult rats than in the adolescent rats. Conclusively, exposure to IMI even at very low concentration could induce multiple neurobehavioral aberrations and neurotoxic impacts, especially in adults.