Topal, AhmetAlak, GoncaOzkaraca, MustafaYeltekin, Ash CilingirComakli, SelimAcil, GurdalAtamanalp, Muhammed2025-05-102025-05-1020170045-65351879-129810.1016/j.chemosphere.2017.02.0472-s2.0-85013059699https://doi.org/10.1016/j.chemosphere.2017.02.047https://hdl.handle.net/20.500.14720/11954Alak, Gonca/0000-0002-7539-1152; Cilingir Yeltekin, Asli/0000-0003-0071-7434; Comakli, Selim/0000-0002-8744-7686The extensive use of imidacloprid, a neonicotinoid insecticide, causes undesirable toxicity in non targeted organisms including fish in aquatic environments. We investigated neurotoxic responses by observing 8-hydroxy-2-deoxyguanosine (8-OHdG) activity, oxidative stress and acetylcholinesterase (AChE) activity in rainbow trout brain tissue after 21 days of imidacloprid exposure at levels of (5 mg/L, 10 mg/L, 20 mg/L). The obtained results indicated that 8-OHdG activity did not change in fish exposed to 5 mg/L of imidacloprid, but 10 mg/L and 20 mg/L of imidacloprid significantly increased 8-OHdG activity compared to the control (p < 0.05). An immunopositiv reaction to 8-OHdG was detected in brain tissues. The brain tissues indicated a significant increase in antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)) compared to the control and there was a significant increase in malondialdehyde (MDA) levels (p < 0.05). High concentrations of imidacloprid caused a significant decrease in AChE enzyme activity (p < 0.05). These results suggested that imidacloprid can be neurotoxic to fish by promoting AChE inhibition, an increase in 8-OHdG activity and changes in oxidative stress parameters. Therefore, these data may reflect one of the molecular pathways that play a role in imidacloprid toxicity. (C) 2017 Elsevier Ltd. All rights reserved.eninfo:eu-repo/semantics/closedAccessImidaclopridPesticideOxidative Stress8-OhdgAcetylcholinesteraseFishBrainToxicityArticle175Q1Q118619128219821WOS:000397691200022