Acute oxidant and inflammatory effects of imidacloprid on the mammalian central nervous system and liver in rats

Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet flea control programme because it’s high specificity as an insecticide. Imidacloprid toxicity on mammalian tissues has not been adequately evaluated. In the present study, potential acute neuro and liver toxic effects of imidacloprid were analyzed in rats as a model of mammalian using antioxidant–oxidant and inflammatory system. 10 μM imidacloprid was administrated intravenously and 2 h post-administration, the rats were sacrificed, liver and brains were surgically removed. Exposure to imidacloprid led to significant increases in nitric oxide concentrations in brain, liver and plasma samples. The quantitative mRNA transcriptional analyses demonstrated that imidacloprid-elevated production of NO levels due to the induction of iNOS in liver, but neither nNOS nor iNOS were induced in brain. The oxidant-generating enzymes xanthine oxidase and myeloperoxidase activities in both tissues were elevated and significant lipid peroxidation in liver and plasma was observed. The antioxidant catalase, superoxide dismutase and glutathione peroxidase activities were differently responded to imidacloprid administration. Significant intracellular glutathione depletion was also measured in both tissues. Imidacloprid treatment up-regulated inflammatory cytokines TNF-α, IL-6 and IL-1β mRNA transcriptions by 2.5- to 5.2-fold increases in both brain and liver. Conversely, anti-inflammatory mediator IL-10 mRNA was down-regulated in both organs. These results suggest that imidacloprid cause oxidative stress and inflammation in central nervous system and liver in non-target organisms in rats.