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An insight into the toxic effects of imidacloprid through measurements of cholinesterase activities and markers of oxidative stress in the blood and brain of male Wistar rats

Imidacloprid is the first neonicotinoid insecticide that acts as a selective toxicant on nicotinic acetylcholine receptors in insects [1, 2]. It is used for crop protection worldwide, as well as for non-agricultural uses [1]. Food is one of the main routes of human imidacloprid exposure [3]. Due to the ever-growing evidence for toxic effects of imidacloprid in animals and humans [4, 5, 6] and need to investigate them in more detail, we evaluated the effects of subchronic oral exposure to environmentally relevant doses of imidacloprid on relevant biochemical markers of toxicity in the blood and brain of adult male Wistar rats. Following a 28-day oral treatment with imidacloprid at 0.06 mg/kg b. w./day, 0.8 mg/kg b. w./day and 2.25 mg/kg b. w./day we measured total cholinesterase, acetylcholinesterase and butyrylcholinesterase activities as markers of cholinergic toxicity, and levels of lipid peroxidation, glutathione and reactive oxygen species as well as activities of glutathione peroxidase, superoxide dismutase and catalase as markers of oxidative stress. Exposure to low doses of imidacloprid did not cause significant changes in total cholinesterase, acetylcholinesterase and butyrylcholinesterase activity in rat blood and brain tissue. Concerning the influence on biomarkers of oxidative stress, treatment with the lowest dose of imidacloprid (which corresponds to the acceptable daily intake for imidacloprid) resulted with increased levels of lipid peroxidation and reactive oxygen species and decreased activities of antioxidative enzymes superoxide dismutase and catalase. The most pronounced effect was noticed in plasma. The highest levels of lipid peroxidation were detected in both plasma and brain tissue after treatment with the lowest dose of imidacloprid, being significantly elevated in plasma. Reactive oxygen species levels were also highest and significantly increased at the lowest dose in plasma. Superoxide dismutase activity in erythrocytes increased depending on the dose, being statistically significant at the highest dose. Treatment with the highest applied dose of imidacloprid also caused significantly increased activities of glutathione peroxidase in both plasma and brain tissue. Decreased superoxide dismutase and catalase activities were found in the plasma of rats treated with the lowest dose of imidacloprid. No changes in glutathione levels were found in the treated rats. Taken together, our findings suggest that oral 28-day exposure to low doses of imidacloprid caused a disturbance of redox homeostasis, i.e. the regulation of formation and removal of reactive oxygen species from the body system. These results call for further studies at molecular level to explain the toxicity of neonicotinoids after long-term exposure to environmentally relevant doses.

neonicotinoid insecticide, cholinergic toxicity, lipid peroxidation, reactive oxygen species, antioxidative enzymes

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