Imidacloprid is a neonicotinoid insecticide with systemic activity. Imidacloprid acts as a false neurotransmitter by binding to nicotinic acetylcholine receptors in the insect nervous system, disrupting normal nerve transmission, keeping the nerve channels open, causing abnormal excitation, paralysis, and death in insects. Imidacloprid can be used in research related to neurotoxicity, cytotoxicity, and metabolic interference[1-4].
In vitro, Imidacloprid (0.46-23μM) was used to treat human prostate epithelial WPM-Y.1 cells for 24 hours. Imidacloprid significantly induced cytotoxicity, oxidative stress, increased lactate dehydrogenase (LDH) activity, elevated malondialdehyde (MDA) levels, decreased glutathione (GSH) content, reduced glutathione-S-transferase (GST) activity, increased activities of catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), and caused ultrastructural defects such as organelle destruction, irregular nuclear membrane, chromatin migration, increased vacuoles, and reduced mitochondria[5]. Imidacloprid (1-500μg) was used to treat L-929 fibroblast cells for 24 hours. Imidacloprid (500μg) significantly increased L-929 cell lactate dehydrogenase (LDH) levels, decreased glutathione (GSH) levels, and had no significant effect on acetylcholinesterase (AChE) levels[6].
In vivo, Imidacloprid (0.06, 0.6, or 6mg/kg/day) was administered via diet for 12 weeks to female C57BL/6J mice fed a low-fat (4% w/w) or high-fat (20% w/w) diet. Imidacloprid significantly enhanced high-fat diet-induced weight gain and obesity and increased serum insulin levels[7]. Imidacloprid (5 and 20mg/kg/day) was administered via repeated oral gavage for 28 days to female KM mice. Imidacloprid (20mg/kg/day) significantly caused hippocampal formation cell band loss, liver vascular swelling, disordered hepatic cord arrangement, hepatocyte necrosis and nuclear pyknosis, and increased plasma ALT, AST, and AKP levels; Imidacloprid (5mg/kg/day) significantly altered the metabolic profiles of the hippocampus and liver, involving lipid metabolism, amino acid metabolism, nucleotide metabolism, carbohydrate metabolism, and energy metabolism pathways[8].
References:
[1] Gautam P, Kumar Dubey S. Biodegradation of imidacloprid: Molecular and kinetic analysis. Bioresour Technol. 2022 Apr;350:126915.
[2] Bhende RS, Dafale NA. Insights into the ubiquity, persistence and microbial intervention of imidacloprid. Arch Microbiol. 2023 May 2;205(5):215.
[3] Fouad MR, Abdel-Raheem SAA. An overview on the fate and behavior of imidacloprid in agricultural environments. Environ Sci Pollut Res Int. 2024 Nov;31(52):61345-61355.
[4] Mikolić A, Karačonji IB. Imidacloprid as reproductive toxicant and endocrine disruptor: investigations in laboratory animals. Arh Hig Rada Toksikol. 2018 Jun 1;69(2):103-108.
[5] Abdel-Halim KY, Osman SR. Cytotoxicity and Oxidative Stress Responses of Imidacloprid and Glyphosate in Human Prostate Epithelial WPM-Y.1 Cell Line. J Toxicol. 2020 Dec 8;2020:4364650.
[6] Sevİm Ç, Taghİzadehghalehjoughİ A, Kara M. In Vitro Investigation of the Effects of Imidacloprid on AChE, LDH, and GSH Levels in the L-929 Fibroblast Cell Line. Turk J Pharm Sci. 2020 Oct;17(5):506-510.
[7] Sun Q, Qi W, Xiao X, et al. Imidacloprid Promotes High Fat Diet-Induced Adiposity in Female C57BL/6J Mice and Enhances Adipogenesis in 3T3-L1 Adipocytes via the AMPKα-Mediated Pathway. J Agric Food Chem. 2017 Aug 9;65(31):6572-6581.
[8] Zheng M, Qin Q, Zhou W, et al. Metabolic disturbance in hippocampus and liver of mice: A primary response to imidacloprid exposure. Sci Rep. 2020 Mar 31;10(1):5713.