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.
Imidacloprid是一种具有内吸活性的新烟碱类杀虫剂。Imidacloprid通过作为错误的神经递质与昆虫神经系统的烟碱型乙酰胆碱受体结合，干扰正常神经传导，使神经传输保持开放状态，引起昆虫异常兴奋和麻痹死亡。Imidacloprid可用于神经毒性、细胞毒性、干扰代谢等相关研究[1-4]。
在体外，Imidacloprid（0.46-23μM）处理人前列腺上皮WPM-Y.1细胞24小时。Imidacloprid显著诱导细胞毒性、氧化应激、乳酸脱氢酶（LDH）活性增加、丙二醛（MDA）水平升高、谷胱甘肽（GSH）含量降低、谷胱甘肽-S-转移酶（GST）活性降低、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）活性增加，并导致超微结构缺陷如细胞器破坏、核膜不规则、染色质迁移、空泡增加、线粒体减少[5]。Imidacloprid（1-500μg）处理L-929成纤维细胞24h。Imidacloprid（500μg）显著增加L-929细胞乳酸脱氢酶（LDH）水平，下降低谷胱甘肽（GSH）水平，对乙酰胆碱酯酶（AChE）水平无显著影响[6]。
在体内，Imidacloprid（0.06、0.6或6mg/kg/day）通过饮食给药持续12周，用于处理喂食低脂（4% w/w）或高脂（20% w/w）饲料的雌性C57BL/6J小鼠。Imidacloprid显著增强了高脂饮食诱导的体重增加和肥胖，并增加了血清胰岛素水平[7]。Imidacloprid（5和20mg/kg/day）通过重复口服给药持续28天，用于处理雌性KM小鼠。Imidacloprid（20mg/kg/day）显著导致海马形成细胞带缺失、肝脏血管肿胀、肝索排列紊乱、肝细胞坏死和核固缩，并增加血浆ALT、AST和AKP水平；Imidacloprid（5mg/kg/day）显著改变海马和肝脏的代谢谱，涉及脂质代谢、氨基酸代谢、核苷酸代谢、碳水化合物代谢和能量代谢途径[8]。