In Vitro Investigation of the Effects of Imidacloprid on AChE, LDH, and GSH Levels in the L-929 Fibroblast Cell Line.

Objectives There are several types of pesticides to control pests and several new types coming into use that could be less toxic compared to the old ones. Pesticide-induced oxidative stress, which is one of the main mechanisms of toxicity, is the research area focused most on over the last decade. There are several different studies in the literature on whether pesticide exposure induces oxidative stress parameter-mediated toxicity. Pesticide-induced oxidative stress level depends on the biochemical features of mammalian systems. Imidacloprid is a neonicotinoid pesticide in wide use that is considered safe; however, it has been reported in different studies that it may cause changes in oxidative stress parameters. Materials and Methods We investigated the dose- and time-dependent effects of imidacloprid on acetylcholinesterase (AChE), lactate dehydrogenase (LDH), and glutathione (GSH) levels in the L-929 fibroblast cell line. The effects of 1-500 μg imidacloprid dose range on AChE, GSH, and LDH were investigated. Results LDH levels were significantly increased dose dependently in the 250 and 500 ng imidacloprid groups compared to the control group. GSH levels nonsignificantly decreased dose dependently and GSH levels were lower in the 500 ng imidacloprid group compared to the control group. There were no significant differences between the groups in AChE levels. Conclusion These results indicated that high doses of imidacloprid may induce oxidative stress in fibroblast cells.

[1]  Sozan A. Ali,et al.  Dose-related impacts of imidacloprid oral intoxication on brain and liver of rock pigeon (Columba livia domestica), residues analysis in different organs. , 2019, Ecotoxicology and environmental safety.

[2]  Yongtao Han,et al.  The metabolism distribution and effect of imidacloprid in chinese lizards (Eremias argus) following oral exposure. , 2018, Ecotoxicology and environmental safety.

[3]  L. Bláha,et al.  Acute and (sub)chronic toxicity of the neonicotinoid imidacloprid on Chironomus riparius. , 2018, Chemosphere.

[4]  W. Jiao,et al.  Chronic brain toxicity response of juvenile Chinese rare minnows (Gobiocypris rarus) to the neonicotinoid insecticides imidacloprid and nitenpyram. , 2018, Chemosphere.

[5]  P. Uchil,et al.  Analysis of Cell Viability by the Lactate Dehydrogenase Assay. , 2018, Cold Spring Harbor protocols.

[6]  K. Cha,et al.  The relationship between serum ammonia level and neurologic complications in patients with acute glufosinate ammonium poisoning: A prospective observational study , 2018, Human & experimental toxicology.

[7]  H. Gil,et al.  Seizures in patients with acute pesticide intoxication, with a focus on glufosinate ammonium , 2018, Human & experimental toxicology.

[8]  S. Réhman,et al.  Pesticide-induced oxidative stress and antioxidant responses in tomato (Solanum lycopersicum) seedlings , 2018, Ecotoxicology.

[9]  A. Anadón,et al.  Mechanism of Neonicotinoid Toxicity: Impact on Oxidative Stress and Metabolism. , 2018, Annual review of pharmacology and toxicology.

[10]  H. Arslan,et al.  Imidacloprid exposure cause the histopathological changes, activation of TNF-α, iNOS, 8-OHdG biomarkers, and alteration of caspase 3, iNOS, CYP1A, MT1 gene expression levels in common carp (Cyprinus carpio L.) , 2017, Toxicology reports.

[11]  D. Goulson,et al.  The environmental risks of neonicotinoid pesticides: a review of the evidence post 2013 , 2017, bioRxiv.

[12]  G. Alak,et al.  Neurotoxic responses in brain tissues of rainbow trout exposed to imidacloprid pesticide: Assessment of 8-hydroxy-2-deoxyguanosine activity, oxidative stress and acetylcholinesterase activity. , 2017, Chemosphere.

[13]  A. Calas,et al.  Characterization of seizures induced by acute exposure to an organophosphate herbicide, glufosinate-ammonium , 2016, Neuroreport.

[14]  P. Badgujar,et al.  Evaluation of imidacloprid-induced neurotoxicity in male rats: A protective effect of curcumin , 2014, Neurochemistry International.

[15]  V. Garg,et al.  Disposition and acute toxicity of imidacloprid in female rats after single exposure. , 2014, Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association.

[16]  K. S. Khera,et al.  Physiological, biochemical and histological alterations induced by administration of imidacloprid in female albino rats. , 2014, Pesticide biochemistry and physiology.

[17]  A. Tsatsakis,et al.  Development and application of LC–APCI–MS method for biomonitoring of animal and human exposure to imidacloprid. , 2013, Chemosphere.

[18]  Jonggun Kim,et al.  Imidacloprid, a neonicotinoid insecticide, induces insulin resistance. , 2013, The Journal of toxicological sciences.

[19]  Kathleen A. Durkin,et al.  Neuroactive insecticides: targets, selectivity, resistance, and secondary effects. , 2013, Annual review of entomology.

[20]  Junsoo Lee,et al.  Imidacloprid, a neonicotinoid insecticide, potentiates adipogenesis in 3T3-L1 adipocytes. , 2013, Journal of agricultural and food chemistry.

[21]  D. Goulson,et al.  Neonicotinoid Pesticide Reduces Bumble Bee Colony Growth and Queen Production , 2012, Science.

[22]  Henk A. Tennekes,et al.  Time-Dependent Toxicity of Neonicotinoids and Other Toxicants:Implications for a New Approach to Risk Assessment , 2011 .

[23]  M. Biziuk,et al.  Determination of organophosphorus and organonitrogen pesticides in water samples , 2010 .

[24]  L. P. Srivastava,et al.  Effect of imidacloprid on antioxidant enzymes and lipid peroxidation in female rats to derive its No Observed Effect Level (NOEL). , 2010, The Journal of toxicological sciences.

[25]  L. Žorić,et al.  Lactate dehydrogenase and oxidative stress activity in primary open-angle glaucoma aqueous humour. , 2010, Bosnian journal of basic medical sciences.

[26]  F. Xie,et al.  The role of cellular oxidative stress in regulating glycolysis energy metabolism in hepatoma cells , 2009, Molecular Cancer.

[27]  Mohammad Abdollahi,et al.  Pesticides and oxidative stress: a review. , 2004, Medical science monitor : international medical journal of experimental and clinical research.

[28]  J. Casida,et al.  Imidacloprid, Thiacloprid, and Their Imine Derivatives Up-Regulate the α4β2 Nicotinic Acetylcholine Receptor in M10 Cells , 2000 .

[29]  J. Casida,et al.  Imidacloprid, thiacloprid, and their imine derivatives up-regulate the alpha 4 beta 2 nicotinic acetylcholine receptor in M10 cells. , 2000, Toxicology and applied pharmacology.