Comparison of the toxicity of pure compounds and commercial formulations of imidacloprid and acetamiprid on HT-29 cells: Single and mixture exposure

Baysal, Merve; Atlı-Eklioğlu, Özlem

doi:10.1016/j.fct.2021.112430

Cited by 10 publications

(3 citation statements)

References 109 publications

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“…In the HepG2 hepatic cell line, a significant decrease in the reduced/oxidised glutathione ratio, indicative of oxidative stress, was observed after 0.5 mM IMI treatment over 24 h [39]. In the colorectal HT-29 cell line, increased oxidative stress and ROS were observed in experiments of both pure IMI and commercial formulations of IMI [16]. In the WPM-Y.1 prostate epithelial cell line, significant increases in the enzymatic activities of catalase, glutathione peroxidase, and glutathione reductase were also observed when comparing IMI-treated and control cells [9].…”

Section: Discussionmentioning

confidence: 95%

“…Additionally, there are no previous studies on human astrocyte cells and IMI exposure. However, several in vitro studies have quantified responses of human nAChRs and toxicity after IMI exposure at concentrations ranging from 0.1 to 4 mM [11,12,16,17]. Thus, in the experiments, the cells were exposed to various concentrations of IMI (0.02-2 mM), or not (controls), for varying periods of time and then used for analyses of cell viability, lysosomal membrane permeabilisation (LMP), cellular ROS production, and autophagy protein markers.…”

Section: Cell Cultures and Experimental Conditionsmentioning

confidence: 99%

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Imidacloprid Induces Lysosomal Dysfunction and Cell Death in Human Astrocytes and Fibroblasts—Environmental Implication of a Clinical Case Report

Eriksson,

Ward,

Vainikka

et al. 2023

Cells

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Imidacloprid (IMI), a neonicotinoid insecticide, has potential cytotoxic and genotoxic effects on human and experimental models, respectively. While being an emerging environmental contaminant, occupational exposure and related cellular mechanisms are unknown. Herein, we were motivated by a specific patient case where occupational exposure to an IMI-containing plant protection product was associated with the diagnosis of Bell’s palsy. The aim was to investigate the toxic effects and cellular mechanisms of IMI exposure on glial cells (D384 human astrocytes) and on human fibroblasts (AG01518). IMI-treated astrocytes showed a reduction in cell number and dose-dependent cytotoxicity at 24 h. Lower doses of IMI induced reactive oxygen species (ROS) and lysosomal membrane permeabilisation (LMP), causing apoptosis and autophagic dysfunction, while high doses caused significant necrotic cell death. Using normal fibroblasts, we found that IMI-induced autophagic dysfunction and lysosomal damage, activated lysophagy, and resulted in a compensatory increase in lysosomes. In conclusion, the observed IMI-induced effects on human glial cells and fibroblasts provide a possible link between IMI cytotoxicity and neurological complications observed clinically in the patient exposed to this neonicotinoid insecticide.

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Section: Discussionmentioning

confidence: 95%

Section: Cell Cultures and Experimental Conditionsmentioning

confidence: 99%

Imidacloprid Induces Lysosomal Dysfunction and Cell Death in Human Astrocytes and Fibroblasts—Environmental Implication of a Clinical Case Report

Eriksson,

Ward,

Vainikka

et al. 2023

Cells

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“…Acetamiprid (ACE), a new kind of chlorinated nicotinoid insecticide, with strong contact and stomach toxicity, as well as excellent internal absorption activity, is widely used in the control of aphid, whitefly, thrips and other pests on vegetables because of its quick insecticidal effect, low dosage, high activity, wide insecticidal spectrum and long duration [ 1 , 2 ]. Although ACE is a low-toxicity pesticide, current studies have shown that it has certain genotoxicity and cytotoxicity, has adverse effects on the nervous system and reproductive system of animals, and poses a threat to human health [ 3 , 4 , 5 , 6 , 7 , 8 , 9 ]. To limit its use, national and international organizations established maximum residue levels (MRLs) for ACE.…”

Section: Introductionmentioning

confidence: 99%

Determination of Acetamiprid Residues in Vegetables by Indirect Competitive Chemiluminescence Enzyme Immunoassay

Zhu

Shi

et al. 2022

Foods

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Acetamiprid (ACE) is widely used in various vegetables to control pests, resulting in residues and posing a threat to human health. For the rapid detection of ACE residues in vegetables, an indirect competitive chemiluminescence enzyme immunoassay (ic-CLEIA) was established. The optimized experimental parameters were as follows: the concentrations of coating antigen (ACE-BSA) and anti-ACE monoclonal antibody were 0.4 and 0.6 µg/mL, respectively; the pre-incubation time of anti-ACE monoclonal antibody and ACE (sample) solution was 30 min; the dilution ratio of goat anti-mouse-HRP antibody was 1:2500; and the reaction time of chemiluminescence was 20 min. The half-maximum inhibition concentration (IC50), the detection range (IC10–IC90), and the detection limit (LOD, IC10) of the ic-CLEIA were 10.24, 0.70–96.31, and 0.70 ng/mL, respectively. The cross-reactivity rates of four neonicotinoid structural analogues (nitenpyram, thiacloprid, thiamethoxam, and clothianidin) were all less than 10%, showing good specificity. The average recovery rates in Chinese cabbage and cucumber were 82.7–112.2%, with the coefficient of variation (CV) lower than 9.19%, which was highly correlated with the results of high-performance liquid chromatography (HPLC). The established ic-CLEIA has the advantages of simple pretreatment and detection process, good sensitivity and accuracy, and can meet the needs of rapid screening of ACE residues in vegetables.

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Cytotoxicity, morphological and ultrastructural effects induced by the neonicotinoid pesticide, imidacloprid, using a rat Leydig cell line (LC-540)

Ibrahim,

Ferreira,

Venter

et al. 2023

Environmental Toxicology and Pharmacology

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Comparison of the toxicity of pure compounds and commercial formulations of imidacloprid and acetamiprid on HT-29 cells: Single and mixture exposure

Cited by 10 publications

References 109 publications

Imidacloprid Induces Lysosomal Dysfunction and Cell Death in Human Astrocytes and Fibroblasts—Environmental Implication of a Clinical Case Report

Imidacloprid Induces Lysosomal Dysfunction and Cell Death in Human Astrocytes and Fibroblasts—Environmental Implication of a Clinical Case Report

Determination of Acetamiprid Residues in Vegetables by Indirect Competitive Chemiluminescence Enzyme Immunoassay

Cytotoxicity, morphological and ultrastructural effects induced by the neonicotinoid pesticide, imidacloprid, using a rat Leydig cell line (LC-540)

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