Abstract
Imidacloprid is the most widely used pesticide of the neonicotinoid class. Neonicotinoid toxicities against various insects are well known. Nevertheless, there are rising evidences that neonicotinoids exert cytotoxic effects on different non-target organisms including mammals, fish, birds etc. Besides, depending on pesticide application, the exposed plants absorb some part of used neonicotinoids and their residues are detected in agricultural products worldwide. Thus, the continuous consumption of fruits and vegetables contaminated with neonicotinoids is a high risk factor for humans despite the low doses. Intestine epithelial cells are the first targets of the neonicotinoid cytotoxicity in humans because of its direct way of administration. The epithelial cells provide the barrier function of the intestinal system via specialized intercellular adhesion. The effects of imidacloprid on the intestine barrier function and inflammatory cytokines production are still unknown. In the present study, we exposed the human Caucasian colon adenocarcinoma (Caco-2) epithelial cells to low doses (0.10–0.75 µg/mL) of imidacloprid in order to assess the expression of tight and adherens junctions proteins, occludin and E-cadherin, and production of proinflammatory cytokine TNF α and iNOS. Imidacloprid induced dose-dependent decline in both occludin and E-cadherin levels. By contrast, TNF-α and iNOS contents were upregulated in imidacloprid-exposed Caco-2 cells. Decrease in tight and adherens junctions proteins indicates that the barrier function of intestine epithelial cells could be damaged by imidacloprid administration. In addition, TNF-α and iNOS upregulation indicates that imidacloprid is potent to activate proinflammatory response in enterocytes. Thus, imidacloprid can affect intestine barrier function through the increase of proinflammatory cytokine production and decrease in adhesiveness of enterocytes. The further assessment of the role of adhesion proteins and inflammatory cytokines in neonicotinoid pesticide cytotoxicity as it affects enterocyte barrier function is required to highlight the risk factor of use of neonicotinoids.
Highlights
Imidacloprid is a chloronicotinyl compound and belongs to the neonicotinoid pesticide family designed in the late 1990s
The objective of our work is to study the expression of tumour necrosis factors (TNF)-α, inducible oxide nitrogen synthase (iNOS), occludin and E-cadherin as the molecular markers of inflammatory changes and intercellular adhesion integrity in Caco-2 intestine cells exposed to imidacloprid
It should be mentioned that 0.10 μg/mL dose had no effect on the Reactive oxygen species (ROS) production (Fig. 1b)
Summary
Imidacloprid is a chloronicotinyl compound and belongs to the neonicotinoid pesticide family designed in the late 1990s. Neonicotinoids have selective synaptic specificity targeting the neuronal nicotinic acetylcholine receptors (nAChR) as the agonists of high affinity. These receptors are responsible for the control of ligand-gated ion channels and for rapid neurotransmission (Tomizawa & Yamamoto, 1993). Research has revealed that neonicotinoids exhibit the highest selective toxicity for insects in comparison with mammals, due to the unique structure of insect nAChR receptors and higher affinity with them (Liu & Casida, 1993). Different kinds of toxicity were detected for neonicotinoids, and for several neonicotinoids metabolites which exert affinity for nAChR
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