Genotoxicity of imidacloprid in relation to metabolic activation and composition of the commercial product

Costa, Chiara; Silvari, Virginia; Melchini, Antonietta; Catania, Stefania; Heffron, J. J. A.; Trovato, A.; Pasquale, R. De

doi:10.1016/j.mrgentox.2008.09.018

Cited by 80 publications

(67 citation statements)

References 25 publications

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“…Our population was mainly exposed to pesticides belonging to neonicotinoids, pyrethroids and organophosphates, all suspected to be carcinogenic [1,9].…”

Section: Discussionmentioning

confidence: 99%

IL-17 and IL-22 serum levels in greenhouse workers exposed to pesticides

et al. 2014

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“…Our population was mainly exposed to pesticides belonging to neonicotinoids, pyrethroids and organophosphates, all suspected to be carcinogenic [1,9].…”

Section: Discussionmentioning

confidence: 99%

IL-17 and IL-22 serum levels in greenhouse workers exposed to pesticides

et al. 2014

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“…Exposure of the human peripheral blood lymphocytes to imidacloprid (0.05 to 0.5 mg/l) significantly increased the levels of SCE and MN and enhanced DNA strand breaks (Feng et al 2005); however, imidacloprid (0.1 to 100 μg/ml) did not affect the frequency of SCE and MN formation (Demsia et al 2007). In the presence and absence of S9 mix, imidacloprid (20 μM) significantly increased the frequency of MN in the peripheral blood lymphocytes and DNA strand breaks in the leukocytes (Costa et al 2009). Recently, De Arcaute et al (2014 demonstrated that imidacloprid can be considered a harmful agent with genotoxic effects at both DNA and chromosomal levels.…”

Section: Avermectin Exerted In Vivo and In Vitro Cytotoxic Actions Inmentioning

confidence: 97%

“…Imidacloprid acts as a selective agonist of the nicotinic acetylcholine receptor subtypes in insects; it is classified as a toxicity class II agent (EPA 1994;WHO 2002) with low mammalian toxicity (Tomizawa and Casida 2003). So, it is widely used in animal health and crop protection with soil, seed, and foliar applications (Tomizawa and Casida 2005;Costa et al 2009). However, imidacloprid was found to induce DNA damage in a dose-related manner in earthworms as well as to increase the frequency of adducts in calf thymus DNA, indicating agent-induced genotoxicity (Shah et al 1997;Zang et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic and genotoxic effects of abamectin, chlorfenapyr, and imidacloprid on CHOK1 cells

Al‐Sarar

Abobakr

Bayoumi

et al. 2015

Environ Sci Pollut Res

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The cytotoxicity and genotoxicity of abamectin, chlorfenapyr, and imidacloprid have been evaluated on the Chinese hamster ovary (CHOK1) cells. Neutral red incorporation (NRI), total cellular protein content (TCP), and methyl tetrazolium (MTT) assays were followed to estimate the mid-point cytotoxicity values, NRI50, TCP50, and MTT50, respectively. The effects of the sublethal concentration (NRI25) on glutathione S-transferase (GST), glutathione reductase (GRD), glutathione peroxidase (GPX), and total glutathione content have been evaluated in the presence and absence of reduced glutathione (GSH), vitamin C, and vitamin E. The genotoxicity was evaluated using chromosomal aberrations (CA), micronucleus (MN) formation, and DNA fragmentation techniques in the presence and absence of the metabolic activation system, S9 mix. Abamectin was the most cytotoxic pesticide followed by chlorfenapyr, while imidacloprid was the least cytotoxic one. The glutathione redox cycle components were altered by the tested pesticides in the absence and presence of the tested antioxidants. The results of genotoxicity indicate that abamectin, chlorfenapyr, and imidacloprid have potential genotoxic effects on CHOK1 cells under the experimental conditions.

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“…On the other hand, diverse studies about genotoxic and/ or cytotoxic effects obtained with pure and commercial formulations of diverse pesticides indicate that commercial formulations may contain additional unsafe xenobiotics supporting the importance of evaluating not only the active principle but also the commercial formulation, which in fact constitutes the real hazard from agrochemicals (42)(43)(44)(45)(46)(47)(48)(49)(50)(51).…”

Section: Discussionmentioning

confidence: 99%

Assessment of genotoxicity of Lannate-90® and its plant and animal metabolites in human lymphocyte cultures

Valencia-Quintana

Gómez‐Arroyo

Sánchez-Alarcón

et al. 2016

Archives of Industrial Hygiene and Toxicology

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This study evaluated direct and metabolic genotoxic effects caused by Lannate-90 ® , a methomyl-based formulation (90 % active ingredient), in human lymphocyte cultures using sister chromatid exchange assay (SCE). Two processes were used for the plant promutagens evaluation: in vivo activation, applying the insecticide systemically in plants for 4 h and subsequently adding plant metabolites containing extracts to lymphocyte cultures; and in vitro activation, where the insecticide was incubated with Vicia faba S10 mix plus human lymphocyte culture. Direct treatment with the insecticide significantly increased SCE frequency in human lymphocytes (250-750 mg L ® to treat human lymphocytes, a dose-response relationship was observed. In lymphocyte cultures treated directly with the insecticide for 2 h, a negative response was obtained. When S10 mix was added, SCE frequency did not change significantly. Meanwhile, a mixture of S9 mammalian metabolic mix and Lannate-90 ® increased the SCE frequency, with an observed concentration-dependent response. Although Lannate-90 ® induced cellular death at the highest concentrations, it did not cause a delay in cell proliferation in any of the treatments, confirming its genotoxic action. This study is one of the first to evaluate and compare the direct effect of Lannate-90 ® in two bioassays, animal and vegetal, and the effect of plant and animal metabolism on its genotoxic potential.

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Genotoxicity of imidacloprid in relation to metabolic activation and composition of the commercial product

Cited by 80 publications

References 25 publications

IL-17 and IL-22 serum levels in greenhouse workers exposed to pesticides

IL-17 and IL-22 serum levels in greenhouse workers exposed to pesticides

Cytotoxic and genotoxic effects of abamectin, chlorfenapyr, and imidacloprid on CHOK1 cells

Assessment of genotoxicity of Lannate-90® and its plant and animal metabolites in human lymphocyte cultures

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