Genotoxicity of imidacloprid in relation to metabolic activation and composition of the commercial product.
ABSTRACT Imidacloprid is a neonicotinoid insecticide combining excellent efficiency against parasites with low toxicity for mammals. Commercially, it is co-formulated with dimethyl sulfoxide, methylpyrrolidone, propylene carbonate and mineral oil, which can modify its bioavailability and toxicological profile for humans following occupational exposure. A combined in vitro approach employing the comet assay and the micronucleus test was used to assess the genotoxicity of imidacloprid in relation to formulation, metabolic activation and exposure level. Human peripheral blood lymphocytes from unexposed healthy volunteers were treated with imidacloprid (0.2, 2 and 20 μM) and with equimolar concentrations of a commercial product, with and without addition of S9 fraction. Imidacloprid significantly increased the comet score and the frequency of micronuclei only at the highest concentration tested. DNA damage was slightly more severe with the commercial product, and was increased, though not significantly, by metabolic activation. Formation of reactive oxygen species (ROS) does not seem to be involved as a mechanism of genotoxicity, but this result may be explained by the insufficient sensitivity of the 2',7'-dichlorofluorescein diacetate assay at the test concentrations of imidacloprid. These results suggest that at concentrations<20 μM imidacloprid is not genotoxic to human lymphocytes in vitro. Nonetheless, the presence of co-formulants in the commercial product and occupational exposure, along with poor safety procedures, may present an increased risk for DNA fragmentation and chromosomal aberrations.
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ABSTRACT: Imidacloprid insecticide was selected to study its effects on biochemical (total protein, acetylcholinestrase and nucleic acids) and histological (liver) parameters in female albino mice at orally administered doses of 25, 50 and 75% LD 50 Imidacloprid and 40 mg/kg bw Cyclophosphamide (CP) and distilled water (DW). Significant decrease in total protein (P<0.01), acetylcholinestrase (P<0.001) and DNA (P<0.05) were observed with increase in doses as compared to control group whereas slight dose dependent significant increase was noticed for RNA (P<0.01). The change noticed in DNA and RNA for low dose of Imidacloprid was insignificant. The maximum damage with CP and 75% LD 50 Imidacloprid dose were noticed. Liver of mice showed degeneration of hepatocytes, dilation of sinusoids, irregular hepatic cords arrangement, leucocytes infiltration, necrosis and hemorrhages. This reveals biochemical and histotoxicity induction by Imidacloprid so awareness about its judicious use by farmers/users is of pivotal importance to have safe next generations.02/2014; 8(1):2319-2399.
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ABSTRACT: Acetamiprid is a member of the neonicotinoid group of insecticides commonly used against wide range of insect pests. In the present study, in vitro cytotoxicity and genotoxicity of technical grade acetamiprid was evaluated on the human intestinal CaCo-2 cells. Cytotoxicity was evaluated using the clonogenic survival and the results indicated that acetamiprid was cytotoxic on CaCo-2 cells. The cells were than treated with acetamiprid concentrations exhibit greater than 75% clonogenic survival for 24 h, to assess genotoxicity using the micronucleus, comet and γH2AX foci formation assays. Our results indicate that, under the experimental conditions used, acetamiprid has cytotoxic and genotoxic potential on human intestinal cells.Pesticide Biochemistry and Physiology 11/2012; 104(3):212–217. · 2.11 Impact Factor
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ABSTRACT: Altered immune function may be an indicator of increased potential for the development of immunologically based diseases such as cancer, hypersensitivity and autoimmunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 08/2014;