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: Neonicotinoids are subjected to vigilance because of environmental contaminations and deleterious effects on bees. Imidacloprid (IMI) is one of the most representative insecticides of this family. At chronic exposure, concentration-effect relationships are non linear. An insect model should allow a better description of this toxicity. We compared the lethal concentration 50% (LC50) of IMI for a Drosophila-field strain, after acute and chronic exposure. Relative to the acute LC50, the chronic LC50 was lowered by a factor of 29 for males (1.3 mM/45 µM), 52 for larvae (157 µM/3µM) and more than 172 for females (>3.1mM/18µM). Chronic exposure also revealed significant lethal and sublethal effects, at concentrations 3-5 orders of magnitude lower than the chronic LC50. Mean mortalities reached 28% (at 3.91 nM) and 27% (at 39.1 nM) for females and males, respectively. Fecundity decreased of 16% at 1.96 nM. Mating increased of 30% at 0.391 nM. The LOEC (Lowest Observed Effect Concentration: 0.391 nM) was 46000 times lower than the chronic LC50 for males; it was 115000 times lower than the chronic LC50 for females. This study illuminates effects that neonicotinoids can induce at very low concentrations. This is of particular interest for non-target insects and for insect dependent species.Environmental Science & Technology 03/2014; · 5.48 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 08/2014; 63(11). · 2.14 Impact Factor
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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.