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.
"Decreased N/C in epithelial and stromal cells might be due to pesticides-induced toxicity. Genotoxicity and DNA damaging effects of MCZ (Calviello et al., 2006) and IMI (Costa et al., 2009) have been shown in mammalian in vitro systems. Thyroid disruption also reflected form impaired plasma levels of the hormones of pituitary–thyroid axis i.e. "
[Show abstract][Hide abstract] ABSTRACT: Thyroid is an important homeostatic regulator of metabolic activities as well as endocrine mechanisms including those of reproduction. Present investigation elucidated the thyroid disrupting potential of a neonicotinoid imidacloprid and a dithiocarbamate mancozeb in a seasonally breeding wildlife bird, Red Munia (Amandava amandava) who is vulnerable to these two pesticides through diet (seed grains and small insects). Adult male birds were exposed to 0.5% LD50 mg kg−1 bw d−1 of both the pesticides through food for 30 days during the preparatory and breeding phases. Weight, volume and histopathology of thyroid gland were distinctly altered. Disruption of thyroid follicles reflected in nucleus-to-cytoplasm ratio (N/C) in epithelial and stromal cells, epithelial cell hypertrophy and altered colloid volume. Impairment of thyroid axis was pesticide and phase specific as evident from the plasma levels of thyroid (T4 and T3) and pituitary (TSH) hormones. In preparatory phase, plasma TSH was increased in response to decrease of T4 on mancozeb exposure showing responsiveness of the hypothalamic–pituitary–thyroid (HPT) axis to feedback regulation. On imidacloprid exposure, however, plasma levels of both T4 and TSH were decreased indicating non-functioning of negative feedback mechanism. Increased plasma T3 in response to both the pesticides exposure might be due to synthesis from non-thyroidal source(s) in a compensatory response to decrease level of T4. In breeding phase, impairment of HPT axis was more pronounced as plasma T4, T3 and TSH were significantly decreased in response to both mancozeb and imidacloprid. Thus, low dose pesticide exposure could affect the thyroid homeostasis and reproduction.
"Thus, the genotoxicity of pesticides is currently of worldwide concern. Genotoxic effects of different types of neonicotinoid insecticides have been investigated by several researchers       . However, a literature survey showed that the studies dealing with the genotoxic effects of Acetamiprid are extremely scarce   The genotoxic potentials of pesticides have been studied both in in vitro and in vivo systems using different end points, such as the cytokinesis block micronuclei (CBMN), comet and gH2AX foci assays   . "
[Show abstract][Hide abstract] 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.
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