Developmental and Biochemical Effects of Imidacloprid on Chick Embryos (original) (raw)
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Malformations and Teratogenic Effects of Imidacloprid on Chick Embryo
2014
Imidacloprid is one of the most commonly used insecticides worldwide belonging to the family of neonicotinoids and relatively new, systemic insecticide chemically related to the tobacco toxin nicotine. Like nicotine, it acts on nervous system. Worldwide, it is considered to be one of the insecticides used in the largest volume. It has a wide diversity of uses in agriculture, on turf, on pets, and for household pests. The present study was carried out in department of Anatomy Govt. Medical College, Ambedkar Nagar and Santosh Medical College Ghaziabad U.P. on 240 fertile eggs of white leghorn chicken obtained from government poultry farm after taking permission from animal ethical committee. Chicken eggs after having been exposed to Imidacloprid with doses of 10μg, 15μg, 25μg, and 40μg in a volume of 10μl, 15μl, 25μl and 40μl respectively and control same as test group. The embryos were terminated on 20 and 21 days, egg shell broken with a scalpel and embryos removed. Gross morphologi...
Effects of Neonicotinoid Insecticide Imidacloprid on Hematological Parameters in Chick Embryos
2015
In order to meet the growing food demand, use of pesticides is a common feature in agriculture now a day but extensive use of pesticide has resulted in global contamination of the environment. Imidacloprid is one of the major representatives of the new generation of neonicotinoid insecticides. The objective of current study is to examine the hematological parameters and developmental defects after exposure of imidacloprid in chick embryos. Present study was carried out on 300 fertile eggs of white leghorn chicken. Imidacloprid exposure increases the risks of developmental defects and mild toxic effects on hematological parameters in chick embryos. © 2015 Elixir All rights reserved. ARTICLE INF O Artic le history: Received: 24 March 2015; Received in revised form: 16 May 2015; Accepted: 18 May 2015;
Environmental Toxicology, 2010
Developmental toxicity of two different classes of commercial formulations of insecticides was studied by in ovo treatment of fertilized Rhode Island Red eggs. The first one was a combination of chlorpyrifos and cypermethrin and the second one was spinosad, a fermentation product of soil bacterium, Actinomycetes. In this study, the combination pesticide and spinosad of different concentrations were administered as a single dose in ovo in volumes of 50 μL per each egg on day “0” of incubation. Embryonic growth and development, morphological and skeletal malformations, and hatchability were assessed. The combination insecticide induced explicit alterations in the embryonic growth and development and resulted in malformations particularly to the axial and appendicular skeletal structures, whereas the changes were trivial in case of the spinosad exposure. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2012.
Mammalian Susceptibility to a Neonicotinoid Insecticide after Fetal and Early Postnatal Exposure
Scientific Reports
Neonicotinoids have become the most widely used class of insecticides worldwide. Although numerous studies have documented neonicotinoid toxicity in bees and other insects, the effects of exposure during early development in mammals remain largely unexplored. We assessed the effects of the neonicotinoid imidacloprid (IMI) in adult male and female mice after in utero and early postnatal exposure. Pregnant mice were infused with IMI (0.5 mg/kg/day) from gestational day 4 to the end of nursing at postnatal day 21. The young adult offspring were studied in a series of biochemical and behavioral tests. To assess reproducibility, the behavioral analyses were conducted in three separate studies using multiple exposed litters. Exposure to IMI reduced fecundity, and in adult offspring, decreased body weight in male but not female pups. Offspring from IMI-treated mothers displayed lower triglycerides, elevated motor activity, enhanced social dominance, reduced depressive-like behavior, and a diminution in social aggression compared to vehicle treated controls. Low levels of IMI were detected in the brains and livers of the treated mothers, while trace levels were detected in some offspring. Our results demonstrate that transient exposure to a neonicotinoid over the early developmental period induces long-lasting changes in behavior and brain function in mice. Neonicotinoid pesticides are the most widely used and among the most effective insecticides on the planet 1-3. Neonicotinoids were designed to be structurally similar to the potent toxin nicotine, and therefore act on central nervous system (CNS) nicotinic acetylcholine receptors (nAChRs; ref. 4). While it has been widely assumed that neonicotinoids are selective for insect nAchRs with little or no activity toward mammalian receptors, the validity of this assumption has recently been challenged 5-7. Thus, it becomes imperative to more rigorously investigate potential detrimental off-target effects of neonicotinoids on mammals including humans, livestock, and wildlife that may be exposed during pesticide application, or via contaminated food and water 8-12. Imidacloprid (IMI), a member of the chloronicotinyl nitroguanidine chemical family, was the first neonicotinoid to be commercialized and remains one of the most widely used insecticides 10. It has been reported to act as a full agonist at house fly nAChRs 12 , or as a partial nAChR agonist in bees 13,14 , and chicken and Drosophila/chicken hybrid nAChRs expressed in Xenopus laevis oocytes 15. In addition to structurally mimicking nicotine, IMI possesses the additional properties of being persistent in plants and soil and displaying high systemic toxicity against insects. An ideal insecticide is expected to quickly kill selected pests that harm crops while leaving other desirable species unaffected. However, several studies have reported off-target effects of IMI. For example, sublethal doses of IMI have been shown to cause neurotoxicity 16 , disrupt olfactory discrimination 17 , decrease sperm viability and fecundity, impair immunity, and alter responses to pheromones in bees and other insects 18-21. Studies conducted on adult mammals have shown that acute exposure to IMI at relatively high doses induces impaired immunity in both mice and rats 22,23 , genotoxicity in rabbits 24 , compromised reproductive function in rats (specifically, abnormal sperm morphology 25), and oxidative stress and/or increased mortality in rats and
Toxicology: Open Access, 2016
Objective: This study was undertaken to explore relationships between level of imidacloprid in the serum and semen quality among men farmers in addition to investigating histopathological findings in treated mature male rats. Methods and results: Our research entailed two parts; firstly, human part done on farm workers (n=35) with age between (Mean ± SD 34.3±6.4) and healthy volunteers (n=25) their ages were (35.6±8.2) years old asked to provide semen and blood samples. A significant negative correlation between sperm concentration, motility, with serum and seminal Imidacloprid (IMI), its main metabolite 6-chloronicotinic acid (6-CINA) and cotinine , was identified in farmers (r= − 0.489; p<0.05). Second part of research was done on adult male rats that had been divided into a total of five groups 10 each. Two groups served as control one as negative and the other as positive. The other three experimental groups were given 45, 90 and 450 mg/kg body weight Imidacloprid in corn orally by a gavage process for fifteen days respectively. There was a significant difference in luteinizing hormone (LH), follicular stimulating hormone (FSH), testestrone (tes), Estradiol 2 (E2), prolactin and semen quality in IMI treated rats when compared to control groups. Vacuolar degeneration of germinal epithelium and loss of spermatids, seminiferous tubules suggesting inhibition of spermatogenesis was recorded in IMI treated rats. Conclusion: Toxic effects to male reproductive system can be considered as an outcome of IMI exposure and infertility problems can be expected in chronically exposed subjects.
Toxicology Research, 2014
Imidacloprid (IMI) and clothianidin (CTD) are the most important of the neonicotinoid insecticides known to target the nicotinic acetylcholine receptor (nAChR) in insects and, potentially, in mammals. In the present study, we aimed to investigate if daily oral administration of IMI and CTD at low subchronic doses for 90 days has any deleterious effects on the biochemical parameters of infant and adult male rats. Animals were randomly divided into five groups of seven rats each: controls, IMI-infant and IMI-adult treatments at 4 mg per kg BW per day, and CTD-infant and CTD-adult treatments at 12 mg per kg BW per day by oral gavage. Kidneys of rats exposed to IMI and CTD showed biochemical changes. Based on the biochemical studies it is evident that IMI and CTD produce significant effects in male rats at 4 and 12 mg per kg per day of exposure. In conclusion, the present animal experiments revealed that the treatment with IMI and CTD at NOAEL (no observed adverse effect level) dose-levels causes changes in kidney biochemical parameters which seem to be dependent on the pesticide and age of the animal (infant or adult).
Cell Biochemistry and Function, 2012
We investigated whether treatment with imidacloprid would induce morphological changes, DNA fragmentation, antioxidant imbalance and apoptosis in the reproductive system of developing male rats. Twenty-four male rats were included in this 90-day study, starting at 7 days of age. The rats were divided into four groups. The first group was used as control. The second, third and fourth groups received oral 0.5-, 2-and 8-mg/kg imidacloprid, respectively. Serum, sperm and testis samples were collected from all groups at the end of the experimental period. The weights of the epididymis, vesicula seminalis, epididymal sperm concentration, body weight gain, testosterone and reduced glutathione values were lower in the imidacloprid-treated groups than that in the controls. All treated groups had increased lipid peroxidation, fatty acid concentrations and higher rates of abnormal sperm. Apoptosis and fragmentation of seminal DNA were higher in rats treated at the two higher doses of imidacloprid. These results show that this compound has a negative effect on sperm and testis of rats.
Mammalian Detrimental Effects of Imidacloprid Residues in Tomato Fruits
Research Journal of Environmental Toxicology, 2015
Imidacloprid, a neonicotinoid pesticide, was used extensively to control whitefly (Bemisia tabaci) on tomato crop worldwide. Current study aimed to determine residue amounts of imidacloprid in tomato fruits after different time intervals of application and to evaluate their detrimental effects on white albino rats. Results revealed that the initial deposit (residue amount after 1 h of last spray application) was 0.316 mg kgG 1 and decreased to 0.32, 0.23, 0.21, 0.14, 0.12 and 0.11 mg kgG 1 after 3, 5, 7, 10, 14 and 21 days of last spray, respectively and the half-life time was 10.16 days. Toxicity of repeated sub-lethal doses equal to 0.109, 0.116, 0.210, 0.316 and 42.5 mg kgG 1 b.wt. dayG 1 for 45 days were tested. Results reported herein revealed significant adverse effects on haematological (PCV (%), RBCs and WBCs), biochemical parameters (total protein (g dLG 1 ) and glucose (mg dLG 1 )) and liver, kidney and cardiac function parameters of male rats at 0.316 and 42.5 mg kgG 1 b.wt. dayG 1 . Current study highlighted that there was no residual toxicity of imidacloprid after 14 days of last application.
Exposure to neonicotinoid insecticides induces embryotoxicity in mice and rabbits
Toxicology, 2017
Highlights Neonicotinoid insecticides negatively affect early embryonic development. Thiacloprid impairs the developmental capacities and qualitative parameters of both mouse and rabbit preimplantation embryos cultured in vitro. During the preimplantation period, oral administration of thiacloprid at the acute reference dose impairs cell proliferation in mouse blastocysts.