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Imidacloprid Sale

(Synonyms: 吡虫啉) 目录号 : GC30895

A neonicotinoid insecticide

Imidacloprid Chemical Structure

Cas No.:138261-41-3

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥491.00
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100mg
¥446.00
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200mg
¥714.00
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500mg
¥1,607.00
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实验参考方法

Animal experiment:

Rats: Adult females are divided into four groups. One group is served as control and is given corn oil as vehicle through gavage. Three groups are given 5, 10, and 20 mg/kg/day imidacloprid to female rats for 90 days. Body weight, food consumption and clinical signs of toxicity are recorded throughout the period of experiment. Urine is collected at initial and 90 days for urine analysis. Individual animals from each group are weighed weekly and body weight is recorded[4]. Mice: Imidacloprid is administered orally daily at 10, 5, or 2.5mg/kg over 28 days. Specific parameters of humoral and cellular immune response including hemagglutinating antibody (HA) titer to sheep red blood cells (SRBC; T-dependent antigen), delayed type hypersensitivity (DTH) response to SRBC, and T-lymphocyte proliferation in response to phytohemagglutinin (PHA) are evaluated[6].

References:

[1]. Kim J, et al. Imidacloprid, a neonicotinoid insecticide, induces insulin resistance. J Toxicol Sci. 2013;38(5):655-60.
[2]. Kara M, et al. Insecticide imidacloprid influences cognitive functions and alters learning performance and related gene expression in a rat model. Int J Exp Pathol. 2015 Oct;96(5):332-7.
[3]. Crosby EB, et al. Neurobehavioral impairments caused by developmental imidacloprid exposure in zebrafish. Neurotoxicol Teratol. 2015 May-Jun;49:81-90.
[4]. Bhardwaj S, et al. A 90 days oral toxicity of imidacloprid in female rats: morphological, biochemical and histopathological evaluations. Food Chem Toxicol. 2010 May;48(5):1185-90.
[5]. Kapoor U, et al. Effect of imidacloprid on antioxidant enzymes and lipid peroxidation in female rats to derive its No Observed Effect Level (NOEL). J Toxicol Sci. 2010 Aug;35(4):577-81.
[6]. Badgujar PC, et al. Immunotoxic effects of imidacloprid following 28 days of oral exposure in BALB/c mice. Environ Toxicol Pharmacol. 2013 May;35(3):408-18.

产品描述

Imidacloprid is a broad-spectrum neonicotinoid insecticide that is effective against sucking and biting insects and insects of the Coleopteran and Lepidoptera orders.1,2 It is an agonist of insect acetylcholine receptors (nAchRs) with Ki values of 1.9, 2.1, 290, and 50 nM for M. persicae and D. melanogaster receptors, rat brain membranes, and rat recombinant receptors containing α4β2 subunits, respectively.3,4 Imidacloprid is lethal to M. persicae with LD95 values of approximately 2 and 160 pg/aphid via oral and topical administration, respectively.2 It impairs aversive learning and memory retention in honey bees following chronic sublethal exposure of 20.8 ppb.5 In a mouse model of high-fat diet-induced obesity, imidacloprid (0.06-6 mg/kg per day) increases body weight gain and adiposity and impairs glucose metabolism without increasing total food intake.6

1.Elbert, A., Overbeck, H., Iwaya, K., et al.Imidacloprid, a novel systemic nitromethylene analogue insecticide for crop protectionBrighton Crop Protection Conference, Pests and Diseases21-28(1990) 2.Elbert, A., Becker, B., Hartwig, J., et al.Imidacloprid - A new systemic insecticidePflanzenschutz-Nachrichten Bayer (German Edition)44(2)113-136(1991) 3.Kagabu, S., Maienfisch, P., Zhang, A., et al.5-Azidoimidacloprid and an acyclic analogue as candidate photoaffinity probes for mammalian and insect nicotinic acetylcholine receptorsJ. Med. Chem.43(26)5003-5009(2000) 4.Tomizawa, M., and Casida, J.E.Selective toxicity of neonicotinoids attributable to specificity of insect and mammalian nicotinic receptorsAnnu. Rev. Entomol.48339-364(2003) 5.Zhang, E., and Nieh, J.C.The neonicotinoid imidacloprid impairs honey bee aversive learning of simulated predationJ. Exp. Biol.218(Pt 20)3199-3205(2015) 6.Sun, Q., Xiao, X., Kim, Y., et al.Imidacloprid promotes high fat diet-induced adiposity and insulin resistance in male C57BL/6J miceJ. Agric. Food Chem.64(49)9293-9306(2016)

Chemical Properties

Cas No. 138261-41-3 SDF
别名 吡虫啉
Canonical SMILES O=[N+](/N=C1NCCN\1CC2=CC=C(Cl)N=C2)[O-]
分子式 C9H10ClN5O2 分子量 255.66
溶解度 DMSO : ≥ 300 mg/mL (1173.43 mM) 储存条件 Store at -20°C
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1 mM 3.9114 mL 19.5572 mL 39.1144 mL
5 mM 0.7823 mL 3.9114 mL 7.8229 mL
10 mM 0.3911 mL 1.9557 mL 3.9114 mL
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Research Update

Imidacloprid as reproductive toxicant and endocrine disruptor: investigations in laboratory animals

Imidacloprid, a neonicotinoid insecticide, has been used worldwide due to its selective toxicity for insects. Its residues may enter the food chain, which is why it is important to investigate the potential adverse effects of imidacloprid exposure. This review summarises current knowledge of the reproductive toxicity and disruptive endocrine effects of imidacloprid in laboratory animals. Investigations, conducted mostly on laboratory rats, have shown adverse effects of imidacloprid on the reproductive ability in both parental and offspring generation as well as on the development of the offspring. Like many pesticides, imidacloprid may also act as endocrine disrupting chemical (EDC). It may disrupt the metabolic homeostasis, contribute to obesity, and disrupt steroidogenesis by inhibiting cytochrome P450 (CYP) enzyme activities. All these adverse effects of imidacloprid may pose a serious risk for reproduction and development with long-term consequences in adulthood.

Chronic Effects of Imidacloprid on Honey Bee Worker Development-Molecular Pathway Perspectives

Sublethal dosages of imidacloprid cause long-term destructive effects on honey bees at the individual and colony levels. In this review, the molecular effects of sublethal imidacloprid were integrated and reported. Several general effects have been observed among different reports using different approaches. Quantitative PCR approaches revealed that imidacloprid treatments during the adult stage are expressed as changes in immuneresponse, detoxification, and oxidation-reduction response in both workers and queens. In addition, transcriptomic approaches suggested that phototransduction, behavior, and somatic muscle development also were affected. Although worker larvae show a higher tolerance to imidacloprid than adults, molecular evidence reveals its potential impacts. Sublethal imidacloprid treatment during the larval stage causes gene expression changes in larvae, pupae, and adults. Transcriptome profiles suggest that the population and functions of affected differentially expressed genes, DEGs, vary among different worker ages. Furthermore, an early transcriptomic switch from nurse bees to foragers was observed, suggesting that precocious foraging activity may occur. This report comprehensively describes the molecular effects of sublethal dosages of imidacloprid on the honey bee Apis mellifera. The corresponding molecular pathways for physiological and neurological responses in imidacloprid-exposed honey bees were validated. Transcriptomic evidence suggests a global and sustained sublethal impact of imidacloprid on honey bee development.

Biodegradation of imidacloprid: Molecular and kinetic analysis

Imidacloprid (C9H10ClN5O2) is the most widely used insecticide. Its persistence and toxic nature have caused a detrimental effect on living biota. Thus its removal from the contaminated environment has become imperative. The present study aimed to isolate bacterial species from pesticide-contaminated sites and assess their potential for biodegradation of imidacloprid. The 16S rRNA analysis revealed the genetic relatedness of isolates to Sphingobacterium sp., Agrobacterium sp., Pseudomonas sp., and Bacillus sp. Batch biodegradation studies showed that Sphingobacterium sp. and Agrobacterium sp. were the most promising isolates as they degraded 81.0% and 84.9%, respectively, of imidacloprid at the concentration of 95 mg/L via co-metabolism. Kinetic study (Vmax/Ks ratio) also suggested the high degradation efficiency of these isolates. Imidacloprid-guanidine (C9H11ClN4) was identified as the metabolite. This report highlights the potential of bacteria for imidacloprid degradation and could be utilized for the formulation of strategies for the remediation of imidacloprid contaminated environments.

Trace determination of imidacloprid and its major metabolites in wheat-soil system

Trace analysis method is a reliable basis for studying the translocation and metabolism of imidacloprid used as an insecticide in wheat, and it clarifies whether biologically active metabolites including residual imidacloprid, have long-lasting insecticidal potency against wheat aphids under seed treatment during the entire growth period. In this study, a highly sensitive analytical method was established to determine the residues of imidacloprid and its six metabolites (5-hydroxy imidacloprid, imidacloprid olefin, imidacloprid guanidine, imidacloprid urea, 6-chloronicotinic acid, and imidacloprid nitrosimine) in wheat-soil systems, such as in wheat leaves, wheat ears, wheat grains, roots, and soil. All the compounds were extracted using an ACN:water (8:2, v/v) mixture and purified by dispersive solid-phase extraction. The average recoveries ranged from 74.4% to 109.5% for all matrices, with intra- and inter-day variations of less than 14.9%. The limit of quantitation was in the range of 0.001-0.005 mg/kg. The method is demonstrated to be sensitive and accurate for monitoring imidacloprid and its metabolites at trace levels during the entire growth period under field conditions.

Imidacloprid treatments induces cyanobacteria blooms in freshwater communities under sub-tropical conditions

Imidacloprid is one of the most used neonicotinoid insecticides all over the world and is considered as a contaminant of concern due to its high toxicity potential to aquatic organisms. However, the majority of the studies that have evaluated the effects of imidacloprid on aquatic organisms were conducted under temperate conditions. In the present study, a mesocosm experiment was conducted under sub-tropical conditions to assess the effects of imidacloprid on the structure (macroinvertebrates, zooplankton and phytoplankton) and functional endpoints of an aquatic ecosystem and to compare the results with similar temperate and (sub-)tropical mesocosm studies. Imidacloprid (0, 0.03, 0.3 and 3 ?g/L) was applied to 13 mesocosms weekly over a period of 4 weeks, followed by a one month recovery period. At the community level a lowest NOECcommunity of 0.03 ?g/L was calculated for the zooplankton, phytoplankton and macroinvertebrate communities. The highest sensitivity to imidacloprid (NOEC < 0.03 ?g/L) were observed for Gerris sp., Diaptomus sp. and Brachionus quadridentatus. Imidacloprid induced population declines of the larger zooplankton species (Diaptomus sp. and Ostracoda) resulted in increased rotifer abundances and shifted the phytoplankton community to a graze resistant gelatinous cyanobacteria dominated ecosystem. These cyanobacteria blooms occurred at all different concentrations and could pose an important public health and environmental concern. Although there are some differences in species and community sensitivity between the present and the other (sub-)topical mesocosm studies, it can be observed that all show a similar general community response to imidacloprid. Under (sub-)tropical conditions, the toxic effects of imidacloprid occur at lower concentrations than found for temperate ecosystems.