PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Neonicotinoids”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2001

Neonicotinoid insecticides alter diapause behavior and survival of overwintering white grubs (Coleoptera: Scarabaeidae).

The chloronicotinyl, imidacloprid, and the thianicotinyl, thiamethoxam, are effective insecticides against white grubs when applied as preventative treatments during or immediately after egg laying. Their efficacy sharply declines when the grubs reach late-instar stage. As both imidacloprid and thiamethoxam act on post-synaptic nicotinic acetylcholine receptors and modify insect behavior, we hypothesized that the two compounds will interfere with overwintering behavior of scarabs, thus reducing their ecological fitness and exposing them to increased winter mortality. We tested this hypothesis by applying the two compounds curatively against late second-instar and early third-instar Popillia japonica and Cyclocephala borealis grubs in turfgrass. Imidacloprid provided control of P japonica equivalent to the most widely used curative organophosphate, trichlorfon, by 14 days after treatment, but thiamethoxam had no affect. In contrast, both imidacloprid and thiamethoxam caused significant reductions in C borealis populations. Both insecticides altered the overwintering behavior of P japonica by significantly reducing the normal downward movement of grubs in October. Halofenozide, an ecdysone agonist, also caused rapid mortality of the late second-instar C borealis equivalent to trichlorfon, but had no affect on P japonica. In another experiment on a site naturally infested with entomopathogenic nematodes, the exclusive treatment of third-instar P japonica with imidacloprid resulted in no significant mortality in the autumn (up to 15 days after treatment), but caused a significant reduction in the survival of overwintered grubs. There was an increase in the numbers of grubs infected with nematodes in the imidacloprid and trichlorfon treatments compared with control, but these differences were significant only for trichlorfon. These results indicate that imidacloprid can effectively control late second-instars of both P japonca and C borealis and can significantly reduce survival of overwintered third-instar P japonica by altering their normal overwintering behavior.

Animals↗
PubMedDate not supplied

Synthesis of a novel [125I]neonicotinoid photoaffinity probe for the Drosophila nicotinic acetylcholine receptor.

The insect nicotinic acetylcholine receptor (nAChR) is the target for the major insecticide imidacloprid (IMI) and for the first candidate photoaffinity probe described here. Addition to 1-[(6-chloro-3-pyridinyl) methyl]-4,5-dihydro-2-nitromethylene-1H-imidazolidine (the nitromethylene analog of the nitroimine IMI) of formaldehyde and any one of several primary amines is known to give hexahydro-8-nitroimidazo[1,2-c]pyrimidine derivatives. These imidazopyrimidines with a wide range of N-substituents were found to inhibit [3H]IMI binding to the Drosophila or Musca nAChR by 50% (IC50) at 0.7-38 nM. Esterification of the N-(2-hydroxyethyl) derivative with 2-azido-5-(trimethylstannyl)-benzoic acid and then iododestannylation using Na125I and chloramine-T provide the candidate photoaffinity probe 6-[2-(2-azido-5-[125I]iodobenzoyl) ethyl]-1-[(6-chloro-3-pyridinyl)methyl]-1,2,3,5,6,7-hexahydro-8 -nitroimidazo[1,2-c]pyrimidine. This compound (unlabeled) has an IC50 of 8 nM for [3H]-IMI binding in Drosophila head membranes, and the 125I-labeled photoaffinity probe labels only a 66 kDa protein(s) at a specific site inhibited by (-)-nicotine, consistent with the insecticide-binding subunit of the nAChR.

Affinity Labels↗
PubMed2000

Role of loop D of the alpha7 nicotinic acetylcholine receptor in its interaction with the insecticide imidacloprid and related neonicotinoids.

1. The nitroguanidine insecticide imidacloprid along with a second generation of related compounds including nitenpyram, all nicotinic acetylcholine (ACh) receptor ligands, are used increasingly in many countries. Site-directed mutagenesis and heterologous expression in Xenopus laevis oocytes have been deployed to investigate mutants (G189D and G189E) of the chicken alpha7 homomer-forming nicotinic receptor subunit which are predicted to enhance the negative charge at the negative subsite (loop D) of the ACh binding site. 2. Xenopus oocytes expressing wild-type alpha7 nicotinic receptors respond to imidacloprid with rapid inward currents. Imidacloprid and nitenpyram are partial agonists, whereas ACh, (-)-nicotine and (+)-epibatidine are full agonists. 3. Compared to wild-type alpha7, the mutant G189D and G189E receptors are much less sensitive to the insecticides, whereas their sensitivity to (-)-nicotine, ACh and (+)-epibatidine is only slightly reduced. In contrast, G189N and G189Q mutants are sensitive not only to ACh, (-)-nicotine and (+)-epibatidine, but also to the two insecticides. Thus reduction of the insecticide-sensitivity by the mutations G189D and G189E are attributed to an increase in negativity of loop D. Desnitro-imidacloprid (DN-IMI), an imidacloprid derivative lacking the nitro group is a potent agonist on the G189D and G189E mutants suggesting an important role of loop D in nicotinic receptor interactions with the nitro group of nitroguanidine insecticides.

Animals↗
PubMed2005

Toxicity of four systemic neonicotinoids to adults of Anoplophora glabripennis (Coleoptera: Cerambycidae).

As part of the ongoing evaluation of different systemic insecticides for prophylactic treatment of trees, responses of the beetle Anoplophora glabripennis (Motschulsky) (Coleoptera: Cerambycidae) to different doses of four systemic neonicotinyl insecticides were studied. Adult beetles were provided with twigs or leaves of trees treated with different concentrations of imidacloprid to evaluate the toxicity of the insecticide through ingestion or contact or through both. Adult beetles also were provided with twigs of host plant treated with clothianidin, dinotefuran, and thiamethoxam to establish dose response of the beetle to these insecticides. Levels of individual insecticides in twigs and leaves were determined by using the "parent" method with high-performance liquid chromatography, and these levels were compared with the applied concentrations to determine their relationship. The LC50 values for detected level of each insecticide in twigs was 5.1 ppm at 24 h, 2.9 at 48 h, and 1.9 ppm at 72 h for imidacloprid; 1.1 ppm at 72 h for clothianidin; 2.2 ppm at 72 h for dinotefuran; and 1.0 ppm at 72 h for thiamethoxam. Our results indicate that mortality of adult beetles resulted not only from the ingestion and contact toxicity but also possibly from the antifeedant effect of imidacloprid.

Animals↗
PubMed2005

Effects of a neonicotinoid insecticide (acetamiprid) on acetylcholinesterase activity and cuticular hydrocarbons profil in German cockroaches.

Acetamiprid was incorporated into the diet at 2% dose corresponding to the LD50 and orally administrated to newly emerged adults of the German cockroach Blattella germanica and investigated on acetylcholinesterase activity and cuticular hydrocarbons profil. Acetylcholinesterase specific activity was determined on adult males and females after 24, 48 and 72 hours of treatment. Pentanic extracts of cuticular hydrocarbons in males and females after 6 days of treatment were analysed by gas chromatography. Data revealed an increase in acetylcholinesterase activity in both sexes from the control series. However, a significant inhibition in AChE was observed after treatment at 24, 48 and 72 hours especially in females. In addition, hydrocarbons profils were found qualitatively similar in all groups of insects. However, slight quantitative differences between sexes in control series were noted. Acetamiprid feminize the cuticular profil in males with significant reduction of cuticular compound, and these allowed separation of insects into two groups using multivariate analysis.

Acetylcholinesterase↗
PubMed2001

Neonicotinoids: insecticides acting on insect nicotinic acetylcholine receptors.

Imidacloprid is increasingly used worldwide as an insecticide. It is an agonist at nicotinic acetylcholine receptors (nAChRs) and shows selective toxicity for insects over vertebrates. Recent studies using binding assays, molecular biology and electrophysiology suggest that both alpha- and non-alpha-subunits of nAChRs contribute to interactions of these receptors with imidacloprid. Electrostatic interactions of the nitroimine group and bridgehead nitrogen in imidacloprid with particular nAChR amino acid residues are likely to have key roles in determining the selective toxicity of imidacloprid. Chemical calculation of atomic charges of the insecticide molecule and a site-directed mutagenesis study support this hypothesis.

Animals↗
PubMed2005

Biorational insecticides: mechanism and cross-resistance.

Potency and cross-resistance of various biorational insecticides, exemplified by the whitefly Bemisia tabaci, have been studied. Bemisia tabaci were exposed to the juvenile hormone mimic pyriproxyfen for the past 12 years resulting in an over 2,000-fold resistance, but there was no appreciable cross-resistance with the benzoylphenyl urea novaluron. Similarly, no cross-resistance was found between pyriproxyfen and the two neonicotinoids, acetamiprid and imidacloprid. On the other hand, a slight cross-resistance of 5-13-fold was observed with another neonicotinoid thiamethoxam. Among the neonicotinoids, a resistant strain of B. tabaci to thiamethoxam (approximately 100-fold) showed no appreciable cross-resistance to either acetamiprid or imidacloprid, while another strain 500-fold resistant to thiamethoxam resulted in a mild of 4-6-fold resistance to acetamiprid and imidacloprid. In other assays, B. tabaci strain resistant to thiamethoxam (approximately 100-fold) had no cross-resistance to pyriproxyfen. Our findings indicate that no appreciable cross-resistance was observed between the benzoylphenyl urea novaluron, the juvenile hormone mimic pyriproxyfen, and the neonicotinoids acetamiprid and imidacloprid. Hence, these compounds could be used as components in insecticide resistance management programs.

Animals↗
PubMed2026

Pesticide occurrence, transformation, and transport from wastewater treatment plants into stream networks with diverse land uses.

Neonicotinoid insecticides and strobilurin fungicides are detected in many environmental compartments and have been associated with negative environmental and human health implications. Wastewater treatment plants (WWTPs) are often hotspots for introducing such contaminants into the environment. Therefore, the occurrence of strobilurin fungicides, neonicotinoids, and their metabolites at two WWTPs with varying land uses and population sizes was investigated. Polar organic chemical integrative samplers were deployed in WWTP influent and effluent and placed upstream and downstream of the effluent mixing zone for 2 weeks in April and July 2022. Biosolids were also collected at each time point. Neonicotinoids were detected with the highest frequency (68%), followed by strobilurin fungicides (49%) and neonicotinoid metabolites (31%). Time-weighted average concentrations for influent/effluent ranged from 85.2 ± 87.8 to 409.4 ± 74.5 ng/L. Pesticide concentrations, specifically the metabolites, typically increased from influent to effluent, resulting in effluent having higher pesticide loads than influent. Pesticide concentrations varied between the upstream and downstream monitoring locations by analyte, with WWTP samples in the highly developed region having significantly higher concentrations of pesticides and less variation by monitoring period. Chronic ecotoxicity benchmarks for freshwater invertebrates for imidacloprid were surpassed in treated effluent at both WWTPs in July and in the downstream monitoring location in the heavily developed area. Findings support the need for further exploration of pesticide contributions from WWTPs to river systems, specifically related to metabolite contributions to downstream streams and their effects on aquatic environments.

Water Pollutants, Chemical↗
PubMed2003

Conserving vedalia beetle, Rodolia cardinalis (Mulsant) (Coleoptera: Coccinellidae), in citrus: a continuing challenge as new insecticides gain registration.

The effects of insecticides used for California citrus pest management were evaluated using larval and adult stages of vedalia beetle, Rodolia cardinalis (Mulsant). This predatory beetle is essential for control of cottony cushion scale Icerya purchasi (Williston) (Homoptera: Margarodidae) in San Joaquin Valley citrus. When adult beetles were exposed to treated citrus leaves, adult survival was significantly reduced by the foliar neonicotinoid imidacloprid and the pyrethroid cyfluthrin. Progeny production was significantly reduced by imidacloprid, cyfluthrin, fenpropathrin, and buprofezin. Buprofezin, pyriproxifen, and foliar imidacloprid also significantly reduced successful development of larvae into the adult stage. When vedalia stages were fed insecticide-treated cottony cushion scale reared on Pittosporum tobira (Thunb.) Ait, toxic effects were more severe than contact toxicity alone. Adult beetle survival was most profoundly reduced by the pyrethroids and to a lesser extent the foliar neonicotinoids acetamiprid and imidacloprid. Progeny production and larval development to adulthood were reduced by all insecticides but were most severely affected by pyriproxifen and the pyrethroids. Systemically applied neonicotinoids were toxic to vedalia larvae feeding on cottony cushion scale that had ingested these insecticides. These data demonstrate that IGRs, neonicotinoid insecticides, and pyrethroid insecticides have a significant, negative impact on vedalia beetles. Depending on the rate of insecticide used, the number and timing of applications, and the level of coverage of the tree, disruption of vedalia can be minimized. However, the situation is made difficult when pests such as citrus thrips Scirtothrips citri (Moulton) (Thysanoptera: Thripidae), forktailed bush katydid Scuddaria furcata Brunner von Wattenwyl (Orthoptera: Tettigoiniidae), or glassy-winged sharpshooter Homalodisca coagulata Say (Homoptera: Cicadellidae) require these pesticide treatments during periods of vedalia beetle activity.

Animals↗
PubMed2000

Imidacloprid, thiacloprid, and their imine derivatives up-regulate the alpha 4 beta 2 nicotinic acetylcholine receptor in M10 cells.

Neonicotinoids are the most important new class of insecticides of the last decade. They act as nicotinic acetylcholine receptor (AChR) agonists. This investigation tests the hypothesis for the first time that neonicotinoid insecticides and their imine derivatives up-regulate the alpha 4 beta 2 nicotinic AChR subtype, which represents >90% of the high-affinity [(3)H]nicotine binding sites in mammalian brain. The alpha 4 beta 2 receptor stably expressed in mouse fibroblast M10 cells was assayed after 3 days' exposure to the test compound, as [(3)H]nicotine binding following immunoisolation by monoclonal antibody (mAb 299) or as [(125)I]mAb 299 labeling for cell surface receptors. We found that imidacloprid (IMI) (one of the most important insecticides) and thiacloprid (THIA) increased [(3)H]nicotine binding levels (up-regulation of the alpha 4 beta 2 AChRs) by five- to eightfold with EC50s of approximately 70,000 and 19,000 nM, respectively, compared with 760 nM for (-)-nicotine. In contrast, two imine analogs [the desnitro metabolite of IMI (DNIMI) and the descyano derivative of THIA] gave up-regulation by eightfold and EC50s of 870 and 500 nM, respectively. The potency order for up-regulation by the five aforementioned compounds was correlated with their in vitro IC50s for inhibiting [(3)H]nicotine binding (r(2) = 0.99, n = 5), indicating that binding to the alpha 4 beta 2 receptor initiates the up-regulation. A potent olefin derivative of the THIA imine up-regulated with an EC50 of 22 nM. DNIMI-induced up-regulation mainly occurred intracellularly rather than at the cell surface. These findings in alpha 4 beta 2-expressing M10 cells indicate the possibility that some neonicotinoid insecticides or their metabolites, on accidental human exposure or when used for flea control on dogs, may also up-regulate the receptor in mammals.

Animals↗
PubMed2006

Unique and common metabolites of thiamethoxam, clothianidin, and dinotefuran in mice.

The established neonicotinoid insecticides have chloropyridylmethyl (imidacloprid, thiacloprid, acetamiprid, and nitenpyram), chlorothiazolylmethyl (thiamethoxam or TMX and clothianidin or CLO) or tetrahydrofuranylmethyl (dinotefuran or DIN) substituents. We recently reported the metabolic fate of the chloropyridylmethyl neonicotinoids in mice as the first half of a comparative study that now considers the chlorothiazolylmethyl and tetrahydrofuranylmethyl analogues. TMX, CLO, two desmethyl derivatives (TMX-dm and CLO-dm), and DIN were administered ip to mice at 20 mg/kg for characterization of metabolites and pharmacokinetic analysis of brain, liver, plasma, and urine by HPLC/DAD and LC/MSD. Each compound is excreted 19-55% unmetabolized in urine within 24 h, and tissue residues are largely dissipated by 4 h. Thirty-seven metabolites of TMX, TMX-dm, CLO, and CLO-dm are identified by comparison with synthetic standards or their structures are proposed by molecular weights and 35Cl:37Cl ratios often supplemented by previous reports or sequence studies in which intermediates are readministered. A facile reaction sequence involves TMX --> TMX-dm or CLO --> CLO-dm. CLO-dm, reported to be a contributor to TMX hepatocarcinogenesis in mice, is unexpectedly remethylated in part to CLO in brain. The nitrosoguanidine, aminoguanidine, and urea derivatives of the parent compounds are detected in the tissues and methylnitroguanidine, methylguanidine, and nitroguanidine in the urine. Chlorothiazolecarboxaldehyde from oxidative cleavage of TMX and CLO is quite persistent in brain, liver, and particularly plasma compared with chloropyridinecarboxaldehyde and tetrahydrofurancarboxaldehyde from the other neonicotinoids. Chlorothiazolecarboxylic acid is conjugated with glycine or glucuronic acid or converted to S-methyl and mercapturate derivatives. DIN metabolism involves nitro reduction, N-demethylation, N-methylene hydroxylation, and amine cleavage, and tetrahydrofuranylmethyl hydroxylation at the 2-, 4-, and 5-positions giving 29 tentatively identified metabolites. The diversity of biodegradable sites and multiple pathways insures against parent compound accumulation but provides intermediates reported to be active as nicotinic agonists and inducible nitric oxide synthase inhibitors.

Animals↗
PubMed2005

A nicotinic acetylcholine receptor mutation conferring target-site resistance to imidacloprid in Nilaparvata lugens (brown planthopper).

Neonicotinoids, such as imidacloprid, are nicotinic acetylcholine receptor (nAChR) agonists with potent insecticidal activity. Since its introduction in the early 1990s, imidacloprid has become one of the most extensively used insecticides for both crop protection and animal health applications. As with other classes of insecticides, resistance to neonicotinoids is a significant threat and has been identified in several pest species, including the brown planthopper, Nilaparvata lugens, a major rice pest in many parts of Asia. In this study, radioligand binding experiments have been conducted with whole-body membranes prepared from imidacloprid-susceptible and imidacloprid-resistant strains of N. lugens. The results reveal a much higher level of [3H]imidacloprid-specific binding to the susceptible strain than to the resistant strain (16.7 +/- 1.0 and 0.34 +/- 0.21 fmol/mg of protein, respectively). With the aim of understanding the molecular basis of imidacloprid resistance, five nAChR subunits (Nlalpha1-Nlalpha4 and Nlbeta1) have been cloned from N. lugens.A comparison of nAChR subunit genes from imidacloprid-sensitive and imidacloprid-resistant populations has identified a single point mutation at a conserved position (Y151S) in two nAChR subunits, Nlalpha1 and Nlalpha3. A strong correlation between the frequency of the Y151S point mutation and the level of resistance to imidacloprid has been demonstrated by allele-specific PCR. By expression of hybrid nAChRs containing N. lugens alpha and rat beta2 subunits, evidence was obtained that demonstrates that mutation Y151S is responsible for a substantial reduction in specific [3H]imidacloprid binding. This study provides direct evidence for the occurrence of target-site resistance to a neonicotinoid insecticide.

Amino Acid Sequence↗
PubMed2007

Insect nicotinic acetylcholine receptor gene families: from genetic model organism to vector, pest and beneficial species.

Nicotinic acetylcholine receptors (nAChRs) mediate fast synaptic transmission in the insect nervous system and are targets of a major group of insecticides, the neonicotinoids. Analyses of genome sequences have shown that nAChR gene families remain compact in diverse insect species, when compared to their mammalian counterparts. Thus, Drosophila melanogaster and Anopheles gambiae each possess 10 nAChR genes while Apis mellifera has 11. Although these are among the smallest nAChR gene families known, receptor diversity can be considerably increased by alternative splicing and mRNA A-to-I editing, thereby generating species-specific subunit isoforms. In addition, each insect possesses at least one highly divergent nAChR subunit. Species-specific subunit diversification may offer promising targets for future rational design of insecticides that act on particular pests while sparing beneficial insects. Electrophysiological studies on cultured Drosophila cholinergic neurons show partial agonist actions of the neonicotinoid imidacloprid and super-agonist actions of another neonicotinoid, clothianidin, on native nAChRs. Recombinant hybrid heteromeric nAChRs comprising Drosophila Dalpha2 and a vertebrate beta2 subunit have been instructive in mimicking such actions of imidacloprid and clothianidin. Unitary conductance measurements on native nAChRs indicate that more frequent openings of the largest conductance state may offer an explanation for the superagonist actions of clothianidin.

Alternative Splicing↗
PubMed2000

Characterization of nicotinic acetylcholine receptors from the insects Aphis craccivora, Myzus persicae, and Locusta migratoria by radioligand binding assays: relation to thiamethoxam action.

Thiamethoxam, a new neonicotinoid insecticide acting at nicotinic acetylcholine receptors, was characterized in competition binding assays with [3-H]-imidacloprid, a specific nicotinic ligand, using membranes from the aphids Aphis craccivora and Myzus persicae, and from the locust Locusta migratoria. In all insects, Scatchard analysis suggested two binding sites for imidacloprid with Kd values in the range of 1 nM and 10 nM, respectively. The Hill values were significantly below 1 (range of 0.63 to 0.85). In contrast to imidacloprid and nicotine, the potency of thiamethoxam to displace [3-H]-imidacloprid varied considerably among these insects. Thiamethoxam was more active than nicotine on Aphis receptors but 100-fold less in Locusta, a nontarget insect. Comparable relations were found to nithiazine. In Myzus, the inhibition curve for thiamethoxam was shallow. This suggested a heterogeneous receptor population displaying a range of binding affinities to thiamethoxam in this aphid. In all three insects, the other neonicotinoid insecticides studied competed with [3-H]-imidacloprid in the same order: thiacloprid > imidacloprid > or = acetamiprid > nitenpyram. N-Methylation of imidacloprid strongly reduced the affinity to the imidacloprid site, whereas N-demethylation of thiamethoxam resulted in a comparable increase of affinity. Supplementary assays were performed with (-)-[3-H]-nicotine and [3-H]-alpha-bungarotoxin on locust membranes. Overall, the data suggested that the outstanding insecticidal properties of thiamethoxam may be due to either a different binding site on nicotinic receptors, or receptor isoforms, or specific pharmakokinetic behavior, rather than to exceptional affinity to one of the examined binding sites.

Animals↗
PubMed2006

Effect of imidacloprid on the reproduction of acaricide-resistant and susceptible strains of Tetranychus urticae Koch (Acari: Tetranychidae).

Occasional reports linking neonicotinoid insecticide applications to field population outbreaks of the two-spotted spider mite, Tetranychus urticae Koch, have been a topic of concern for integrated pest management (IPM) programmes, particularly in apples. In order to shed light on the factors which may contribute to the occasional field population increase of T. urticae following the application of neonicotinoid insecticides, greenhouse experiments have been set up. Four different T. urticae strains, namely GSS (acaricide-susceptible), WI (organophosphate-selected), USA (a largely uncharacterised strain) and Akita (METI (mitochondrial electron transport inhibitor) acaricide-resistant and cross-resistant to dicofol), were compared for their fecundity without insecticide treatment and for their ovipositional response to foliar and drench applications of the field-relevant dose of imidacloprid (100 mg litre(-1)). Without insecticide treatment, strain GSS laid significantly more eggs (162.50 (+/- 5.43)) than the multiple resistant strain Akita (139.90 (+/- 5.54)) during a 16 day oviposition period. With imidacloprid treatment the highest effect was observed with GSS, with a significantly reduced number of eggs in drench (143.40 (+/- 4.22)) and foliar (144.60 (+/- 5.85)) applications. For strains Akita and USA, no significant differences were observed in oviposition between imidacloprid treatments and controls. The proportion of F1 female offspring decreased significantly with drench application for GSS and WI, while no differences were observed among strains in the survival of F1 immature stages, except for strain USA. The viability of eggs was relatively high (from 82.9 (+/- 4.5)% for USA to 95.2 (+/- 1.2)% for GSS) and not affected by imidacloprid treatments.

Animals↗