Neonicotinoids Impact All Aspects of Bird Life: A Meta-Analysis.

Worldwide, bird populations are declining dramatically. This is especially the case in intensely used agricultural areas where the application of neonicotinoid insecticides is thought to-unintendedly-cause a cascade of negative impacts throughout food webs. Additionally, there could be direct (sub-) lethal impacts of neonicotinoids on birds, but to date there is no comprehensive quantitative assessment to confirm or rule out this possibility. Therefore, we use a meta-analytical approach synthesising 1612 effect sizes from 49 studies and show that neonicotinoids consistently harm bird health, behaviour, reproduction, and survival. Thus, in addition to reduced food availability, the negative direct effects of exposure to neonicotinoids likely contribute to bird population declines globally. Our outcomes are pivotal to consider in future risk assessments and pesticide policy: despite localised bans, the metabolites and residues of neonicotinoids remain present in the environment and in birds and will thus have long-lasting direct effects on both the individual and the population levels.

Neonicotinoids differentially modulate nicotinic acetylcholine receptors in immature and antral follicles in the mouse ovary†.

Neonicotinoids are the most widely used insecticides in the world. They are synthetic nicotine derivatives that act as nicotinic acetylcholine receptor agonists. Although parent neonicotinoids have low affinity for the mammalian nicotinic acetylcholine receptor, they can be activated in the environment and the body to positively charged metabolites with high affinity for the mammalian nicotinic acetylcholine receptor. Imidacloprid, the most popular neonicotinoid, and its bioactive metabolite desnitro-imidacloprid differentially interfere with ovarian antral follicle physiology in vitro, but their effects on ovarian nicotinic acetylcholine receptor subunit expression are unknown. Furthermore, ovarian nicotinic acetylcholine receptor subtypes have yet to be characterized in the ovary. Thus, this work tested the hypothesis that ovarian follicles express nicotinic acetylcholine receptors and their expression is differentially modulated by imidacloprid and desnitro-imidacloprid in vitro. We used polymerase chain reaction, RNA in situ hybridization, and immunohistochemistry to identify and localize nicotinic acetylcholine receptor subunits (α2, 4, 5, 6, 7 and ß1, 2, 4) expressed in neonatal ovaries (NO) and antral follicles. Chrnb1 was expressed equally in NO and antral follicles. Chrna2 and Chrnb2 expression was higher in antral follicles compared to NO and Chrna4, Chrna5, Chrna6, Chrna7, and Chrnb4 expression was higher in NO compared to antral follicles. The α subunits were detected throughout the ovary, especially in oocytes and granulosa cells. Imidacloprid and desnitro-imidacloprid dysregulated the expression of multiple nicotinic acetylcholine receptor subunits in NO, but only dysregulated one subunit in antral follicles. These data indicate that mammalian ovaries contain nicotinic acetylcholine receptors, and their susceptibility to imidacloprid and desnitro-imidacloprid exposure varies with the stage of follicle maturity.

Pharmacology and molecular modeling studies of sulfoxaflor, flupyradifurone and neonicotinoids on the human neuronal α7 nicotinic acetylcholine receptor.

We conducted electrophysiological and molecular docking studies using a heterologous expression system (Xenopus oocytes) to compare the effects of four neonicotinoids (acetamiprid, imidacloprid, clothianidin and thiamethoxam), one sulfoximine, (sulfoxaflor), and one butenolide (flupyradifurone), on human α7 neuronal nicotinic acetylcholine receptors (nAChRs). All neonicotinoids (except thiamethoxam), as well as the recently introduced nAChR competitive modulators, flupyradifurone and sulfoxaflor, appear to be weaker agonists than acetylcholine. Two mutations in loop C (E211N and E211P) and one mutation in loop D (Q79K), known to be involved in the binding properties of neonicotinoids were introduced to the α7 wild type. Interestingly, the acetylcholine and nicotine-evoked activation was not modified in human α7 mutated receptors, but the net charge was enhanced for clothianidin and imidacloprid, respectively. Flupyradifurone responses strongly increased under the Q79K mutation. The molecular docking investigations demonstrated that the orientations and interactions of the ligands considered were in accordance with those observed experimentally. Specifically, the charged fragments of acetylcholine and nicotine, used as reference ligands, and their neonicotinoid homologs were found to be surrounded by aromatic residues, with key interactions with Trp171 and Y210. Furthermore, the molecular docking investigations predicted the water-mediated interaction between the carbonyl oxygen of acetylcholine and the Nsp2 nitrogen of the pyridine ring for nicotine (as well as for the majority of the corresponding neonicotinoid fragments) and main chain NH of L141. The docking scores, extending over a significant range of 6 kcal/mol, showed that most neonicotinoids were poorly stabilized in the α7 nAChR compared to acetylcholine, except sulfoxaflor.

Physiological and gene expression responses of Protohermes xanthodes (Megaloptera: Corydalidae) larvae to imidacloprid.

Megaloptera larvae are important bioindicator species and potential resource insects. To further cultivate their economic role, their living environment must be examined in more detail. In this study, we analyzed the physiological and biochemical effects of a sublethal dose of imidacloprid, a widely used neonicotinoid insecticide, on the larvae of Protohermes xanthodes. After treatment with imidacloprid, P. xanthodes larvae exhibited clear symptoms of poisoning, including the head curling up toward the ventral surface. Additionally, the activity of acetylcholinesterase was significantly inhibited following exposure. The activities of glutathione S-transferases initially continuously increased but showed a slight decrease after 8 days. Catalase activity initially increased and then decreased following imidacloprid treatment; superoxide dismutase activity fluctuated over time, and peroxidase activity continuously increased. The expression levels of HSP70s genes were evaluated using qRT-PCR. These results indicate that P. xanthodes larvae exhibit a toxic response to imidacloprid exposure, manifested as oxidative stress, as observed through behavioral and physiological indicators.

Toxicokinetics Explain Differential Freshwater Ecotoxicity of Nanoencapsulated Imidacloprid Compared to Its Conventional Active Ingredient.

Agricultural applications of nanotechnologies necessitate addressing safety concerns associated with nanopesticides, yet research has not adequately elucidated potential environmental risks between nanopesticides and their conventional counterparts. To address this gap, we investigated the risk of nanopesticides by comparing the ecotoxicity of nanoencapsulated imidacloprid (nano-IMI) with its active ingredient to nontarget freshwater organisms (embryonic Danio rerio, Daphnia magna, and Chironomus kiinensis). Nano-IMI elicited approximately 5 times higher toxicity than IMI to zebrafish embryos with and without chorion, while no significant difference was observed between the two invertebrates. Toxicokinetics further explained the differential toxicity patterns of the two IMI analogues. One-compartmental two-phase toxicokinetic modeling showed that nano-IMI exhibited significantly slower elimination and subsequently higher bioaccumulation potential than IMI in zebrafish embryos (dechorinated), while no disparity in toxicokinetics was observed between nano-IMI and IMI in D. magna and C. kiinensis. A two-compartmental toxicokinetic model successfully simulated the slow elimination of IMI from C. kiinensis and confirmed that both analogues of IMI reached toxicologically relevant targets at similar levels. Although nanopesticides exhibit comparable or elevated toxicity, future work is of utmost importance to properly understand the life cycle risks from production to end-of-life exposures, which helps establish optimal management measures before their widespread applications.

Imidacloprid removal by modified graphitic biochar with Fe/Zn bimetallic oxides.

Coping with the critical challenge of imidacloprid (IMI) contamination in sewage treatment and farmland drainage purification, this study presents a pioneering development of an advanced modified graphitic white melon seed shells biochar (Fe/Zn@WBC). The Fe/Zn@WBC demonstrates a substantial enhancement in adsorption efficiency for IMI, achieving a remarkable removal rate of 87.69% within 30 min and a significantly higher initial adsorption rate parameter h = 4.176 mg g-1·min-1. This significant improvement outperforms WBC (12.22%, h = 0.115 mg g-1·min-1) and highlights the influence of optimized adsorption conditions at 900 °C and the graphitization degree resulting from Fe/Zn bimetallic oxide modification. Characterization analysis and batch sorption experiments including kinetics, isotherms, thermodynamics and pH factors illustrate that chemical adsorption is the main type of adsorption mechanism responsible for this superior ability to remove IMI through pore filling, hydrogen bonding, hydrophobic interaction, electrostatics interaction, π-π interactions as well as complexation processes. Furthermore, we demonstrate exceptional stability of Fe/Zn@WBC across a broad pH range (pH = 3-11), co-existing ions presence along with humic acid under various real water conditions while maintaining high removal efficiency. This study presents an advanced biochar adsorbent, Fe/Zn@WBC, with efficient adsorption capacity and easy preparation. Through three regeneration cycles via pyrolysis method, it demonstrates excellent pyrolysis regeneration capabilities with an average removal efficiency of 92.02%. The magnetic properties enable rapid separation facilitated by magnetic analysis. By elucidating the efficacy and mechanistic foundations of Fe/Zn@WBC, this research significantly contributes to the field of environmental remediation by providing a scalable solution for IMI removal and enhancing scientific understanding of bimetallic oxides-hydrophilic organic pollutant interactions.

Improving the stability, foliar utilization and biological activity of imidacloprid delivery systems: Size effect of nanoparticles.

Nanotechnology could improve the effectiveness and functionality of pesticides, but the size effect of nanopesticides on formulation performance and the related mechanisms have yet to be explored, hindering the precise design and development of efficient and eco-friendly nanopesticides. In this study, two non-carrier-coated imidacloprid formulations (Nano-IMI and Micro-IMI) with identical composition but varying particle size characteristics were constructed to exclude other interferences in the size effect investigation. Nano-IMI and Micro-IMI both exhibited rod-like structures. Specifically, Nano-IMI had average vertical and horizontal axis sizes of 239.5 nm and 561.8 nm, while Micro-IMI exhibited 6.7 µm and 22.1 µm, respectively. Compared to Micro-IMI, the small size effect of Nano-IMI affected the arrangement of interfacial molecules, reduced surface tension and contact angle, thereby improving the stability, dispersibility, foliar wettability, deposition and retention of the nano-system. Nano-IMI exhibited 1.3 times higher toxicity to Aphis gossypii Glover compared to Micro-IMI, attributed to its enhanced foliar utilization efficiency. Importantly, the Nano-IMI did not intensify the toxicity to non-target organism Apis mellifera L. This study systematically elucidates the influence of size effect on key indicators related to the effectiveness and safety, providing a theoretical basis for efficient and safe application of nanopesticides and critical insights into sustainable agriculture and environmental development.

Toxicity evaluation of novel imidacloprid nanoribbons, using somatic mutation and fitness indexes in Drosophila melanogaster.

Nanoribbons of imidacloprid, a systemic and chloronicotinyl insecticide, were successfully synthesized by laser-induced fragmentation/exfoliation of imidacloprid powders suspended in water, with widths ranging from 160 to 470 nm, lengths in the micron scale, and thickness of a few atoms layers. The aim of the present study was to examine the effects of acute and chronic exposure to imidacloprid (IMC) bulk and compare its effects with synthesized imidacloprid nanoribbons (IMCNR) on larval and adult viability, developmental time, olfactory capacity, longevity, productivity, and genotoxicity in Drosophila melanogaster. Larvae or adults were exposed at 0.01, 0.02, or 0.03 ppm to IMC or IMCNR. Results demonstrated that IMCNR produced a significant reduction in viability and olfactory ability. IMC did not significantly alter viability and olfactory ability. Similarly, marked differences on longevity were detected between treatment with IMC and IMCNR where the lifespan of males treated with IMC was significantly higher than control while IMCNR produced a reduction. As for productivity, developmental time, and genotoxicity, no marked differences were found between both forms of IMC.

Exposure to Imidacloprid under variable conditions disturbs the muscle fatty acid profile of a fresh water non target fish: Labeo rohita.

Economy of Pakistan is heavily dependent upon agriculture and extensive use of pesticide is quiet common to enhance the crop yield. Imidacloprid is among the first choice pesticides in Pakistan and it has been reported that through run off along with water it ends up in water bodies affecting non target aquatic fauna. Through the present investigation, we are reporting the effects of Imidacloprid on the fatty acids composition of a non-target, commercially important carp: Labeo rohita. Fish were exposed to sub lethal concentration of Imidacloprid (120 mgL1) for 2, 4 and 8 days (short term) as well as for 16, 32 and 64 days (long term experimental conditions). Pesticide untreated controls were also maintained for each treatment. Following the specific Imidacloprid exposure, fatty acid composition (%) was determined in the muscle of all experimental groups by using gas chromatography. Fish exposed to Imidacloprid for 8 days had reduced Palmitic acid (p = 0.02) and elevated muscle Arachidic acid (p < 0.001) than control group. Labeo rohita exposed to the pesticide for 32 days had elevated muscle Oleic (p = 0.02) and Linoleic acid (p = 0.02) while fish exposed to Imidacloprid to 64 days had reduced muscle Palmitic (p = 0.04) and Oleic acid (p = 0.03). In conclusion, we are reporting that the exposure to sub lethal concentration of Imidacloprid disturb the muscle fatty acid composition of Labeo rohita that may affect its food quality. The effects were more pronounced under long term experimental conditions and were probably due to potentiating lipid peroxidation and disturbed fish metabolism upon Imidacloprid exposure.

Rifampicin synergizes the toxicity of insecticides against the green peach aphid, Myzus persicae.

Myzus persicae is an important pest that has developed resistance to nearly all currently used insecticidal products. The employment of insecticide synergists is one of the effective strategies that need to be developed for the management of this resistance. Our study showed that treatment with a combination of the antibiotic, rifampicin, with imidacloprid, cyantraniliprole, or clothianidin significantly increased their toxicities against M. persicae, by 2.72, 3.59, and 2.41 folds, respectively. Rifampicin treatment led to a noteworthy reduction in the activities of multifunctional oxidases (by 32.64%) and esterases (by 23.80%), along with a decrease in the expression of the CYP6CY3 gene (by 58.57%) in M. persicae. It also negatively impacted the fitness of the aphids, including weight, life span, number of offspring, and elongation of developmental duration. In addition, bioassays showed that the combination of rifampicin and a detoxification enzyme inhibitor, piperonyl butoxide, or dsRNA of CYP6CY3 further significantly improved the toxicity of imidacloprid against M. persicae, by 6.19- and 7.55-fold, respectively. The present study suggests that development of active ingredients such as rifampicin as candidate synergists, show promise to overcome metabolic resistance to insecticides in aphids.

Impact of imidacloprid exposure on gestational hyperglycemia: A multi-omics analysis.

Imidacloprid (IMI), a commonly utilized neonicotinoid insecticide, has been identified to adversely impact glucose homeostasis. Pregnant women are believed to be more sensitive to toxins than non-pregnant women, and the impact of IMI exposure on gestational hyperglycemia remain unclear. To explore the impact, pregnant mice fed a high-fat diet were exposed to different doses (0.06, 0.6, 6 mg/kg bw/day) of IMI by gavage. Glucose homeostasis-related parameters were measured. The glucose homeostasis influenced by IMI treatment was explored through integrating gut microbiota, metabolomic and transcriptomic analysis. Results showed that IMI-H (6 mg/kg bw/day) exposure notably restricted gestational weight gain and perturbed glucose homeostasis characterized by reduced glucose tolerance and insulin sensitivity, alongside elevated levels of fasting blood glucose and insulin. Multi-omics analysis revealed that IMI-H exposure induced significant changes in the richness and composition of the gut microbiome. The metabolite profiles of serum samples and cecal contents, and transcriptome of liver and ileum were all affected by IMI-H treatment. The altered gut microbiota, metabolites and genes exhibited significant correlations with glucose homeostasis-related parameters. These differential metabolites and genes were implicated in various metabolic pathways including bile secretion, glucagon signaling pathway, lipid metabolism, fatty acid metabolism. Significant correlations were observed between the altered gut microbiota and caecum metabolome as well as liver transcriptome. For example, the abundance of Oscillibacter was strongly correlated with gut microflora-related metabolites (Icosenoic acid, Lysosulfatide, and fluticasone) and liver differential genes (Grin3b, Lifr, and Spta1). Together, IMI exposure resulted in significant changes in microbial composition, along with alterations in certain metabolites and genes associated with metabolic process, which may promote gestational hyperglycemia.

Fluorometric detection of copper and imidacloprid using nitrogen-doped graphitic carbon dots: A promising method for environmental monitoring.

Pesticides in environmental samples pose significant risks to ecosystems and human health since they require precise and efficient detection methods. Imidacloprid (IMI), a widely used neonicotinoid insecticide, exemplifies these hazards due to its potential toxicity. This study addresses the urgent need for improved monitoring of such contaminants by introducing a novel fluorometric method for detecting IMI using nitrogen-doped graphite carbon dots (N-GCDs). The sensor operates by quenching fluorescence through the interaction of Cu2+ ions with N-GCDs. Subsequently, IMI binds to the imidazole group, chelates with Cu2+, and restores the fluorescence of N-GCDs. This alternating fluorescence behavior allows for the accurate identification of both Cu2+ and IMI. The sensor exhibits linear detection ranges of 20-100 nM for Cu2+ and 10-140 µg/L for IMI, with detection limits of 18 nM and 1.2 µg/L, respectively. The high sensitivity of this sensor enables the detection of real-world samples, which underscores its potential for practical use in environmental monitoring and agricultural safety.

Protective effect of melatonin on imidacloprid-induced pyroptosis and ferroptosis by mediating peptidoglycan in the gut of the common carp (Cyprinus carpio).

Imidacloprid (IMI) is a contaminant widespread in surface water, causing serious intestinal damage in the common carp. Melatonin (MT), an endogenous indoleamine hormone, plays a crucial role in mitigating pesticide-induced toxicity. Our previous research has demonstrated that MT effectively reduces the production of intestinal microbial-derived signal peptidoglycan (PGN) induced by IMI, thereby alleviating intestinal tight junction injuries in the common carp. In this study, we performed a transcriptomic analysis to explore the effect of MT on the IMI exposure-induced gut damage of the common carp. The results elucidated that the ferroptosis, mitogen-activated protein kinases (MAPKs), and nucleotide oligomerization domain (NOD)-like signaling pathways were significantly associated with IMI exposure and MT treatment. Meanwhile, the exposure to IMI resulted in the formation of pyroptotic bodies and distinct morphological features of ferroptosis, both mitigated with the addition of MT. Immunofluorescence double staining demonstrated that MT abolished the elevated expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and Gasdermin D (GSDMD) induced by IMI, as well as reduced expression of ferritin heavy chains (FTH) and glutathione peroxidase 4 (GPX4) in gut tissues. Subsequently, we found that the exposure to IMI or PGN enhanced the expression of toll-like receptors (TLR) 2 (a direct recognition receptor of PGN) triggering the P38MAPK signaling pathway, thereby aggravating the process of pyroptosis and ferroptosis of cell models. The addition of MT or SB203580 (a P38MAPK inhibitor) significantly reduced pyroptotic cells, and also decreased iron accumulation. Consequently, these results indicate that MT alleviates IMI-induced pyroptosis and ferroptosis in the gut of the common carp through the PGN/TLR2/P38MAPK pathway.

Glutathione S-transferase directly metabolizes imidacloprid in the whitefly, Bemisia tabaci.

The whitefly Bemisia tabaci poses a significant threat to various crops and ornamental plants and causes severe damage to the agricultural industry. Over the past few decades, B. tabaci has developed resistance to several pesticides, including imidacloprid. Therefore, elucidating the mechanism that leads to insecticide detoxification is very important for controlling B. tabaci and managing whitefly resistance to neonicotinoid insecticides. Among insect detoxification enzymes, glutathione S-transferase (GST) is an important phase II detoxification enzyme that helps detoxify exogenous toxic substances. In this study, we cloned the BtGSTz1 gene and observed that its expression level was greater in imidacloprid-resistant populations than sensitive populations of B. tabaci. By silencing BtGSTz1 via RNA interference, we found a significant increase in the mortality of imidacloprid-resistant B. tabaci. Additionally, prokaryotic expression and in vitro metabolism studies revealed that the recombinant BtGSTz1 protein could metabolize 36.36% of the total imidacloprid, providing direct evidence that BtGSTz1 plays a crucial role in the detoxification of imidacloprid. Overall, our study elucidated the role of GSTs in physiological activities related to insecticide resistance, which helps clarify the resistance mechanisms conferred by GSTs and provides useful insights for sustainable integrated pest management.

microRNA-3037 targeting CYP6CY2 confers imidacloprid resistance to Sitobion miscanthi (Takahashi).

The wheat aphid Sitobion miscanthi is a dominant and destructive pest in agricultural production. Insecticides are the main substances used for effective control of wheat aphids. However, their extensive application has caused severe resistance of wheat aphids to some insecticides; therefore, exploring resistance mechanisms is essential for wheat aphid management. In the present study, CYP6CY2, a new P450 gene, was isolated and overexpressed in the imidacloprid-resistant strain (SM-R) compared to the imidacloprid-susceptible strain (SM-S). The increased sensitivity of S. miscanthi to imidacloprid after knockdown of CYP6CY2 indicates that it could be associated with imidacloprid resistance. Subsequently, the posttranscriptional regulation of CYP6CY2 in the 3' UTR by miR-3037 was confirmed, and CYP6CY2 participated in imidacloprid resistance. This finding is critical for determining the role of P450 in relation to the resistance of S. miscanthi to imidacloprid. It is of great significance to understand this regulatory mechanism of P450 expression in the resistance of S. miscanthi to neonicotinoids.

Assessment of imidacloprid induced genotoxicity in Pethia conchonius (Rosy barb), a common freshwater fish of India.

Imidacloprid is one of the highly efficient, globally used neonicotinoid groups of insecticides. The indiscriminate use of imidacloprid is contaminating large water bodies affecting not only the target organisms but also non-target organisms including fish. The present study aimed to assess the extent of nuclear DNA damage by imidacloprid in Pethia conchonius a freshwater fish in India using comet and micronucleus assays. The LC50 value of imidacloprid was estimated to be 227.33 mg L-1. Based on the LC50-96 h value, three sub-lethal concentrations of imidacloprid, SLC I -18.94 mg L-1, SLC II -28.41 mg L-1 and SLC III -56.83 mg L-1 were used to detect its genotoxic effect at DNA and cellular level. The imidacloprid exposed fishes exhibited higher DNA damage and nuclear abnormalities (p < 0.05) than the control. The %head DNA, %tail DNA, tail length and the frequency of micronuclei with other nuclear abnormalities like blebbed and notched nuclei were significantly higher than the control in a time and concentration-dependent manner. The DNA damage parameters such as %head DNA (29.107 ± 1.843), %tail DNA (70.893 ± 1.843), tail length (361.431 ± 8.455) micronucleus (1.300 ± 0.019), notched (0.844 ± 0.011) and blebbed (0.811 ± 0.011) nuclei were found to be highest for SLC III (56.83 mg L-1) at 96 h. The findings indicate that IMI is highly genotoxic in fish and other vertebrates leading to mutagenic/clastogenic effects. The study will be helpful in optimization of the imidacloprid use.

Design, Synthesis, and Synergistic Activities of Eight-Membered Carbon Bridged Neonicotinoid Derivatives.

Insecticide synergists are an effective approach to increase the control efficacy and reduce active ingredient usage. In order to explore neonicotinoid-specific synergists with novel scaffolds and higher potency, a series of eight-membered carbon bridged neonicotinoid derivatives were designed and synthesized in accordance with our previous research. The synergistic effects of the target compounds on neonicotinoids in Aphis craccivora were evaluated, and the structure-activity relationships were summarized. The results indicated that most of the target compounds exhibited significant synergistic effects on imidacloprid in A. craccivora at low concentrations. In particular, compound 1 at a concentration of 1 mg/L reduced the LC50 value of imidacloprid from 0.856 mg/L to 0.170 mg/L. Meanwhile, compound 1 also increased the insecticidal activity of most neonicotinoid insecticides belonging to the Insecticide Resistance Action Committee (IRAC) 4 A subgroup against A. craccivora. The present study might be meaningful for directing the design of neonicotinoid-specific synergists.

Decreases in the number of microglia and neural circuit dysfunction elicited by developmental exposure to neonicotinoid pesticides in mice.

Neonicotinoids are insecticides widely used in the world. Although neonicotinoids are believed to be toxic only to insects, their developmental neurotoxicity in mammals is a concern. Therefore, we examined the effects of developmental exposure to neonicotinoids on immune system in the brain and post-developmental behaviors in this study. Imidacloprid or clothianidin was orally administered to dams at a dosage of 0.1 mg/kg/day from embryonic day 11 to postnatal day 21. Imidacloprid decreased sociability, and both imidacloprid and clothianidin decreased locomotor activity and induced anxiety, depression and abnormal repetitive behaviors after the developmental period. There was no change in the number of neurons in the hippocampus of mice exposed to imidacloprid. However, the number and activity of microglia during development were significantly decreased by imidacloprid exposure. Imidacloprid also induced neural circuit dysfunction in the CA1 and CA3 regions of the hippocampus during the early postnatal period. Exposure to imidacloprid suppressed the expression of csf1r during development. Collectively, these results suggest that developmental exposure to imidacloprid decreases the number and activity of microglia, which can cause neural circuit dysfunction and abnormal behaviors after the developmental period. Care must be taken to avoid exposure to neonicotinoids, especially during development.

Resveratrol alleviates imidacloprid-induced mitochondrial apoptosis, necroptosis, and immune dysfunction in chicken lymphocyte lines by inhibiting the ROS/MAPK signaling pathway.

Imidacloprid (IMI) is a neonicotinoid insecticide with the highest global market share, and IMI exposure in the environment can negatively affect many nontarget organisms (a general term for organisms affected by drugs other than target organisms). Resveratrol (RSV), a non-flavonoid polyphenolic organic compound derived from peanuts, grapes, and other plants, has anti-inflammatory and antioxidant effects. It is currently unclear how RSV protects against cell damage caused by IMI. Therefore, we established an experimental model of chicken lymphocyte lines exposed to 110 µg/mL IMI and/or 0.5 µM RSV for 24 h. According to the experimental results, IMI markedly raised intracellular reactive oxygen species levels and diminished the activity of the cellular antioxidant enzymes (CAT, SOD, and GPx), leading to MDA accumulation and decreased T-AOC. JNK, ERK, and P38, the essential components of the mitogen-activated protein kinase (MAPK) signaling pathway, were also expressed more when IMI was present. Additionally, IMI resulted in upregulation of mitochondrial apoptosis (Caspase 3, Caspase 9, Bax, and Cyt-c) and necroptosis (Caspase 8, RIPK1, RIPK3, and MLKL) related factors expression, downregulation of Bcl-2 expression, induction of upregulation of cytokine IL-6 and TNF-α expression, and downregulation of IFN-γ expression. The combined treatment of RSV and IMI significantly reduced cellular oxidative stress levels, inhibited the MAPK signaling pathway, and alleviated IMI-induced mitochondrial apoptosis, necroptosis, and immune dysfunction. To summarize, RSV antagonized IMI-induced mitochondrial apoptosis, necroptosis, and immune dysfunction in chicken lymphocyte lines by inhibiting the ROS/MAPK signaling pathway.

Kill two birds with one stone: colorimetric/fluorescence immunosensor based on Au@Pt nanozyme for sensitive detection of imidacloprid.

Gold-platinum (Au@Pt) nanozymes with high catalytic activity and stability were designed to improve the stability of the enzyme-linked immunosorbent assay (ELISA), and a two-mode signal output was used to enhance the sensitivity and confidence of the assay. This study reports the two-mode signal output based on Au@Pt nanozyme to catalyzed 3,3',5,5'-tetramethylbenzidine (TMB) reaction. Oxidized 3,3',5,5'-tetramethylbenzidine (ox-TMB) has wide absorption spectrum, providing excellent optical density capabilities and fluorescence quenching. The detection limits of imidacloprid were 0.88 µg/L and 1.14 µg/L in colorimetric and fluorescence modes, respectively. Multiple-mode strategy improves detection accuracy, increases the confidence of experimental results, and broadens detection modes. Two modes can meet the requirements of accurate and flexible multi-mode sensing in different application situations.