The toxicity effects of imidacloprid and chlorpyrifos on oxidative stress and blood biochemistry in Cyprinus carpio.

This study aimed to assess the toxicity effects of chlorpyrifos and imidacloprid, alone and in combination, on oxidative biomarkers and blood biochemistry of Cyprinus carpio. A total of 324 common carp (Cyprinus carpio) were distributed among 27 tanks and exposed to concentrations of 0.0, 100, and 200 µg L-1 of chlorpyrifos and 0.0, 10.0, and 20.0 µg L-1 of imidacloprid for 28 days. Changes in enzyme activities in the plasma of fish exposed to chlorpyrifos depended on the dose. In contrast, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), creatine phosphokinase (CPK), gamma-glutamyl transferase (GGT) activities were significantly increased in fish exposed to imidacloprid, alone and in combination with chlorpyrifos. However, the activity of butyrylcholinesterase (BChE) was significantly decreased. Exposure to imidacloprid and chlorpyrifos, alone and in combination, increased glucose, urea, cholesterol, triglycerides, and creatinine levels, whereas total protein and albumin levels were significantly decreased. The activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), and catalase (CAT) was significantly increased, while glutathione reductase (GR) was significantly decreased. Additionally, although the total antioxidant capacity (TAN) was significantly decreased, malondialdehyde (MDA) levels increased after exposure to imidacloprid and chlorpyrifos, alone and in combination. In conclusion, exposure to imidacloprid and chlorpyrifos, alone and in combination, induced oxidative stress and altered blood biochemistry in carp fish. Moreover, imidacloprid and chlorpyrifos had synergistic effects on some oxidative and biochemical biomarkers.

Factors contributing to pesticide contamination in riverine systems: The role of wastewater and landscape sources.

Wastewater treatment plant (WWTP) discharges can be a source of organic contaminants, including pesticides, to rivers. An integrated model was developed for the Potomac River watershed (PRW) to determine the amount of accumulated wastewater (ACCWW) and calculate predicted environmental concentrations (PECs) for 14 pesticides in non-tidal National Hydrography Dataset Plus Version 2.1 stream segments. PECs were compared to measured environmental concentrations (MECs) from 32 stream sites that represented a range of ACCWW and land use to evaluate model performance and to assess possible non-WWTP loading sources. Agreement between PECs and MECs was strongest for insecticides, followed by fungicides and herbicides. Principal component analysis utilizing optical fluorescence and ancillary water quality data further separated wastewater from urban runoff sources. Pesticides that indicated relatively larger sources from WWTPs included dinotefuran, fipronil, carbendazim, thiabendazole, and prometon while imidacloprid, azoxystrobin, propiconazole, tebuconazole, and diuron were more strongly related to urban runoff. However, PECs generally comprised a low proportion of MECs, which suggests dominant loading sources beyond WWTP discharges. Cumulative potential toxicity was higher for sites with greater ACCWW and/or located in developed areas. Imidacloprid, fipronil, and carbendazim accounted for the largest portion of predicted potential toxicity across sites. The chronic aquatic life toxicity benchmarks for freshwater invertebrates were exceeded for 82 % of the imidacloprid detections (n = 28) and 47 % of the fipronil detections (n = 19). These results not only highlight the significant ecological implications of pesticide contamination from WWTP discharges but also underscores the potential legacy effects from accumulated soil and groundwater sources, emphasizing the need for management strategies to mitigate both current and historical impacts on aquatic ecosystems.

Changes in the proteome of Apis mellifera acutely exposed to sublethal dosage of glyphosate and imidacloprid.

Uncontrolled use of pesticides has caused a dramatic reduction in the number of pollinators, including bees. Studies on the effects of pesticides on bees have reported effects on both metabolic and neurological levels under chronic exposure. In this study, variations in the differential expression of head and thorax-abdomen proteins in Africanized A. mellifera bees treated acutely with sublethal doses of glyphosate and imidacloprid were studied using a proteomic approach. A total of 92 proteins were detected, 49 of which were differentially expressed compared to those in the control group (47 downregulated and 2 upregulated). Protein interaction networks with differential protein expression ratios suggested that acute exposure of A. mellifera to sublethal doses of glyphosate could cause head damage, which is mainly associated with behavior and metabolism. Simultaneously, imidacloprid can cause damage associated with metabolism as well as, neuronal damage, cellular stress, and impairment of the detoxification system. Regarding the thorax-abdomen fractions, glyphosate could lead to cytoskeleton reorganization and a reduction in defense mechanisms, whereas imidacloprid could affect the coordination and impairment of the oxidative stress response.

Role of IRE1α/XBP1/CHOP/NLRP3 Signalling Pathway in Neonicotinoid Imidacloprid-Induced Pancreatic Dysfunction in Rats and Antagonism of Lycopene: In Vivo and Molecular Docking Simulation Approaches.

Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse effects on the pancreas following oral consumption of imidacloprid neonicotinoids (45 mg/kg daily for 30 days) and the potential protective effects of lycopene (LYC) administration (10 mg/kg/day for 30 days) with IMI exposure in male Sprague-Dawley rats. The apoptotic, pyroptotic, inflammatory, oxidative stress, and endoplasmic reticulum stress biomarkers were evaluated, along with the histopathological alterations. Upon IMI administration, noticeable changes were observed in pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress biomarkers, inflammatory, pyroptotic, and apoptotic biomarkers were also observed following IMI administration. LYC effectively reversed these alterations by reducing oxidative stress markers (e.g., MDA) and enhancing antioxidant enzymes (SOD, CAT). It downregulated ER stress markers (IRE1α, XBP1, CHOP), decreased pro-inflammatory cytokines (TNF-α, IL-1ß), and suppressed pyroptotic (NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the histopathological and ultrastructure alterations brought on by IMI toxicity.

Photocatalytic removals of imidacloprid insecticide in TiO2- and Fe2O3-immobilized porous geopolymer granules.

In this study, geopolymer catalysts were synthesized by incorporating different TiO2 (0, 7, and 14 wt%) and Fe2O3 content (0, 7, 14, and 20 wt%) into porous metakaolin-based geopolymer granules. TiO2- and Fe2O3-immobilized geopolymer granules were applied for photocatalytic removals of imidacloprid under UV-C irradiation. The analysis of the surface morphology of the Fe2O3 catalyst revealed its larger surface area predominated with meso- and macro-pores thus providing a larger area for photocatalysis. Meanwhile, the TiO2 catalyst had TiO2 nanoparticles filled up those mesopores and macropores in geopolymer resulting in its denser structure therefore limiting access of imidacloprid to the reactive sites. To maximize its photocatalytic activities, Fe2O3 and TiO2 could be immobilized into porous geopolymer matrix up to 20 and 14 wt%, respectively. The developed porous geopolymer had relatively stable imidacloprid adsorption capacities regardless of the TiO2 and Fe2O3 contents in their texture. After UV irradiation, their removal efficiencies were 94.85-100% and the photocatalytic degradation increased with the increase in TiO2 content (from 0 to 14 wt%) and Fe2O3 content (from 14 to 20 wt%). Nevertheless, Fe2O3-immobilized geopolymer granules posed a significantly higher kinetic rate (1.966 h-1) compared to that of TiO2 (0.154 h-1) at the same catalyst content (14 wt%). The newly developed Fe2O3-immobilized porous geopolymer catalysts could be effectively reused over 10 successive cycles during which the imidacloprid could be completely removed.

Low-temperature subcritical water dechlorination composites of waste PVC/coal fly ash with powerful sensing activity for chemiluminescent detection of acetamiprid and imidacloprid.

Pesticide residues in agricultural products are serious threat to people's health. Real-time monitoring of pesticides residues in the environment and agricultural products posed challenges to sustainable methods with high analytical performance for pesticide detection. Herein, waste PVC/coal fly ash (the mass ratio of PVC and coal fly ash was 4:1) was dechlorinated in subcritical water at low temperature to achieve nearly 100 % dechlorination of PVC and obtain carbon-based composite materials (CM-Fe/Al/Si-dPVC) with strong sening activity. For CM-Fe/Al/Si-dPVC, CFe bonding resulted in strong electron migration, and nano/µm SiO2 and Al2O3 doping in the layered polyene C matrix provided large specific surface area, and silicon hydroxyl created good heterogeneous catalytic interfaces. CM-Fe/Al/Si-dPVC could strongly trigger luminol chemiluminescence (CL) reaction and produce intense CL signals. Neonicotinoid pesticides (acetamiprid and imidacloprid) bonded with CM-Fe/Al/Si-dPVC through coordination chelation and hydrogen bonding, which shielded the catalytic active site and increased the Fermi level of system, thus quenching CL reaction. Inspired by these, a cheap CL assay was constructed for detecting neonicotinoids combinations of acetamiprid and imidacloprid (NICs). The detection limits of NICs were 0.7 ng/L. Satisfactory recoveries were obtained for real agricultural products and environmental samples. The results of life cycle evaluation (LCA) revealed that the strategy had significantly small global warming potential (GWP). This work presented a sustainable method with environmental benefits for the detection of neonicotinoids, and also opened up new way for the recycling of organic solid wastes.

Increased spontaneous activity and progressive suppression of adult neurogenesis in the hippocampus of rat offspring after maternal exposure to imidacloprid.

Imidacloprid (IMI) is a widely used neonicotinoid insecticide that poses risks for developmental neurotoxicity in mammals. The present study investigated the effects of maternal exposure to IMI on behaviors and adult neurogenesis in the hippocampal dentate gyrus (DG) of rat offspring. Dams were exposed to IMI via diet (83, 250, or 750 ppm in diet) from gestational day 6 until day 21 post-delivery on weaning, and offspring were maintained until adulthood on postnatal day 77. In the neurogenic niche, 750-ppm IMI decreased numbers of late-stage neural progenitor cells (NPCs) and post-mitotic immature granule cells by suppressing NPC proliferation and ERK1/2-FOS-mediated synaptic plasticity of granule cells on weaning. Suppressed reelin signaling might be responsible for the observed reductions of neurogenesis and synaptic plasticity. In adulthood, IMI at ≥ 250 ppm decreased neural stem cells by suppressing their proliferation and increasing apoptosis, and mature granule cells were reduced due to suppressed NPC differentiation. Behavioral tests revealed increased spontaneous activity in adulthood at 750 ppm. IMI decreased hippocampal acetylcholinesterase activity and Chrnb2 transcript levels in the DG on weaning and in adulthood. IMI increased numbers of astrocytes and M1-type microglia in the DG hilus, and upregulated neuroinflammation and oxidative stress-related genes on weaning. In adulthood, IMI increased malondialdehyde level and number of M1-type microglia, and downregulated neuroinflammation and oxidative stress-related genes. These results suggest that IMI persistently affected cholinergic signaling, induced neuroinflammation and oxidative stress during exposure, and increased sensitivity to oxidative stress after exposure in the hippocampus, causing hyperactivity and progressive suppression of neurogenesis in adulthood. The no-observed-adverse-effect level of IMI for offspring behaviors and hippocampal neurogenesis was determined to be 83 ppm (5.5-14.1 mg/kg body weight/day).

Heterologous expression and characterization of two delta glutathione S-transferases genes involved in imidacloprid metabolism in Grapholita molesta.

Glutathione S-transferases (GSTs) are multifunctional enzymes, and insect GSTs play a pivotal role in the metabolism of insecticides. Grapholita molesta is a worldwide pest that causes substantial economic losses to the fruit industry. However, it remains unclear how imidacloprid, a commonly used insecticide in orchards, is metabolized by G. molesta. In the present study, the synergist diethyl maleate (DEM), which inhibits the GST activity, exhibited a 22-fold synergistic ratio against imidacloprid. Two new GST genes, GmGSTD2 (OR096251) and GmGSTD3 (OR096252), were identified and successfully cloned, showing the highest expression in the Malpighian tubes. Knockdown of GmGSTD2 and GmGSTD3 by RNA interference, increased the mortality of G. molesta from 28% to 47% following imidacloprid treatment. Both recombinant GmGSTD2 and GmGSTD3 proteins exhibited 1-chloro-2,4-dinitrobenzene (CDNB) activity and could be inhibited by imidacloprid in vitro, with maximum inhibition was 60% for GmGSTD2 and 80% for GmGSTD3. These results suggested that GSTs participate in the metabolism of imidacloprid with GmGSTD2 and GmGSTD3 playing key roles in this process.

ZIF-8-wrapped AgNPs modified with ß-cyclodextrin for sensitive detection of thiacloprid and imidacloprid by SERS technology.

The high efficient surface-enhanced Raman scatterring (SERS) methods to detect thiacloprid and imidacloprid were established using ZIF-8-wrapped Ag nanoparticles (AgNPs) modified with ß-cyclodextrin (ß-CD). The substrate of ZIF-8/ß-CD@AgNPs was characterized by ultraviolet visible spectra (UV-vis), thermogravimetric analysis (TGA), X-ray diffraction (XRD), transmission electron microscopy (TEM) and scanning transmission electron microscopy (STEM). The interaction between the substrate and thiacloprid/imidacloprid was also explored. The optimum measurement conditions were obtained by response surface model based on single-factor experiments. Enhancement factors (EFs) of thiacloprid and imidacloprid were respectively 2.29 × 106 and 2.60 × 106. A good linearity between the scattering intensity and the concentration of thiacloprid/imidacloprid within 3-1000 nmol L-1/6-400 nmol L-1 was established. The interference experiments indicated that the methods had good selectivity. The SERS methods were successfully applied to detect thiacloprid and imidacloprid in several vegetables samples. The recoveries ranged from 95.5 % to 105 % (n = 5). The detection limits (LODs) (S/N = 3) for thiacloprid and imidacloprid were 1.50 and 0.83 nmol L-1, respectively.

Evaluating the Safety of Imidacloprid FS Seed Treatment Use in Potato Production: A Case Study from China.

This study evaluated the residue behavior and dissipation dynamics of a new imidacloprid FS 600 seed treatment in potato cultivation systems in Shandong and Jilin, China. Sensitive and accurate UPLC-MS/MS methods were established to quantify imidacloprid residues in potatoes, potato plants, and soil. Results showed that imidacloprid dissipation followed a first-order kinetic model, with half-lives ranging from 6.9 to 26.7 days in plants and 19.8 to 28.9 days in soil. At harvest, the highest average residues in potatoes and soil were 0.778 mg/kg and 0.149 mg/kg, respectively. The dietary risk assessment indicated a chronic risk quotient (CRQ) of 39.73% for adults, indicating minimal risk to human consumers, while the ecological risk quotient (ERQ) and ecotoxicity exposure ratio (TER) revealed low to moderate toxicity to earthworms, warranting caution in the use of this formulation. This research provides valuable data for assessing the safety of imidacloprid FS seed treatment in potato cultivation.

Development and Validation of a High-Performance Liquid Chromatography Diode Array Detector Method to Measure Seven Neonicotinoids in Wheat.

Neonicotinoids (NEOs), used as insecticides against aphids, whiteflies, lepidopterans, and beetles, have numerous detrimental impacts on human health, including chronic illnesses, cancer, infertility, and birth anomalies. Monitoring the residues in food products is necessary to guarantee public health and ecological balance. The present work validated a new method to measure seven neonicotinoid insecticides (acetamiprid ACT, clothianidin CLT, dinotefuran DNT, imidacloprid IMD, nitenpyram NTP, thiacloprid TCP, and thiamethoxan THT) in wheat. The analytical procedure was based on simple and fast wheat sample cleanup using solid-phase extraction (SPE) to remove interferents and enrich the NEOs, alongside the NEOs' separation and quantification by reverse-phase chromatography coupled with a diode array detector (DAD). The validation process was validated using the accuracy profile strategy, a straightforward decision tool based on the measure of the total error (bias plus standard deviation) of the method. Our results proved that, in the future, at least 95% of the results obtained with the proposed method would fall within the ±15% acceptance limits. The test's cost-effectiveness, rapidity, and simplicity suggest its use for determining the levels of acetamiprid, clothianidin, dinotefuran, imidacloprid, nitenpyram, thiacloprid, and thiamethoxam in routine analyses of wheat.

A colloidal gold immunochromatographic method for rapid screening of imidacloprid residues in Chinese herbal medicines.

An imidacloprid colloidal gold immunochromatographic strip was developed in this work, and systematic analytical conditions were deeply investigated. The test strips were used for rapid screening of imidacloprid residues in Chinese herbal medicines. The performance of the colloidal gold test strips was investigated by using five selected Chinese herbal medicines (malt, Coix seed, lotus seed, dried ginger and honeysuckle). As a result, the developed imidacloprid colloidal gold immunochromatographic test strips could be used for rapid screening of imidacloprid residues in 60 kinds of different herbs (including 26 kinds of root/rhizome medicines, 20 kinds of seed/fruit/pericarp medicines, 11 kinds of flower/leaf/whole herb medicines, and 3 kinds of bark/aboveground issues of herb medicines), and the cut-off value was 50 µg/kg. The development of this method can achieve the goal of on-site, rapid and low-cost screening of imidacloprid residues in different herbs, which is of great significance for the quality assurance of herbs.

Structural gonadal lesions observed in Japanese quail (Coturnix coturnix japonica) following exposure during puberty to the neonicotinoid pesticide, imidacloprid.

Exposure to the neonicotinoid insecticide, imidacloprid (IMI), causes reproductive toxicity in mammals and reptiles. However, reports on the effects of IMI on the gonads in birds are grossly lacking. Therefore, this study investigated the effects of pubertal exposure to IMI on the histology, ultrastructure, as well as the cytoskeletal proteins, desmin, smooth muscle actin and vimentin, of the gonads of Japanese quail (Coturnix coturnix japonica). Quails were randomly divided into four groups at 5 weeks of age. The control group was given only distilled water, whereas, the other three experimental groups, IMI was administered by oral gavage at 1.55, 3.1, and 6.2 mg/kg, twice per week for 4 weeks. Exposure to IMI doses of 3.1 and 6.2 mg/kg caused dose-dependent histopathological changes in the ovary and testis. In the ovary, accumulation of lymphocytes, degenerative changes, and necrosis with granulocyte infiltrations were observed, while in the testis, distorted seminiferous tubules, germ cell sloughing, vacuolisations, apoptotic bodies, autophagosomes, and mitochondrial damage were detected. These changes were accompanied by a decreased number of primary follicles (P ≤ 0.05) in the ovary and a decrease (P ≤ 0.05) in the epithelial height, luminal, and tubular diameters of seminiferous tubules at the two higher dosages. In addition, IMI had a negative effect on the immunostaining intensity of desmin, smooth muscle actin, and vimentin in the ovarian and testicular tissue. In conclusion, exposure to IMI during puberty can lead to a range of histopathological alterations in the gonads of Japanese quails, which may ultimately result in infertility.

Those That Remain Caught in the "Organic Matter Trap": Sorption/Desorption Study for Levelling the Fate of Selected Neonicotinoids.

With projections suggesting an increase in the global use of neonicotinoids, contemporary farmers can get caught on the "pesticide treadmill", thus creating ecosystem side effects. The aim of this study was to investigate the sorption/desorption behavior of acetamiprid, imidacloprid, and thiacloprid that controls their availability to other fate-determining processes and thus could be useful in leveling the risk these insecticides or their structural analogues pose to the environment, animals, and human health. Sorption/desorption isotherms in four soils with different organic matter (OC) content were modelled by nonlinear equilibrium models: Freundlich's, Langmuir's, and Temkin's. Sorption/desorption parameters obtained by Freundlich's model were correlated to soil physico-chemical characteristics. Even though the OC content had the dominant role in the sorption of the three insecticides, the role of its nature as well as the chemical structure of neonicotinoids cannot be discarded. Insecticides sorbed in the glassy OC phase will be poorly available unlike those in the rubbery regions. Imidacloprid will fill the sorption sites equally in the rubbery and glassy phases irrespective of its concentration. The sorption of thiacloprid at low concentrations and acetamiprid at high concentrations is controlled by hydrophilic aromatic structures, "trapping" the insecticides in the pores of the glassy phase of OC.

Environmentally relevant concentrations of nickel and imidacloprid induce reproductive toxicity in earthworm (Eisenia fetida fetida).

The current research investigates individual and combined toxicity effects of nickel (Ni) and imidacloprid (IMI) on earthworm species Eisenia fetida fetida. Employing standardized toxicity parameters, we assessed the impact of environmentally relevant concentrations (ERC) of Ni, IMI, and their mixtures on key biomarkers and reproductive fitness of earthworms. Our findings reveal concentration-dependent responses with discernible adverse effects on physiological parameters. The ERC obtained for Ni was 0.095 ppm, and for imidacloprid was 0.01 ppm. Two concentrations (ERC and 1/5th) of both toxicants (individually and in combinations) were further given for 14 days, and parameters like avoidance behaviour, antioxidants, histology, and metabolomic profile were observed. The behaviour of earthworms was noted, where at 24-48 h, it was found to be in control soil, while later, at 72-96 h, they migrated to toxicants-treated soil. Levels of antioxidants (superoxide dismutase, catalase, reduced glutathione, ascorbic acid), lipid peroxidation, and lactate dehydrogenase were elevated in the testis, spermatheca, ovary, and prostate gland in a high concentration of Ni + IMI. Histological studies showed more vacuolization and disruption of epithelium that was increased in the prostate gland of the Ni + IMI high group, decreased number of spermatids, and damaged cell architecture was noted in testis and spermatheca of the Ni + IMI high group. The highest number of metabolites was found in Ni exposed group (181), followed by IMI (131) and Control (125). Thus, this study sheds light on the ecotoxicological effects of combinational exposure of these contaminants on an essential soil-dwelling organism, where IMI was more toxic than Ni, and both toxicants decreased earthworm reproductive fecundity.

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.

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.

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.

Molecular Mechanism Underlying ROS-Mediated AKH Resistance to Imidacloprid in Whitefly.

Synthetic insecticides used to control Bemisia tabaci include organophosphorus, pyrethroids, insect growth regulators, nicotinoids, and neonicotinoids. Among these, neonicotinoids have been used continuously, which has led to the emergence of high-level resistance to this class of chemical insecticides in the whitefly, making whitefly management difficult. The adipokinetic hormone gene (AKH) and reactive oxygen species (ROS) play roles in the development of insect resistance. Therefore, the roles of AKH and ROS in imidacloprid resistance in Bemisia tabaci Mediterranean (MED; formerly biotype Q) were evaluated in this study. The expression level of AKH in resistant B. tabaci MED was significantly lower than that in sensitive B. tabaci (MED) (p < 0.05). AKH expression showed a decreasing trend. After AKH silencing by RNAi, we found that ROS levels as well as the expression levels of the resistance gene CYP6CM1 and its upstream regulatory factors CREB, ERK, and P38 increased significantly (p < 0.05); additionally, whitefly resistance to imidacloprid increased and mortality decreased (p < 0.001). These results suggest that AKH regulates the expression of resistance genes via ROS in Bemisia tabaci.

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.