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.

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.

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.

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.

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.

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.

Imidacloprid (IMI) is one of the top-notch insecticides that adversely affects the body organs including the liver. Malvidin (MAL) is a natural flavonoid which exhibits a wide range of pharmacological properties. This research was designed to evaluate the protective ability of MAL to counteract IMI instigated liver toxicity in rats. Thirty-two rats were divided into four groups including control, IMI (5mg/kg), IMI (5mg/kg) + MAL (10mg/kg) and MAL (10mg/kg) alone treated group. The recommended dosages were administrated through oral gavage for 4 weeks. It was revealed that IMI intoxication disrupted the PI3K/AKT and Nrf-2/Keap-1 pathway. Furthermore, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme-oxygenase-1 (OH-1) and glutathione reductase (GSR) were reduced while upregulating reactive oxygen species (ROS) and malondialdehyde (MDA) levels after IMI treatment. Moreover, IMI poisoning increased the levels of ALT (Alanine aminotransferase), AST (Aspartate transaminase), and ALP (Alkaline phosphatase) while reducing the levels of total proteins and albumin in hepatic tissues of rats. Besides, IMI administration escalated the expressions of Bcl-2-associated protein x (Bax) and cysteine-aspartic acid protease-3 (Caspase-3) while downregulating the expressions of B-cell lymphoma 2 (Bcl-2). Similarly, IMI intoxication, increased the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, IMI disrupted the normal architecture of hepatic tissues. However, MAL treatment remarkably protected the liver tissues via regulating abovementioned disruptions.

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.

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.

We evaluated whether thymol (THY) (30 mg/kg b.wt) could relieve the adverse effects of the neonicotinoid insecticide imidacloprid (IMD) (22.5 mg/kg b.wt) on the liver in a 56-day oral experiment and the probable underlying mechanisms. THY significantly suppressed the IMD-associated increase in hepatic enzyme leakage. Besides, the IMD-induced dyslipidemia was considerably corrected by THY. Moreover, THY significantly repressed the IMD-induced hepatic oxidative stress, lipid peroxidation, DNA damage, and inflammation. Of note, the Feulgen, mercuric bromophenol blue, and PAS-stained hepatic tissue sections analysis declared that treatment with THY largely rescued the IMD-induced depletion of the DNA, total proteins, and polysaccharides. Moreover, THY treatment did not affect the NF-kB p65 immunoexpression but markedly downregulated the Caspase-3 in the hepatocytes of the THY+IMD-treated group than the IMD-treated group. Conclusively, THY could efficiently protect against IMD-induced hepatotoxicity, probably through protecting cellular macromolecules and antioxidant, antiapoptotic, and anti-inflammatory activities.