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The citrus red mite, Panonychus citri (McGregor), is an important spider mite pest in citrus producing areas. Owing to long-term acaricide exposure, resistance has evolved rapidly in recent years. To evaluate the extent of resistance, seven field mite populations sampled from various geographical locations in China during 2015–2018 were tested using the leaf-dip bioassay method to determine their susceptibilities to four acaricides. In comparison with the susceptible strain maintained in the laboratory, low or moderate levels of fenpropathrin resistance, while no resistance to abamectin or cyflumetofen, were found among populations sampled from Liangping, Wanzhou, Daying, and Anyue in Southwestern China during the test period. High levels (>1,000-fold, with LC50 values that were greater than the recommended concentration) of resistance to fenpropathrin had evolved in field populations from Southern China, including Guilin, Nanning, and Yuxi, when compared with that of the susceptible strain. Populations from Guilin and Nanning also evolved high resistance levels to abamectin (1,088-fold and 1,401-fold) and cyflumetofen (2,112-fold and 9,093-fold). All the populations sampled in 2018 showed a moderate or high resistance to bifenazate. Generally, field populations of citrus red mites from Southwestern China were more sensitive to the tested acaricides than those of Southern China.The data provide a foundation for developing acaricide resistance management strategies in these regions.

Residue analyses were conducted for 283 pesticide active ingredients on pepper samples collected from the local markets (between April and November) of Çanakkale province of Turkey by using QuEChERS method and LC–MS/MS and GC–MS/MS devices. In present pepper samples, 35 different pesticide residues were detected. About 25.0% (27 samples) of present samples had single residue and 43.5% (47 samples) had multiple residues. Of the detected pesticides, acetamiprid, triadimenol, imidacloprid, boscalid, pirimiphos-methyl, tebuconazole, and metalaxyl were the most common ones, while carbendazim/benomyl, fenpropathrin, and thiram were the banned ones. Moreover, 24 of the pesticide residues detected were above the MRL values, 19 pesticides were in the “moderately hazardous (II),” and two pesticides were in the “extremely hazardous (Ib)” class (WHO). Present findings revealed that consumer health may be in danger despite all legal measures by the Ministry of Agriculture and Forestry of Turkey, thus greater emphasis should be put on monitoring of pesticide use and residues.

The massive use of pesticides brings considerable environmental and human health impacts. This study conducted an overall assessment of the ecological impact of the extensive pesticide use in China from 1999 to 2018 through the Chemical Footprint (ChF) calculation. The results demonstrated that the primary ecological impacts caused by pesticides occurred in the most central and eastern regions in China, e.g., provinces of Shandong, Henan, Hubei, Anhui, and Jiangsu. The northeastern, some southern and central provinces, e.g., Heilongjiang, Jilin, Liaoning, Yunnan, Guangxi, Guangdong, Ningxia, and Shaanxi, got moderate impacts, whereas the northwest regions, e.g., Qinghai, Xinjiang, and Tibet, had much lighter impacts relatively. The agricultural soil in inland areas and surface sea waters in coastal provinces bore the major impacts of the pesticide pollution in China, shared above 80% of the ChF across all environmental compartments. Chlorpyrifos, pymetrozine, fenpropathrin, pyridaben, atrazine, etc., were the pesticides that had the greatest impacts on the ecosystem, which contributed over 95% of the total ChF of pesticides used in China, although the use amount of these pesticides accounted for less than 10% of the total use amount of all pesticides annually. The study also indicated that the overall ChF of pesticide use in China has been declining since 2010, which was corresponding with the control actions of highly hazardous pesticides, especially the elimination of high toxic organophosphorus insecticides during the past decade.

A molecularly-imprinted electrochemiluminescence sensor was constructed for the determination of fenpropathrin (FPT) by molecular imprinting technology. In this sensing platform, the introduction of CdS@MWCNTs significantly enhanced the initial ECL signal of the luminol-O 2 system. Specifically, MWCNTs was used as a carrier to adsorb more CdS, in which CdS acted as a co-reaction promoter for luminescence. Molecularly imprinted polymer (MIP) containing specific recognition sites of FPT was used as the material for selective recognition. With increasing amount of FPT the ECL signal decreased. Under the optimum conditions, the ECL response was linearly related to the logarithm of FPT concentration. The developed ECL sensor allowed for sensitive determination of FPT and exhibited a wide linear range from 1.0 × 10 − 10 mol L − 1 to 1.0 × 10 − 6 mol L − 1 . The limit of detection was 3.3 × 10 − 11 mol L − 1 (S/ N  = 3). It can be used for the detection of FPT in vegetable samples.

The synthetic pyrethroid pesticide fenpropathrin (FEN) is extensively used worldwide and has frequently been detected in biota and the environment, whilst the negative effects and toxicological mechanisms of FEN on non-target organisms are still unknown. In the present study, healthy immature common carp were treated with FEN (0.45 and 1.35 μg/L) for a duration of 14 days, and the negative impacts and possible mechanisms of FEN on fish were investigated. Biochemical analyses results showed that FEN exposure altered the levels of glucose (GLU), total cholesterol (T-CHO), triglyceride (TG), albumin (ALB), alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) in carp serum, and caused histological injury of the liver and kidney, indicating that FEN may cause hepatotoxicity and nephrotoxicity in carp. In addition, FEN also altered the activities of superoxide dismutase (SOD) and catalase (CAT) in carp serum, upregulated the levels of reactive oxygen species (ROS), and elevated the levels of malondialdehyde (MDA) in the liver and kidney. Meanwhile, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels were also upregulated, indicating that oxidative stress and inflammatory reaction may be involved in the hepatotoxicity and nephrotoxicity caused by FEN. Furthermore, RNA-seq analysis results revealed that FEN treatment induced a diverse array of transcriptional changes in the liver and kidney and downregulated differentially expressed genes (DEGs) were concentrated in multiple pathways, especially cell cycle and DNA replication, suggesting that FEN may induce cell cycle arrest of hepatocytes and renal cells, subsequently inducing hepatotoxicity and nephrotoxicity. Overall, the present study enhances our comprehension of the toxic effects of FEN and provides empirical evidence to support the risk assessment of FEN for non-target organisms.

Introduction: The synthetic pyrethroid derivative fenpropathrin (FNE), a commonly used insecticide, has been associated with various toxic effects in mammals, particularly neurotoxicity. The study addressed the hallmarks of the pathophysiology of Parkinson’s disease upon oral exposure to fenpropathrin (FNE), mainly the alteration of dopaminergic markers, oxidative stress, and molecular docking in rat models. In addition, the protective effect of curcumin-encapsulated chitosan nanoparticles (CRM-Chs-NPs) was also assessed. Methods: In a 60-day trial, 40 male Sprague Dawley rats were divided into 4 groups: Control, CRM-Chs-NPs (curcumin-encapsulated chitosan nanoparticles), FNE (15 mg/kg bw), and FNE + CRM-Chs-NPs. Results: FNE exposure induced reactive oxygen species generation, ATP production disruption, activation of inflammatory and apoptotic pathways, mitochondrial function and dynamics impairment, neurotransmitter level perturbation, and mitophagy promotion in rat brains. Molecular docking analysis revealed that FNE interacts with key binding sites of dopamine synthesis and transport proteins. On the other hand, CRM-Chs-NPs mitigated FNE’s toxic effects by enhancing mitochondrial dynamics, antioxidant activity, and ATP production and promoting anti-inflammatory and antiapoptotic responses. Conclusion: In summary, FNE appears to induce dopaminergic degeneration through various mechanisms, and CRM-Chs-NPs emerged as a potential therapeutic intervention for protecting the nervous tissue microenvironment.

Fenpropathrin has been a commonly used insecticide to control agricultural and household insects over a few decades. Up to now, fenpropathrin residue in soil and water has been often determined due to its widespread use, which poses serious threat to environment and aquatic organisms. The potential of fenpropathrin to affect aquatic lives is still poorly understood. In this study, we used zebrafish (Danio rerio) embryo as an experimental model system to evaluate the toxicity of fenpropathrin to the development of zebrafish nervous system. Zebrafish embryos were separately exposed to fenpropathrin at the dose of 0.016 mg/L, 0.032 mg/L, 0.064 mg/L, starting at 6 h post-fertilizationhpf (hpf) up to 96 hpf. The results showed that fenpropathrin exposure gives rise to physiological, behavioral, and neurodevelopmental impairments in zebrafish embryos, including enhanced acetylcholinesterase (AChE) activity, abnormal swimming behavior, karyopyknosis in brain cells, increased intercellular space, and uneven migration of neuron in brain area. In addition, the expressions of genes concerning neurodevelopment and neurotransmitter system were inhibited following fenpropathrin exposure. We also found that fenpropathrin exposure distinctly induced oxidative stress by increasing reactive oxygen species (ROS) generation and inhibiting the production of antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD). Expectedly, some apoptosis-associated genes were induced and the apoptosis appeared in the brain and heart cells of zebrafish embryos. Moreover, fenpropathrin exposure also inhibited the expressions of genes in Nrf2 signaling pathway, such as heme oxygenase-1 (HO-1) and SOD. In summary, the results of this study indicate that oxidative stress-triggered apoptosis may be an underlying fundamental of fenpropathrin-induced neurotoxicity in zebrafish embryos.

Insecticide resistance in mosquito populations has long been recognized as a significant global public health challenge, motivating the development of new control chemistries. ReMoa Tri is a novel triple-action space spray that employs a different mode of action than traditional adult mosquito control formulations. It combines 3 components: fenpropathrin, a mixed-type I/II pyrethroid; abamectin, a macrocyclic lactone; and C8910, a patented fatty acid chain. As an ultra-low volume adulticide, ReMoa Tri has the potential to target mosquito species that are resistant to pyrethroid and organophosphate-based control materials. To determine whether ReMoa Tri effectively targets resistant mosquito species in Florida's Collier County, United States, we conducted ground-based field cage trials using field-caught pyrethroid-resistant Culex quinquefasciatus (Say) and Aedes aegypti (L.), of which the latter also displayed developing resistance to organophosphates. Trials were also conducted against the same mosquito populations with Merus 3.0, a pyrethrin-based adulticide used by the Collier Mosquito Control District. ReMoa Tri was effective against Collier's pyrethroid-resistant Cx. quinquefasciatus, resulting in more than 95% mortality in semifield cage trials by 24 h postapplication. Similarly, ReMoa Tri applications against Collier's pyrethroid-resistant Ae. aegypti resulted in 72%–89% mortality at 24 h postapplication and 74%–97% mortality at 48 h postapplication. This study represents the first field data on this novel space spray, and its findings shed light on the performance of ReMoa Tri against local mosquito populations that have developed resistance to currently available adulticides.

The acetylcholinesterase (AChE) is involved in termination of synaptic transmission at cholinergic synapses and plays a vital role in the insecticide detection and inhibitor screening. Here, we report the heterologous expression of an AChE from Tetronarce californica (TcA) in Escherichia coli (E. coli) as a soluble active protein. TcA was immobilized in calcium alginate beads; the morphology, biochemical properties, and insecticide detection performance of free and immobilized TcA were characterized. Moreover, we used sequence, structure-based approaches, and molecular docking to investigate structural and functional characterization of TcA. The results showed that TcA exhibited a specific activity of 102 U/mg, with optimal activity at pH 8.0 and 30 °C. Immobilized TcA demonstrated superior thermal stability, pH stability, and storage stability compared to the free enzyme. The highest sensitivity of free TcA was observed with trichlorfon, whereas immobilized TcA showed reduced IC50 values towards tested insecticides by 3 to 180-fold. Molecular docking analysis revealed the interaction of trichlorfon, acephate, isoprocarb, λ-cyhalothrin, and fenpropathrin in the active site gorge of TcA, particularly mediated through the formation of hydrogen bonds and π-π stacking. Therefore, TcA expressed heterologously in E. coli is a promising candidate for applications in food safety and environmental analysis.Key points• T. californica AChE was expressed solubly in prokaryotic system.• The biochemical properties of free/immobilized enzyme were characterized.• The sensitivity of enzyme to insecticides was evaluated in vitro and in silico.

This research assessed the effectiveness of Sambucus nigra (SN) in alleviating hepatorenal injury caused by fenpropathrin (FNP) in rodents. Six equal groups were created from the 30 Wistar rats: Group 1 was the negative control, Groups 2 and 3 were the SN control groups, Group 4 was the FNP group, and Groups 5 and 6 were the FNP + SN combination groups. The hepatoprotective and renoprotective effects of SN were assessed by quantifying serum enzyme markers, including ALT, AST, ALP, blood urea nitrogen, and creatinine. Oxidative stress indicators, RT-PCR analysis, histological examination, and immunohistochemistry studies were conducted on the liver and kidneys to confirm the previously indicated parameters. The rats administered FNP injections displayed increased blood marker enzyme levels, altered oxidant-antioxidant equilibrium, and significant pathogenic changes in hepatic and renal tissues. Furthermore, these rats exhibited elevated levels of caspase-3 and iNOS, linked to the triggered expression of TNF-α and NF-κB genes in these tissues. Administering SN enhanced all the aforementioned toxicological parameters. The prospective hepato-renal therapeutic benefits of SN against impairment of the liver and kidneys induced by FNP have been evidenced through its anti-inflammatory, antioxidant, and anti-apoptotic pathways.