FOOD AND AGRICULTURAL IMMUNOLOGY
·
2014
·
IF 0.984
Xinlin Wei,Yaru Zhao,Baoqin Wang,Yuanfeng Wang
Two kinds of new immunogens and coating antigens had been designed and synthesised by methods of lively ester (DCC) and carbodiimide (EDC), respectively. Preliminary immunosorbent assays indicated that the two target conjugates presented good inhibition ratio against the haptens of cypermethrin in vivo. The results showed that the best efficient titres of anti-cypermethrin rabbit serum in methods of DCC and EDC were 1:32000 and 1:64000, the IC50 of them were 18.907µg/L and 16.877µg/L against the haptens of cypermethrin, respectively. The data indicated that the anti-cypermethrin antibodies in method of EDC had higher sensitivity and higher selectivity than the anti-cypermethrin antibodies in method of DCC. Thus, we can synthesise antigens and anti-bodies with method of EDC. The antibodies of high quality can be effectively used in the field of the rapid detection of pyrethroid pesticide residues in the research of the reagent strips.
研究领域:
分析化学
·
环境科学
·
毒理学
·
农业科学
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DOI
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2025
·
IF 6.2
Zengting Niu,Guotong Sun,Mingtao Tan,Shanchun Yan,Dun Jiang
Heavy metals are prevalent environmental contaminants in pest habitats. This study investigates the tolerance of Hyphantria cunea larvae to β-cypermethrin under cadmium (Cd) stress. Exposure to Cd markedly enhanced larval tolerance to β-cypermethrin. The P450 enzyme was found to be crucial in triggering this cross-tolerance. Notably, Cd exposure significantly upregulated the expression of HcCYP333A29 and HcCYP6AE184 both before and after β-cypermethrin treatment. Silencing these genes reduced the β-cypermethrin tolerance in Cd-exposed larvae. Furthermore, overexpression of HcCYP333A29 and HcCYP6AE184 significantly improved the tolerance of Sf9 cells and Drosophila to β-cypermethrin. Silencing of HcDicer-1, a key gene in the miRNA synthesis pathway, significantly diminished the β-cypermethrin tolerance in Cd-treated larvae. The miR-2739 controlled overexpression of HcCYP333A29, while miR-2854 controlled HcCYP6AE184 overexpression, both of which were essential for β-cypermethrin cross-tolerance in H. cunea larvae under Cd exposure. Collectively, Cd exposure induces cross-tolerance to β-cypermethrin in H. cunea larvae through miRNA-mediated post-transcriptional regulation.
研究领域:
环境毒理学
·
分子生物学
·
昆虫学
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产品关联
DOI
PubMed
高影响因子
MICROCHEMICAL JOURNAL
·
2025
·
IF 5.1
Zhi Chen,Jian Sun,Guoliang Cheng,Yifan Wang,Huanhuan Liu,Hui Lin
Fluorescence assay for in situ and on-site monitoring of pyrethroid pesticides residues from plants is of great value but remains little research. In this study, a fluorescence biosensor Au NCs@BSA, is designed and constructed by embedding Au nanoclusters (Au NCs) in bovine serum albumin (BSA) to transmit on-the-scene cypermethrin pesticide residues messages. Harnessing orange emission and stimuli-responsive performance of Au NCs, as well as the specific strong binding ability of BSA to cypermethrin molecules, Au NCs@BSA is endowed with quantitative response to cypermethrin at μM level within 20 s through promoting fluorescence recovery in conjunction with the transformation of fluorescence images into digital signals. In addition, the interference experiment using common ions and other types of pesticides as coexisting interference substances demonstrated that the sensing system possesses brilliant selectivity and anti-interference ability. By combining the smartphone-based platform and convolutional neural network (CNN-model), different concentrations levels of cypermethrin were accurately identified in real samples. This study opens up a new avenue to engineer simple fluorescence assay for in situ and on-site capturing of the pyrethroid pesticide residue information, favoring the rapid development of agriculture food monitoring.
研究领域:
分析化学
·
食品安全
·
纳米生物技术
·
环境监测
·
农业科学
✓ 已验证
DOI
高影响因子
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
·
2025
·
IF 4.2
Jingran Yang,Ruirui Ding,Ling Qi,Haoran Bi,Jianan Li
Cypermethrin (CMN) is a synthetic pyrethroid insecticide known for its neurotoxic effects, particularly in the hippocampus. To investigate the underlying molecular mechanisms, we conducted integrated microRNA (miRNA) and messenger RNA (mRNA) sequencing in HT22 hippocampal cells treated with 400 μM CMN. We identified 36 differentially expressed miRNAs and 170 target mRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed significant involvement in cell adhesion, extracellular matrix organization, and signaling pathways such as phosphoinositide 3-kinase–protein kinase B signaling pathway (PI3K-Akt), mitogen-activated protein kinase (MAPK), and extracellular matrix (ECM)–receptor interaction. Using six topological algorithms, three hub genes (Col1a2, Fn1, and Pdgfrb) were finally identified. In addition, a miRNA–mRNA regulatory network was constructed, and expression patterns of key miRNAs and mRNAs were validated via reverse transcription polymerase chain reaction (RT-PCR). These findings highlight the critical role of the miRNA–mRNA regulatory network in CMN-induced neurotoxicity. The study provides valuable insights into potential therapeutic targets and preventive strategies for CMN-associated hippocampal damage.
研究领域:
毒理学
·
神经生物学
·
生物信息学
·
分子生物学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2019
·
IF 5.714
Bingnan He,Xia Wang,Jianbo Zhu,Baida Kong,Lai Wei,Yuanxiang Jin,Zhengwei Fu
The immunotoxicity of synthetic pyrethroid (SPs) has garnered much attention, and our previous research demonstrated that β-CYP causes immunotoxicity and oxidative stress in macrophages. Nevertheless, the underlying mechanism remains largely unknown. In this study, the murine macrophage RAW 264.7 cells and murine peritoneal macrophages (PMs) were exposed to β-CYP. The results showed that β-CYP elevated intracellular ROS levels in both RAW 264.7 cells and PMs. Exposure to β-CYP also caused mitochondrial dysfunction with reduced mitochondrial membrane potential (MMP), intracellular ATP level and mitochondrial DNA (mtDNA) content in the two cell types. In addition, exposure of RAW 264.7 cells to β-CYP for 12 h and 24 h enhanced autophagy, with elevated Beclin1, Rab7, Lamp1 and LC3-II expression levels, while 48 h of exposure attenuated autophagy. In contrast, exposure of PMs to β-CYP for 12 h promoted autophagy, whereas exposure for 24 h and 48 h impaired autophagy. Cotreatment with an antioxidant, N-acetyl-L-cysteine (NAC), partially blocked the reduced MMP, intracellular ATP level and autophagy disturbance. Moreover, cotreatment with an autophagy agonist, rapamycin (RAPA), partially blocked mitochondrial dysfunction and oxidative stress in the two cell types, whereas cotreatment with an autophagy inhibitor, 3-methyladenine (3-MA), augmented the abovementioned toxic effects. Furthermore, mitochondrial ROS levels in both RAW 264.7 cells and PMs were elevated by exposure to β-CYP, and molecular docking showed that β-CYP docked with mouse respiratory chain complex I by binding to the ND2, ND4, and ND5 subunits of the protein complex. Taken together, the data obtained in the present study demonstrate that oxidative stress partially mediates mitochondrial dysfunction and autophagy disturbance upon exposure to β-CYP in macrophages, and autophagy plays a protective role against the toxic effects.
研究领域:
免疫毒理学
·
细胞生物学
·
毒理学
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产品关联
DOI
PubMed
高影响因子
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
·
2020
·Vol. 52
·期 8
·821-831
·
IF 2.836
He Bingnan,Wang Xia,Jin Xini,Xue Zimeng,Zhu Jianbo,Wang Caiyun,Jin Yuanxiang,Fu Zhengwei
The toxicity of synthetic pyrethroids has garnered attention, and studies have revealed that pyrethroids promote fat accumulation and lead to obesity in mice. Nevertheless, the effect of β-cypermethrin (β-CYP) on adipogenesis and its underlying mechanism remains largely unknown. In this study, mouse embryo fibroblasts 3T3-L1 cells were exposed to β-CYP, and the cell viability, intracellular reactive oxygen species (ROS) level, autophagy, and adipogenesis were assessed to investigate the roles of oxidative stress and autophagy in the toxic effects of β-CYP on adipogenesis. The results demonstrated that treatment with 100 μΜ β-CYP elevated the ROS level, decreased mitochondrion membrane potential, stimulated autophagy, and enhanced the adipogenesis induced by the mixture of insulin, dexamethasone, and 3-isobutyl-1-methylxanthine. However, co-treatment with N-acetyl-L-cysteine partially blocked the abovementioned effects of β-CYP in 3T3-L1 cells. In addition, co-treatment with rapamycin, an autophagy agonist, enhanced the inductive effect of β-CYP on adipogenesis, whereas co-treatment with 3-methyladenine blocked the enhancement of adipogenesis caused by β-CYP. Moreover, β-CYP also altered the microenvironment of 3T3-L1 cells to an adipogenesis-friendly one by reducing the extracellular expression of miR-34a, suggesting that the culture media of β-CYP-treated 3T3-L1 cells could shift macrophages to M2 type. Taken together, the data obtained in the present study demonstrated that β-CYP promoted adipogenesis via oxidative stress-mediated autophagy disturbance, and it caused macrophage M2 polarization via the alteration of miR-34a level in the microenvironment. The study demonstrated the adipogenesis-promoting effect of β-CYP and unveiled the potential mechanism.
研究领域:
毒理学
·
细胞生物学
·
分子生物学
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产品关联
DOI
PubMed
高影响因子
Bioengineered
·
2021
·
IF 3.269
Jianan Li,Haoran Bi
Cypermethrin (CMN) is a widely used artificial synthetic pesticide that causes neurotoxicity in the hippocampus. However, the underlying toxicological targets and mechanisms remain unclear. In this study, network pharmacology analysis and in vitro models were integrated to investigate the effect and mechanism of CMN-induced hippocampal neurotoxicity. A total of 88 targets of CMN-induced hippocampal neurotoxicity were predicted. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes enrichment (KEGG) analyses suggested that these targets were related to multiple GO terms and signaling pathways. To further investigate underlying mechanism, the top 10 hub targets (Akt1, Tnf, Ptgs2, Casp3, Igf1, Sirt1, Jun, Cat, Il10, and Bcl2l1) were screened. Furthermore, cell viability and lactate dehydrogenase (LDH) assays demonstrated that CMN was toxic to HT22 cells in a time- and dose-dependent manner. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining revealed that treatment with CMN increased the proportion of apoptotic cells. In addition, the real-time quantitative polymerase chain reaction (RT-qPCR) results indicated that CMN altered the mRNA expression levels of most of the hub targets, with the exceptions of Igf1 and Jun. The results demonstrated that multiple targets and signaling pathways were involved in CMN-induced hippocampal neurotoxicity. These findings provided reference values for subsequent studies of the toxicological mechanism of CMN.
研究领域:
毒理学
·
神经科学
·
药理学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2024
·
IF 12.2
Mingtao Tan,Hong Jiang,Rusong Chai,Miao Fan,Zengting Niu,Guotong Sun,Shanchun Yan,Dun Jiang
Heavy metal pollutants are important abiotic environmental factors affecting pest habitats. In this study, Cd pre-exposure significantly increased the tolerance of Lymantria dispar larvae to β-cypermethrin, but did not significantly alter their tolerance to λ-cyhalothrin and bifenthrin. The activation of P450 by Cd exposure is the key mechanism that induces insecticide cross-tolerance in L. dispar larvae. Both before and after β-cypermethrin treatment, Cd exposure significantly increased the expression of CYP6AB224 and CYP6AB226 in L. dispar larvae. Silencing CYP6AB224 and CYP6AB226 reduced the tolerance of Cd-treated L. dispar larvae to β-cypermethrin. Transgenic CYP6AB224 and CYP6AB226 genes significantly increased the tolerance of Drosophila and Sf 9 cells to β-cypermethrin, and the recombinant proteins of both genes could significantly metabolise β-cypermethrin. Cd exposure significantly increased the expression of CnCC and Maf . CnCC was found to be a key transcription factor regulating CYP6AB224 - and CYP6AB226 -activated insecticide cross-tolerance in Cd-treated larvae. Decreasing reactive oxygen species (ROS) levels in the Cd-treated larvae or increasing ROS levels in the untreated larvae reduced or enhanced the expression of CnCC , CYP6AB224 and CYP6AB226 and β-cypermethrin tolerance in L. dispar larvae, respectively. Collectively, Cd exposure confers β-cypermethrin tolerance in L. dispar larvae through the ROS/ CnCC signalling pathway-mediated P450 detoxification. Environmental Implication Heavy metals have been reported to produce cross-tolerance in agricultural insects to insecticides. The growing demand for chemical pest control necessitates expanding research on the widespread occurrence of cross-tolerance to insecticides among pests, particularly forest pests, in areas polluted with heavy metals. In this study, Cd pre-exposure enhanced the cross-tolerance of Lymantria dispar larvae to β-cypermethrin. Cd pre-exposure activated the P450 detoxification system of L. dispar larvae. CYP6AB224 and CYP6AB226 were key detoxify genes to the formation of cross-tolerance. ROS-CnCC signaling pathway was proved to be responsible for activation of detoxify genes.
研究领域:
环境科学
·
昆虫学
·
分子生物学
·
毒理学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2024
·
IF 5.7
Jian Zhu,Yunyan Lai,Yinhua Wu,Jiali Wang,Jiaqi Wei,Hanhong Xu
We screened the contact activity of 32 commercial essential oils (EOs) and their synergistic effect with β-cypermethrin against Blattella germanica. Results showed that the most effective EOs against B. germanica were from Illicium verum, Syzygium aromaticum, and Cinnamomum camphora, with LD50 values of less than 500 μg/insect. The most potent synergistic effects of β-cypermethrin on B. germanica were from Dysphania ambrosioides and Mentha canadensis. Both oils have a co-toxic factor of 133.33. The results of the major compound testing of the EOs showed that trans-anisaldehyde and thymol have the best insecticidal activity against B. germanica, with LD50 values of 141.30 and 138.61 μg/insect, respectively. The compounds with the best synergistic effect on β-cypermethrin were γ-terpinene and linalool at a concentration of 0.5%. The co-toxic factors for γ-terpinene and linalool were 150 and 133.33, respectively, which were similar to the synergistic effect observed with 2% piperonyl butoxide.
研究领域:
昆虫学
·
植物化学
·
害虫管理
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产品关联
DOI
PubMed
高影响因子
ACS Applied Polymer Materials
·
2026
·
IF 5.2
Huang Yanmin,Chen Yanlin,Li Jiansheng,Hu Qiang,Liu Zhiping,Xiong Qipeng,Gan Chunfang,Cui Jianguo
A β-cypermethrin
(CY) nanoformulation (CY@β-CDs/SE)
was constructed via a dual-carrier coencapsulation strategy utilizing
β-cyclodextrin octadecanoate (β-CDs) and starch hexadecanoate
ester (SE). This system leverages the host–guest inclusion
of pesticide molecules within the hydrophobic cavity of β-CDs,
followed by assembly with SE into an outer barrier via hydrophobic
interactions between β-CD and SE side chains, supplemented by
van der Waals forces and interfacial hydrogen bonding. The formulation
significantly enhanced the stability of the active ingredient, exhibiting
a thermal storage degradation of 3.47%, which was 20.4% and 59.0%
lower than those of the single-carrier CY@β-CDs and CY microemulsion
(CYm), respectively. The photolysis half-life ( T 50 ) of CY@β-CDs/SE reached 76.2 h, representing a 75%
and 127% extension compared to CY@β-CDs and CYm, respectively.
Sustained-release studies demonstrated a cumulative release of 79.0%
after 302 h in 20% methanol–water, and release increased markedly
under alkaline (pH = 9) or elevated temperatures (45 ° C), with
dual pH/temperature-responsive behavior. CY@β-CDs/SE maintained
68% insecticidal lethality 25 days postapplication, outperforming
CY@β-CDs (48.0%) and CYm (34.7%). Furthermore, CY@β-CDs/SE
substantially improved the biosafety of β-cypermethrin, achieving
a 96h LC 50 value of 24.7 μg/L in zebrafish , 2.1-fold higher than that of CYm (11.7 μg/L), while also
enhancing the biosafety for rice seed germination. This study establishes
an intelligent delivery system using biodegradable materials, offering
a strategy for pesticide reduction and advancing sustainable agricultural
practices.
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产品关联
DOI
高影响因子
ENVIRONMENT INTERNATIONAL
·
2026
·
IF 10.2
Fan Yu,Shihao Luo,Zhengrong Zhou,Feixia Chen,Jiawei Ying,Qiufang Wu,Yize Wu,Shihua Chen,Xinxin Yao,Feiqin Xie,Wenhui Xu,Ke Xu,Renyi Peng
Cypermethrin (CY), a pyrethroid insecticide, accumulated in aquatic environments and exertd toxic effects on aquatic organisms, impairing their development, nervous system, and immune function. Polystyrene nanoparticles (PS-NPs) readily adsorbed organic contaminants like CY, forming complex pollution systems that resulted in synergistic toxicities. However, the mechanisms behind their hepatotoxicity remained unclear. In this study, both in vivo and in vitro experiments demonstrated that co-exposure to PS-NPs and CY significantly induced liver injury and steatosis in zebrafish larvae, while activating the key lipid synthesis regulator sterol regulatory element-binding protein 1 (SREBP1) in Hep G2 cells. This process displayed typical features of ferroptosis, including oxidative stress, mitochondrial damage, iron dysregulation, and suppression of the antioxidant enzyme glutathione peroxidase 4 (GPX4). Correlation analysis showed a close association between ferroptosis and steatosis. Physiological and genetic verification revealed that Erastin aggravated lipid accumulation by inhibiting GPX4 expression, activating the SREBP1/SCD1 lipid synthesis pathway. Conversely, Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, alleviated oxidative stress, iron overload, and lipid accumulation, while GPX4 overexpression reversed SREBP1/SCD1 activation and improved lipid accumulation, peroxidation, and ferroptosis. This study revealed a novel mechanism by which PS-NPs and CY co-exposure induced ferroptosis-mediated hepatic steatosis through GPX4. These findings provided new insights into the hepatometabolic toxicity of complex pollutants and identified potential targets for preventing related liver diseases.
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产品关联
DOI
PubMed
高影响因子
PEST MANAGEMENT SCIENCE
·
2020
·Vol. 77
·期 4
·2129-2141
·
IF 3.75
Li-Sha Bai,Jing-Jing Xu,Cai-Xia Zhao,Ya-Li Chang,Yan-Ling Dong,Kai-Ge Zhang,Yong-Qiang Li,Yi-Ping Li,Zhi-Qing Ma,Xi-Li Liu
BACKGROUND Carboxylesterase (CarE) is a major class of enzyme involved in the detoxification of toxic xenobiotics in various insect species. Previous work has shown that the carboxylesterase gene CarE001G found in Helicoverpa armigera is more active and can metabolize synthesized pyrethroids, such as β -cypermethrin, one of the commonly used commercial insecticides for lepidopteran pest control. In addition, CarE001G is very special as it has a very specific glycine-rich region located adjacent to its C-terminal. But whether mutations in this unique sequence can change the biochemistry and function of CarE001G are unknown. RESULTS In this study, four variants of CarE001G with different deletions in the glycine-rich region were obtained and functionally expressed in Escherichia coli . The recombinant proteins were purified and confirmed by Western blot and mass spectrometry analyses. These mutant enzymes showed high catalytic efficiency toward the model substrate α -naphthyl acetate. Inhibition study showed that β -cypermethrin had relatively strong inhibition on CarE activities. In vitro metabolism assay showed that the mutant enzymes significantly enhanced their metabolic activities toward β -cypermethrin with specific activities between 4.0 and 5.6 nmol L -1 min −1 mg −1 protein. Molecular docking analyses consistently demonstrated that deletion mutations in the glycine-rich region may facilitate the anchoring of the β -cypermethrin molecule in the active binding pocket of the mutant enzymes. CONCLUSION The data show that deletion mutations can cause qualitative change in the capacity of CarEs in the detoxification of β -cypermethrin. This indicates that deletion mutations in the glycine-rich region may have the potential to cause synthesized pyrethroid (SP) resistance in H. armigera in the future. © 2020 Society of Chemical Industry
研究领域:
昆虫学
·
分子生物学
·
农药毒理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子