Emamectin benzoate-induced toxicity affects intestinal epithelial integrity involving apoptosis.

The frequency presence of emamectin benzoate in agricultural production highlights the need for studying their toxicity against human intestinal epithelial barrier (IEB). Herein, we combined a Caco-2 cell model with transcriptome analysis to assess the intestinal toxicity of emamectin benzoate and its disease-causing potential. Results showed that the half maximal inhibitory concentration (IC) of emamectin benzoate on Caco-2 cell viability after 24, 48, and 72 h of exposure were 18.

Characterization of Neuropeptides from and Functional Analysis of NPF in Diet Intake.

Neuropeptides are involved in many biological processes in insects. However, it is unclear what role neuropeptides play in adaptation to phytochemical flavone. In this study, 63 neuropeptide precursors from 48 gene families were identified in , including two neuropeptide F genes ().

Nicotinamide deficiency promotes imidacloprid resistance via activation of ROS/CncC signaling pathway-mediated UGT detoxification in Nilaparvata lugens.

Metabolic alternation is a typical characteristic of insecticide resistance in insects. However, mechanisms underlying metabolic alternation and how altered metabolism in turn affects insecticide resistance are largely unknown. Here, we report that nicotinamide levels are decreased in the imidacloprid-resistant strain of Nilaparvata lugens, may due to reduced abundance of the symbiotic bacteria Arsenophonus.

Screening and functional validation of the core detoxification genes conferring broad-spectrum response to insecticides in Spodoptera frugiperda.

Background: Fall armyworm, Spodoptera frugiperda, a formidable agricultural pest, has developed resistance to various synthetic insecticides. However, how S. frugiperda utilizes its limited energy and resources to deal with various insecticides remains largely unexplored.

Characterization and functional analysis of UDP-glycosyltransferases reveal their contribution to phytochemical flavone tolerance in Spodoptera litura.

Efficient detoxification is the key factor for phytophagous insect to adapt to phytochemicals. However, the role of uridine diphosphate (UDP)-glycosyltransferases (UGTs) in insect anti-defense to phytochemical flavone is largely unknown. In this study, 52 UGT genes were identified in Spodoptera litura and they presented evident gene duplication.

Role of the epsilon glutathione S-transferases in xanthotoxin tolerance in Spodoptera litura.

Spodoptera litura, a polyphagous lepidopteran pest, demonstrates a remarkable capacity to adapt to varying host plants by efficiently detoxifying phytochemicals. However, the underlying mechanism for this adaptation is not well understood. Herein, twenty eplison glutathione S-transferase genes (GSTes) were characterized and their roles in phytochemical tolerance were analyzed in S.

CYP321A Subfamily P450s Contribute to the Detoxification of Phytochemicals and Pyrethroids in .

Although the induction of cytochrome P450 monooxygenases involved in insect detoxification has been well documented, the underlying regulatory mechanisms remain obscure. In , CYP321A subfamily members were effectively induced by exposure to flavone, xanthotoxin, curcumin, and λ-cyhalothrin, while knockdown of the CYP321A genes increased larval susceptibility to these xenobiotics. Homology modeling and molecular docking analyses showed that these four xenobiotics could stably bind to the CYP321A enzymes.

Genome-Wide Scanning Loci and Differentially Expressed Gene Analysis Unveils the Molecular Mechanism of Chlorantraniliprole Resistance in .

Chlorantraniliprole has been widely used to control, but it has led to the development of chlorantraniliprole resistance. Multiomics analysis of strains with two extreme traits helps to elucidate the complex mechanisms involved. Herein, following genome resequencing and application of the Euclidean distance algorithm, 550 genes within a 16.

Nuclear receptors potentially regulate phytochemical detoxification in Spodoptera litura.

Phytochemicals are a class of potential pesticides for pest control. Our previous studies have demonstrated that the development of Spodoptera litura is suppressed by two phytochemicals, flavone and xanthotoxin. Generally, phytochemical is metabolized by insect detoxification enzyme systems.

Contribution of UDP-glycosyltransferases to chlorpyrifos resistance in Nilaparvata lugens.

As a multigene superfamily of Phase II detoxification enzymes, uridine diphosphate (UDP)-glycosyltransferases (UGTs) play important roles in the metabolism of xenobiotics including insecticides. In this study, 5-nitrouracil, an inhibitor of UGT enzyme activity, effectively increased the toxicity of chlorpyrifos to the chlorpyrifos-resistant strain of Nilaparvata lugens, one of the most resistant rice pests. The enzyme content of UGT in the resistant strain was significantly higher than that in the susceptible strain.

Functional characterization of CYP6AE subfamily P450s associated with pyrethroid detoxification in Spodoptera litura.

The common cutworm, Spodoptera litura, has developed with varying degrees of resistance to most commonly used insecticides. Cytochrome P450 monooxygenases (P450s) with broad substrate specificities have been frequently reported to be involved in insecticide detoxification, but the underlying mechanisms remain obscure. Herein, seven CYP6AE subfamily P450s which possess six classical substrate recognition sites and several conserved catalytic motifs were identified from the genome of S.

The metabolic resistance of Nilaparvata lugens to chlorpyrifos is mainly driven by the carboxylesterase CarE17.

The involvement of carboxylesterases (CarEs) in resistance to chlorpyrifos has been confirmed by the synergism analysis in Nilaparvata lugens. However, the function of specific CarE gene in chlorpyrifos resistance and the transcriptional regulatory mechanism are obscure. Herein, the expression patterns of 29 CarE genes in the susceptible and chlorpyrifos-resistant strains were analyzed.

Uric acid accumulation in DNA-damaged tumor cells induces NKG2D ligand expression and antitumor immunity by activating TGF-β-activated kinase 1.

DNA damage by genotoxic drugs such as gemcitabine and 5-fluorouracil (5-FU) activates the ataxia telangiectasia, mutated (ATM)-Chk pathway and induces the expression of NKG2D ligands such as the MHC class I-related chain A and B (MICA/B). The mechanisms underlying this remain incompletely understood. Here we report that xanthine oxidoreductase (XOR), a rate-limiting enzyme that produces uric acid in the purine catabolism pathway, promotes DNA damage-induced MICA/B expression.