Search Results (525)

This study evaluated the potential of synergistically degraded low-molecular-weight chitosan (LMW-CS) as a functional feed additive to promote growth, antioxidant capacity, innate immunity, and disease resistance in Pacific white shrimp (Litopenaeus vannamei). High-molecular-weight chitosan (HMW-CS, approximately 85 kDa) was degraded using γ-irradiation in combination with H₂O₂ to produce LMW-CS with improved functional properties. Shrimp were fed five experimental diets for 4 weeks: a control diet, HMW-CS0.4 (0.4% w/w), LMW-CS0.1 (0.1% w/w), LMW-CS0.2 (0.2% w/w), and LMW-CS0.4 (0.4% w/w). Growth performance, oxidative stress markers, antioxidant enzyme activities, lysozyme activity, immune-related gene expression, bacterial load, and survival after Vibrio parahaemolyticus challenge were evaluated. The results indicate that dietary LMW-CS supplementation improved growth performance and feed utilization, with LMW-CS0.2 showing significantly higher final weight, total weight gain, and average daily gain than the control group (p < 0.05). Antioxidant assays showed that LMW-CS reduced malondialdehyde levels and increased reduced glutathione, nitric oxide, glutathione reductase, catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase activities in both plasma and hepatopancreas (p < 0.05). Lysozyme activity was significantly enhanced, particularly in the LMW-CS0.4 and HMW-CS0.4 groups (p < 0.05). Gene expression analysis revealed upregulation of genes associated with growth regulation, antimicrobial defense, pathogen recognition, and prophenoloxidase activation, including igf2, cstn, lgbp, lyz, and propo2. Gut microbiota profiling showed that chitosan supplementation altered bacterial community composition, reduced the relative abundance of some Vibrio-associated taxa, and descriptively lowered predicted pathogenic and stress-tolerant bacterial phenotypes. Following the Vibrio parahaemolyticus challenge, shrimp fed LMW-CS0.4 showed the lowest bacterial load and highest survival rate, indicating improved disease resistance (p < 0.05). Overall, synergistically degraded LMW-CS enhanced growth, redox balance, innate immune competence, gut microbial structure, and resistance to V. parahaemolyticus, supporting its potential as an antibiotic-free functional feed additive for sustainable shrimp aquaculture. Full article

Cisplatin is an effective platinum-based chemotherapeutic agent used to treat a variety of cancers. However, its clinical utility is limited by dose-dependent neurotoxicity, yet no approved neuroprotective strategy currently exists. Our integrated cellular, metabolic, and in vivo approaches unraveled the neuroprotective potential of Areca catechu ethyl acetate extract (AC-EA) against cisplatin-induced neurotoxicity. Importantly, AC-EA did not reduce cisplatin-induced cytotoxicity in A549 lung cancer cells. In HT22 hippocampal neurons, AC-EA restored cell viability, suppressed reactive oxygen species generation, preserved mitochondrial-associated fluorescence, and attenuated phosphorylated histone H2AX (γH2AX)-marked DNA damage. AC-EA was associated with increased pNRF2 expression, consistent with activation of NRF2-dependent antioxidant signaling, suppressed inducible nitric oxide synthase iNOS (inducible nitric oxide synthase )-mediated neuroinflammation, and prevented the depletion of total AKT (protein kinase B) protein. Untargeted metabolomics and Caenorhabditis elegans survival assays were performed for mechanistic and in vivo validation. Metabolomics data showed restoration of several critical amino acids, including L-tyrosine and β-alanine, disrupted by cisplatin. Moreover, C. elegans studies confirmed in vivo activation of antioxidants via the SKN-1/GST-4 (glutathione S-transferase 4) pathway. While AC-EA shows neuroprotective potential, arecoline’s toxicity demands caution. To our knowledge, this is the first study to demonstrate the neuroprotective activity of A. catechu against cisplatin-induced neurotoxicity, laying the foundation for developing plant-derived adjunct therapies for chemotherapy-associated neuropathy. Full article

Wheat Fusarium head blight (FHB) is a globally prevalent and destructive fungal disease predominantly caused by Fusarium graminearum. Pydiflumetofen, a novel succinate dehydrogenase inhibitor (SDHI) fungicide, exhibits strong inhibitory activity against F. graminearum; however, the molecular regulatory mechanisms underlying the field-developed resistance in this pathogen remain poorly defined. In the present study, a field-evolved resistant isolate W24-039 and a sensitive isolate W24-016 were subjected to multi-omics analysis. The sequencing results identified compound mutations C89S/A93V in SdhC2, and A21T/S30F in SdhD of the resistant strain, which confer stable fungicide resistance without any detectable fitness costs. Physiological tests revealed that these target mutations sustain the homeostasis of succinate dehydrogenase (SDH) activity and intracellular ATP production. Following pydiflumetofen treatment, the sensitive isolate displayed remarkable declines in SDH activity, intracellular ATP content and deoxynivalenol (DON) biosynthesis, accompanied by markedly elevated cell membrane permeability. Transcriptomic sequencing uncovered 2221 differentially expressed genes (DEGs) in the sensitive strain under fungicide stress, and 2566 DEGs in the resistant isolate under the same conditions. The genes associated with detoxification and drug efflux, including cytochrome P450, glutathione S-transferase (GST), ABC and MFS transporters, were significantly upregulated in the resistant isolate. Metabolomic analysis indicated that differential metabolites were mainly enriched in the tricarboxylic acid (TCA) cycle, amino acid metabolism and membrane lipid biosynthesis pathways. The resistant strain maintained intact TCA cycle operation and accumulated high levels of pivotal metabolites such as phosphatidylcholine, unsaturated fatty acids and reduced glutathione. Integrated multi-omics analysis verified that the ABC transporter and glutathione metabolism pathways serve as core regulatory modules governing fungicide resistance. Collectively, F. graminearum develops resistance via the synergistic effects of SDH compound mutations, enhanced detoxification and efflux, and global metabolic remodeling, demonstrating that target-site mutation alone is not the sole driver of resistance, which is instead controlled by an intricate regulatory network involving multiple coordinated pathways. This study systematically characterizes the resistance regulatory network of F. graminearum against pydiflumetofen, and provides theoretical guidance for the rational application and sustainable field resistance management of this fungicide. Full article

In Senegal, scaling up vector control has significantly reduced malaria, but coastal transmission remains a challenge due to secondary vectors like Anopheles melas. This exophilic and zoophilic species evades conventional indoor interventions, yet its bionomics and insecticide resistance profiles remain poorly characterized due to difficulties in laboratory colonization. Anopheles melas larvae were collected from brackish breeding sites in Mbine Coly (Mbour District). A laboratory colony was established from 26 PCR-confirmed founder females and stabilized up to the F17 generation by optimizing water salinity (10 g/L) and transitioning to communal oviposition. Standardized WHO tube bioassays were conducted on generations F2 to F9 to evaluate susceptibility to pyrethroids, organophosphates, and carbamates, alongside synergist tests using 4% piperonyl butoxide (PBO). The colony showed confirmed resistance to alpha-cypermethrin (81.7% mortality) and suspected resistance to deltamethrin (91.3%) and permethrin (94.3%). Pre-exposure to PBO fully restored susceptibility to deltamethrin and permethrin (100%), and significantly increased alpha-cypermethrin mortality to 96.3% (p < 0.001). While metabolic resistance typically involves multiple enzyme families including cytochrome P450s, glutathione S-transferases (GSTs), and esterases, these synergist results demonstrate a predominant role of cytochrome P450-mediated detoxification pathways in this population. Moderate-intensity resistance was confirmed for alpha-cypermethrin at 5× diagnostic doses. Conversely, the population was 100% susceptible to pirimiphos-methyl and bendiocarb. This study reports the successful long-term colonization of a wild An. melas strain for the first time and provides the first comprehensive evidence of multi-insecticide resistance in this population. The presence of high-intensity, metabolic pyrethroid resistance strongly justifies the immediate deployment of next-generation PBO-LLINs and the integration of organophosphates or carbamates in indoor residual spraying rotations to manage resistance in coastal Senegal. Full article

Background: The main aim of this study was to assess the effects of short-term N-acetylcysteine (NAC) supplementation on concentrations of homocysteine (Hcy) and reduced glutathione (rGSH), blood lipid profile and liver enzyme activities in endurance-trained adults, and to determine whether these effects are modified by methylenetetrahydrofolate reductase (MTHFR) C677T and glutathione S-transferase Pi 1 (GSTP1) A313G. Methods: A total of 56 males and 21 females completed a randomized, double-blind, placebo-controlled crossover trial. Participants received 1200 mg of NAC or a placebo for seven days in a crossover design. Serum Hcy and plasma rGSH concentrations were assessed using dedicated biochemical assays, while blood lipid profile and liver enzyme activities were measured using the biochemical analyzer Konelab 20i. Genotyping was conducted using TaqMan probes. A series of within-subject/between-subject repeated-measures analysis of variance (ANOVA) within a general linear model framework were performed to compare Hcy, rGSH, blood lipid profile and liver enzymes activities before and after the intervention. Results: Hcy concentrations significantly decreased following NAC supplementation (18.58 ± 5.45 µmol/L vs. 16.51 ± 4.97 µmol/L; p = 0.009), although subgroup analysis indicated that the decrease was significant only among females (15.40 ± 4.96 µmol/L vs. 13.60 ± 3.68 µmol/L; p = 0.002) without any significant effect among males. We did not observe any significant changes in rGSH, lipid profile, or liver enzyme activities. There was no interaction between NAC supplementation, MTHFR and GSTP1 genotypes and the changes noted in the parameters we analyzed. Conclusions: In conclusion, short-term NAC supplementation may reduce circulating Hcy concentrations in endurance-trained adults, particularly in females. No consistent effects were observed for rGSH, lipid profile, or liver enzyme activities. Full article

This study aimed to investigate the inhibitory effect of toosendanin (TSN) on the growth and development of Spodoptera litura (Fabricius, 1775), especially in terms of feeding preference, larval growth and development, nutritional indices, and enzyme activities. The feeding preference of S. litura, larval growth and development, and nutritional indices were evaluated using the diet incorporation method. The activities of three detoxification, three digestive, and three antioxidant enzymes were determined using spectrophotometric, micro-assay, and microplate methods. The feeding preference of S. litura exposed to TSN indicated that the larvae had a significant preference for the untreated (control) feed compared with the TSN-supplemented feed. The growth and development results showed a prolongation of the larval developmental period by approximately one instar in S. litura larvae fed TSN-supplemented feed. At the highest concentration (100 μg/g), larval weight was 0.76 times that of the control group, with a 27.34% reduction in the pupation rate and a 23.58% reduction in the emergence rate. All differences were statistically significant compared with the control group. In addition, the pupal and adult deformity rates were significantly higher than those in the control group, being 14.68 and 5.67 times higher, respectively, at this concentration. Growth inhibition increased with increasing TSN concentration. In terms of nutritional efficiency, TSN treatment reduced food intake and decreased food conversion rate, thereby inhibiting the relative growth rate of the 4th instar larvae. Further, TSN treatment significantly increased the activities of trypsin, α-amylase, glutathione S-transferase, carboxylesterase, superoxide dismutase, peroxidase, and catalase, and had no significant effect on lipase activity, and significantly reduced cytochrome P450 enzyme activity. TSN can significantly inhibit the digestion and absorption of nutrients in S. litura larvae, slow down their growth and development, and increase the pupal and adult deformity rates, thereby protecting plants against infestation by S. litura. Full article

Glyphosate (GLY), one of the most extensively applied broad-spectrum herbicides worldwide, frequently contaminates soil and aquatic ecosystems, posing serious threats to human health, non-target organisms, soil microbial communities, and environmental sustainability. In the present study, phytoremediation using Medicago sativa (MS) was evaluated for the removal of GLY from contaminated soil under greenhouse conditions, with remediation efficiency enhanced through inoculation with two bacterial bioagents, Bacillus sp. h10 (BS) and Pseudomonas aeruginosa KZFS4 (PA). Biochemical parameters, including superoxide dismutase (SOD), catalase (CAT), hydrogen peroxide (H₂O₂), and malondialdehyde (MDA), together with detoxification-related gene expression, were investigated in the roots and leaves of MS exposed to GLY stress. The combined application of MS with BS + PA, followed by MS + PA and MS + BS, significantly decreased GLY residues in soil and increased GLY accumulation in plant roots and leaves after 1, 3, 7, and 10 days compared with MS treatment alone. In vitro batch equilibrium experiments demonstrated that BS and PA desorbed 33.63 and 40.56 µg g⁻¹ of GLY, respectively, thereby enhancing its removal from soil. The persistence of GLY was highest in contaminated soil without treatment, exhibiting a half-life (t₁/₂) of 52.66 days, whereas the shortest half-life (6.69 days) was recorded in soil treated with MS combined with BS and PA relative to sterilized contaminated soil. Furthermore, inoculation with BS and PA markedly increased SOD and CAT activities in MS tissues, while significantly reducing H₂O₂ and MDA accumulation, indicating alleviation of oxidative stress. GLY exposure also triggered substantial upregulation of detoxification-associated genes, including cytochrome P450, glutathione S-transferases (GST), glycosyltransferases (GTs), and ABC transporters in MS. These findings demonstrate that the integration of BS and PA with phytoremediation effectively accelerates GLY dissipation and reduces pesticide-associated toxicity in contaminated soils and plants. Full article

To induce embryogenic callus from Pinus thunbergii vegetative organs, and deeply understand the internal mechanism of the process, an orthogonal experimental design of three factors and four levels and proteome analysis were adopted. The results showed that the optimal medium was douglas-fir cotyledon medium (DCR), containing 2.5 mg L⁻¹ 2-4-dichlorophenoxyacetic acid (2,4-D) and 1.0 mg L⁻¹ 6-benzylaminopurine (6-BA), 0.3 g L⁻¹ polyvinylpyrrolidone (PVP), 0.5 g L⁻¹ acid casein hydrolysate (CH), 0.5 g L⁻¹ L-glutamine, 1.0 g L⁻¹ inositol, 6.0 g L⁻¹ agar and 20.0 g L⁻¹ sucrose. Microscopic examinations revealed a distinct embryogenic-like callus (EC) structure, and these ECs finally achieved redifferentiation. Analysis of the interactions between factors detected that although the 6-BA concentration alone was not significant, it became a significant effect factor when interacted with 2,4-D (p < 0.05). Peroxidase (POD), superoxide dismutase (SOD) and soluble sugar (SS) of EC were significantly higher than those of non-embryogenic callus (NEC), and label-free quantitative proteomics analysis showed that different types of PODs including peroxidase 4, phospholipid hydroperoxide glutathione peroxidase, and cationic peroxidase 1 in EC were significantly up-regulated, and they were involved in antioxidant biological processes, located in the intercellular region, and performed molecular functions such as heme binding, so POD was a suitable and stable physiological marker for EC. Four up-regulated proteins in EC included glutathione S-transferase, chalcone flavanone isomerase, phosphoenolpyruvate carboxykinase and endoglucanase. Five EC-specific proteins included indole-3-acetic acid-amido synthetase GH3.1, indole-3-acetate O-methyltransferase 1-like, cytokinin dehydrogenase, MLP-like protein 423 and 2-methoxy-6-polyprenyl-1,4-benzoquinol methylase. These proteins are also potential EC molecular markers. Among these proteins, glutathione S-transferase is beneficial to prevent cell death in EC, while indole-3-acetate O-methyltransferase 1-like and cytokinin dehydrogenase are beneficial to promote EC redifferentiation. Full article

Despite increasing interest in fungal remediation systems for the treatment of persistent contaminants, the mechanisms governing fungal transformation of halogenated organic compounds remain poorly resolved. The aim of this study was to determine whether the transformation of halogenated nitrophenols is driven by isolated extracellular enzymes and cofactor-dependent oxidative activity or instead reflects coordinated system-level fungal metabolism. To address this question, we investigated the transformation of 2-chloro-4-nitrophenol (2C4NP) and 5-fluoro-2-nitrophenol (5F2NP) by ascomycete fungi Caldariomyces fumago (C. fumago) and Curvularia sp. under varying nutrient and cofactor conditions. Whole-culture transformation, crude supernatant activity, purified enzyme assays, intracellular detoxification responses, and genome-resolved functional annotation were integrated to evaluate the relative contributions of extracellular and intracellular processes. Transformation was strongly dependent on fungal species, substrate identity, nutrient availability, and cofactor composition. C. fumago achieved complete transformation of 2C4NP and up to 85.3% transformation of 5F2NP, whereas Curvularia sp. exhibited strict Na₃VO₄-dependent transformation of 5F2NP. Crude supernatants retained partial transformation capacity, achieving ~40–45% substrate depletion under conditions supporting whole-culture activity. Purified chloroperoxidase and laccase showed negligible independent activity and did not reproduce whole-culture transformation behavior. Lignin peroxidase activity was consistently induced during contaminant exposure and peaked during periods of maximum transformation. Cytochrome P450 inhibition did not prevent transformation. Baseline glutathione S-transferase activity was detected in both fungi, and comparative genome analysis identified conserved intracellular detoxification-associated enzyme alongside divergent extracellular oxidative enzyme repertoires. Together, these findings demonstrate that transformation of halogenated nitrophenols by fungi cannot be explained by isolated extracellular enzymes alone but is consistent with coordinated extracellular and intracellular system-level metabolism. These findings highlight an underexplored role for integrated fungal metabolic systems in bioremediation and provide a mechanistic basis for developing a scalable fungal platform for treatment of persistent halogenated contaminants. Full article

Since its first detection in 2010, Aedes albopictus has spread across northern Algeria, where vector control relies on the use of chemical insecticides. This study aimed to evaluate the susceptibility of Ae. albopictus populations from Algiers to commonly used larvicides and adulticides, as well as to characterize the underlying resistance mechanisms. Eggs were collected from three sites in Algiers. The susceptibility of larvae to temephos and Bacillus thuringiensis israelensis (Bti), as well as that of adults to permethrin, deltamethrin, malathion, and bendiocarb was evaluated using WHO bioassays. Genotyping of knockdown resistance (kdr) mutations was performed via PCR and sequencing. Metabolic resistance mechanisms were investigated using CDC bottle bioassays. The larvae were found to be susceptible to temephos and Bti. Bioassays on adults demonstrated susceptibility to deltamethrin, suspected resistance to permethrin, and resistance to malathion and bendiocarb. Genotyping revealed low frequencies of heterozygous kdr mutations (V1016G, I1532T, F1534C/S). Synergist assays highlighted the key role of esterases in malathion resistance, a minimal involvement of glutathione S-transferases and an unexpected antagonistic effect of cytochrome P450 monooxygenases. Although larvicides remain effective, resistance to organophosphates, carbamates, as well as suspected resistance to permethrin, has been detected. Esterase-mediated metabolic resistance and kdr mutations may contribute to this profile. These findings highlight the need for resistance monitoring and integrated vector control to ensure sustainable control of Ae. albopictus. Full article

Asthma is a heterogeneous chronic airway disease in which oxidative stress (OS) plays a central mechanistic role beyond classical immune-mediated inflammation. Reactive oxygen and nitrogen species (ROS/RNS), generated by recruited inflammatory cells and activated airway structural cells, drive epithelial injury, mucus hypersecretion, airway remodeling, and modulate key transcription factors including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. This review synthesizes current evidence on the multilevel redox-based determinants of asthma severity, spanning from genetic polymorphisms to circulating biomarkers. We examine serum antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxiredoxins (PRDXs), and the thioredoxin (Trx) system as dynamic indicators of systemic redox status and disease severity, alongside oxidative enzymes including NADPH oxidases and dual oxidases (NOX/DUOX), xanthine oxidase (XO), and myeloperoxidase (MPO) that serve as upstream sources of airway oxidant burden. Functional genetic polymorphisms in antioxidant genes (SOD2, CAT, glutathione S-transferase mu 1/glutathione S-transferase theta 1 (GSTM1/GSTT1), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2/KEAP1)) and oxidative enzyme genes including nitric oxide synthase 1/2/3 (NOS1/2/3), MPO, cytochrome b-245 alpha chain (CYBA), and xanthine dehydrogenase (XDH) are reviewed as modulators of individual redox capacity and asthma susceptibility, with particular attention to gene–environment interactions. We further discuss oxidative damage biomarkers, including malondialdehyde (MDA), 8-isoprostanes, 4-hydroxynonenal, 8-oxo-7, 8-dihydro-2′-deoxyguanosine, protein carbonyls, 3-nitrotyrosine, and advanced oxidation protein products as indicators of lipid, DNA, and protein oxidation that correlate with disease activity and control. The roles of micronutrient cofactors in modulating antioxidant enzyme function and their potential as contextual biomarkers are also addressed. Additionally, emerging evidence on microRNAs (miRNAs) linked to OS biology in asthma is presented. Finally, we critically evaluate the challenges limiting clinical translation, including biomarker non-specificity, analytical variability, gene–environment complexity, and the absence of standardized reference ranges. This integrated framework supports the development of multilevel redox prognostic panels combining genetic, enzymatic, and oxidative damage readouts for improved asthma phenotyping, severity stratification, and personalized therapeutic approaches. Full article

Thiamethoxam is the main neonicotinoid insecticide used for controlling Riptortus pedestris (Fabricius) (Hemiptera: Alydidae). However, sublethal concentration stress may induce intergenerational transcriptional memory, leading to transcriptional patterns that may contribute to the intergenerational accumulation of metabolic tolerance, and evaluating only the toxicity of the current generation would underestimate the long-term risk. Therefore, this study investigated the effect of parental exposure on the expression of detoxification enzyme genes in offspring. Using transcriptome sequencing, we systematically identified three detoxification enzyme gene families (cytochrome P450 monooxygenases (CYPs), carboxylesterases (CCEs), and glutathione S-transferases (GSTs)) in R. pedestris and compared their differential expression patterns between the parental and filial generations after thiamethoxam treatment at three sublethal concentrations (LC₁₀, LC₃₀, and LC₅₀). In the parental generation, a Theta family GST was consistently upregulated, while in the filial generation, detoxification genes were predominantly downregulated, and the genes upregulated in the parents were not also upregulated in the offspring. Comparisons of parents and offspring at the same concentration revealed that the medium concentration induced the highest number of intergenerationally upregulated genes, exhibiting a non-linear response pattern. These results indicate that parental exposure to sublethal thiamethoxam leaves an intergenerational transcriptional imprint in the offspring, and the transmission pattern involves transcriptional reprogramming rather than simple replication of the parental response, the mechanism of which remains to be determined. This study provides transcriptomic evidence for understanding the metabolic adaptation and intergenerational resistance evolution of R. pedestris to thiamethoxam, offering important reference value for field resistance monitoring and rational insecticide application. Full article

Necrotizing enterocolitis (NEC) is a multifactorial disease associated with prematurity, intestinal hypoperfusion, dysbiosis, and oxidative stress. Interindividual variability in disease occurrence suggests a role for genetic susceptibility. Null genotypes of the GSTM1 and GSTT1 genes result in absent glutathione S-transferase activity and may impair antioxidant defenses. This study investigated whether GSTM1 and GSTT1 null genotypes are associated with NEC development and severity in preterm newborns. This single-center case–control pilot study included 100 preterm newborns (50 NEC and 50 controls). Genotyping was performed by multiplex polymerase chain reaction. Baseline characteristics were comparable between groups (p > 0.05). Stages II-A and II-B accounted for 82% of NEC cases. A significant inverse correlation was observed between gestational age and postnatal age at NEC diagnosis (r = −0.5994; p < 0.0001). The GSTM1-null genotype was more frequent in the NEC group (60% vs. 36%) and was associated with increased disease risk in both unadjusted (OR = 2.667; 95%CI: 1.188–5.986; p = 0.027) and adjusted analyses (aOR = 3.09; 95%CI: 1.29–7.40; p = 0.011). No significant associations were observed for GSTT1, combined genotypes, or disease severity. These findings provide preliminary evidence of an association between the GSTM1-null genotype and NEC susceptibility. Given the exploratory pilot design, these results should be considered hypothesis-generating and require confirmation in larger prospective studies. Full article

Plagiodera versicolora (Coleoptera: Chrysomelidae), the willow leaf beetle, is a leaf-eating pest that generally occurs on salicaceous trees. However, there is a blank of identification and phylogenetic relationship of the detoxification genes in P. versicolora. Here, we identified four detoxification gene families (glutathione S-transferases: GSTs, UDP-glycosyltransferases: UGTs, cytochrome P450 monooxygenases: CYPs and carboxylesterases: COEs) from the adult antennal transcriptome data. In all, 146 candidate detoxification genes including 22 GSTs, 20 UGTs, 60 CYPs, and 44 COEs were identified. We used quantitative real-time PCR technology to explore the tissue expression patterns of 12 PvGSTs in P. versicolora. The results showed that 7 PvGSTs have significantly high expression in antennae, indicating these PvGSTs may play an important role in degrade and/or inactivate the sex pheromones and host volatiles. The identification and phylogenetics of the detoxification genes in P. versicolora extended the database in Coleoptera and contributed to the subsequent in-depth research for function about detoxification genes. Full article

Aedes aegypti and Anopheles darlingi represent health challenges due to synthetic insecticide resistance. Hence, the essential oil from Piper humillimum is an alternative for vector control. In this study, the essential oil (3.5 ± 0.4% yield) alongside germacrene D (61.51%) and δ-cadinene (17.46%) showed larvicidal activity (LC₅₀ of 34.75 to 46.04 µg/mL), accompanied by an increase of hydrogen peroxide (H₂O₂) production (36.67 ± 1.52 to 81.33 ± 1.52 µmol H₂O₂ min⁻¹ mg⁻¹ protein), causing lipid (43.3 ± 6.02 to 81.67 ± 3.05 nmol malondialdehyde mg⁻¹ protein) and protein damages (61.67 ± 6.80 to 83.00 ± 2.64 nmol carbonyls mg⁻¹ protein). Further triggering an increase in superoxide dismutase (83.31 ± 6.80 to 95.00 ± 3.60 U mg⁻¹ protein) and catalase (74.31 ± 7.02 to 82.09 ± 1.00 µmol H₂O₂ min⁻¹ mg⁻¹ protein) activities. In addition, mixed-function oxidases (61.17 ± 11.37 to 73.52 ± 6.42 nmol cyt c min⁻¹ mg⁻¹ protein), α- and β-esterase (38.41 ± 4.04 to 61.31 ± 9.29 µmol min⁻¹ mg⁻¹ protein) levels increased. Conversely, glutathione S-transferase (GST) (11.01 ± 2.00 to 9.67 ± 3.05 µmol min⁻¹ mg⁻¹ protein) and acetylcholinesterase (AChE) (14.33 ± 3.78 to 17.00 ± 1.00 μmol min⁻¹ mg⁻¹ protein) were inhibited, corroborated by molecular docking, with germacrene D and δ-cadinene showing binding energies of −7.9 and −7.9 kcal/mol, 1.63 and 1.94 Ki for AChE, while for GST were −6.4 and 6.6 kcal/mol, and 20.5 and 15.50 Ki, respectively. These results demonstrate that the essential oil from P. humillimum is a promising multi-target alternative for the control of the investigated vectors. Full article