Mechanism and spatial spillover effect of digital economy on common prosperity in the Yellow River Basin of China.

The digital economy has emerged as a new trend in economic development and has profoundly influenced the process of achieving common prosperity. However, current research on the correlation between the digital economy and common prosperity from the perspective of a river basin still needs to be strengthened. Based on this, the present study first theoretically elaborates the conceptual meanings of "digital economy" and "common prosperity", as well as the mechanism by which the digital economy empowers common prosperity. Subsequently, a scientifically-constructed performance evaluation index system for the digital economy and common prosperity is established. Considering the Yellow River Basin as an empirical case study area, this study investigates the mechanism and spatial spillover effects of the digital economy in empowering common prosperity from 2005 to 2020. The research findings reveal that: (1) The Yellow River Basin exhibits a basin characteristic with downstream > midstream > upstream areas regarding the level of common prosperity and digital economy. It indicates that a distinct spatial correlation exists between the two factors. However, the ongoing decrease in both high-level and very high-level areas reflects the lengthy and challenging journey of enhancing the quality and efficiency of the digital economy in empowering common prosperity. (2) The digital economy not only directly impacts common prosperity, but also fosters its development through spatial spillover effects. Among the control factors, informatization and housing levels have a major stimulating effect. (3) There exists a clear regional heterogeneity in how the digital economy affects common prosperity in the Yellow River Basin. Specifically, common prosperity of downstream cities is significantly impacted by the digital economy. The spatial spillover effects of the digital economy on common prosperity exhibit a pronounced "neighborhood as a moat" characteristic. (4) The digital economy facilitates the achievement of shared prosperity through the implementation of mechanisms centered on sharing, affluence, and sustainability. These research findings illuminate the empowering mechanisms and spatial spillover pathways of the digital economy in promoting shared prosperity, aligning with national strategies for ecological conservation and high-quality development in the Yellow River Basin.

The role of KLF5 in gut microbiota and lung adenocarcinoma: unveiling programmed cell death pathways and prognostic biomarkers.

Lung adenocarcinoma (LUAD) is the most important subtype of lung cancer. It is well known that the gut microbiome plays an important role in the pathophysiology of various diseases, including cancer, but little research has been done on the intestinal microbiome associated with LUAD. Utilizing bioinformatics tools and data analysis, we identified novel potential prognostic biomarkers for LUAD. To integrate differentially expressed genes and clinical significance modules, we used a weighted correlation network analysis system. According to the Peryton database and the gutMGene database, the composition and structure of gut microbiota in LUAD patients differed from those in healthy individuals. LUAD was associated with 150 gut microbiota and 767 gut microbiota targets, with Krüppel-like factor 5 (KLF5) being the most closely related. KLF5 was associated with immune status and correlated well with the prognosis of LUAD patients. The identification of KLF5 as a potential prognostic biomarker suggests its utility in improving risk stratification and guiding personalized treatment strategies for LUAD patients. Altogether, KLF5 could be a potential prognostic biomarker in LUAD.

Restoring energy metabolism by NAD+ supplement prevents alcohol-induced liver injury and boosts liver regeneration.

Our previous clinical metabolomics study illustrated that energy metabolism disorder is an underlying pathogenesis mechanism for the development of alcoholic liver disease (ALD). Supplementation of nicotinamide (NAM), the precursor of nicotinamide adenine dinucleotide (NAD+), may restore the energy metabolism homeostasis of ALD and thus serves as potential therapeutics to treat ALD. In this bedside-to-bench study, the protective effect of NAM against ALD was investigated by using the NIAAA mice model (chronic-plus-binge ethanol), and the liver regeneration boosting capability of NAM was evaluated by the partial hepatectomy mice model. Our results showed that NAM supplements not only protected the liver from alcohol-induced injury and improved alcohol-induced mitochondrial structure and function change, but also boosted liver regeneration in postpartial hepatectomy mice by increasing liver NAD+ content. These findings suggested that NAM, a water-soluble form of vitamin B3, can promote liver regeneration and improves liver function by alleviating alcohol-induced energy metabolism disorder.

Arsenite Antiporter PvACR3 Driven by Its Native Promoter Increases Leaf Arsenic Accumulation in Tobacco.

Pteris vittata is the first-reported arsenic (As) hyperaccumulator, which has been applied to phytoremediation of As-contaminated soil. PvACR3, a key arsenite (AsIII) antiporter, plays an important role in As hyperaccumulation in P. vittata. However, its functions in plants are not fully understood. In this study, the PvACR3 gene was heterologously expressed in tobacco, driven by its native promoter (ProPvACR3). After growing at 5 µM AsIII or 10 µM AsV in hydroponics for 1-5 days, PvACR3-expression enhanced the As levels in leaves by 66.4-113 and 51.8-101%, without impacting the As contents in the roots or stems. When cultivated in As-contaminated soil, PvACR3-expressed transgenic plants accumulated 47.9-85.5% greater As in the leaves than wild-type plants. In addition, PvACR3-expression increased the As resistance in transgenic tobacco, showing that enhanced leaf As levels are not detrimental to its overall As tolerance. PvACR3 was mainly expressed in tobacco leaf veins and was likely to unload AsIII from the vein xylem vessels to the mesophyll cells, thus elevating the leaf As levels. This work demonstrates that heterologously expressing PvACR3 under its native promoter specifically enhances leaf As accumulation in tobacco, which helps to reveal the As-hyperaccumulation mechanism in P. vittata and to enhance the As accumulation in plant leaves for phytoremediation.

Multiplexed gene editing in citrus by using a multi-intron containing Cas9 gene.

Several expression systems have been developed in clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 (CRISPR/Cas9) framework allowing for gene editing of disease-associated genes across diverse citrus varieties. In this study, we present a new approach employing a multi-intron containing Cas9 gene plus multiple gRNAs separated with tRNA sequences to target the phytoene desaturase gene in both 'Carrizo' citrange and 'Duncan' grapefruit. Notably, using this unified vector significantly boosted editing efficiency in both citrus varieties, showcasing mutations in all three designated targets. The implementation of this multiplex gene editing system with a multi-intron-containing Cas9 plus a gRNA-tRNA array demonstrates a promising avenue for efficient citrus genome editing, equipping us with potent tools in the ongoing battle against several diseases such as canker and huanglongbing.

What is affecting the improvement of green innovation efficiency in the old industrial base: evidence from Northeast China.

Green innovation is an important driving force for high-quality development and is vital for reinvigorating the old industrial bases in Northeast China. As such, this study investigates the spatial-temporal evolution characteristics and factors influencing green innovation efficiency (GIE) in Northeast China from 2005 to 2020, using the super-efficient EBM-Malmquist model, kernel density estimation, and random forest model. The results show the following. (1) The "growth effect" of technological change is the main force driving GIE improvement; the "horizontal effect" of pure technical efficiency change has started to play an important role; and the club convergence characteristics of GIE in Northeast China have started to be optimized. (2) GIE in Northeast China shows significant spatial differentiation. The urban agglomeration of Mid-southern Liaoning and Harbin-Changchun has had high values for GIE, indicating that green innovation has a cyclic cumulative effect and the spatial pattern of green innovation needs to be further optimized. (3) The random forest model is more accurate and provides more trustworthy results compared with the traditional multiple linear regression model. The results of random forest model measurement illustrate that the number of digital economy enterprises, public finance expenditure, GDP per capita, and vegetation coverage play a positive role in promoting GIE. The proportion of the non-farm population and industrial agglomeration plays a negative role in GIE. In the same period, the contribution of the number of digital economy enterprises≥0.41, public expenditure ≥0.47, GDP per capita≥0.39, and vegetation coverage≥0.36 to GIE reach maximum values and then remain unchanged.

N-hydroxypipecolic acid triggers systemic acquired resistance through extracellular NAD(P).

Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant defense mechanism induced in distal systemic tissues by mobile signals generated at the primary infection site. Despite the discoveries of multiple potential mobile signals, how these signals cooperate to trigger downstream SAR signaling is unknown. Here, we show that endogenous extracellular nicotinamide adenine dinucleotide (phosphate) [eNAD(P)] accumulates systemically upon pathogen infection and that both eNAD(P) and the lectin receptor kinase (LecRK), LecRK-VI.2, are required in systemic tissues for the establishment of SAR. Moreover, putative mobile signals, e.g., N-hydroxypipecolic acid (NHP), trigger de novo systemic eNAD(P) accumulation largely through the respiratory burst oxidase homolog RBOHF-produced reactive oxygen species (ROS). Importantly, NHP-induced systemic immunity mainly depends on ROS, eNAD(P), LecRK-VI.2, and BAK1, indicating that NHP induces SAR primarily through the ROS-eNAD(P)-LecRK-VI.2/BAK1 signaling pathway. Our results suggest that mobile signals converge on eNAD(P) in systemic tissues to trigger SAR through LecRK-VI.2.

Arsenic in the hyperaccumulator Pteris vittata: A review of benefits, toxicity, and metabolism.

Arsenic (As) is a toxic metalloid, elevated levels of which in soils are becoming a major global environmental issue that poses potential health risks to humans. Pteris vittata, the first known As hyperaccumulator, has been successfully used to remediate As-polluted soils. Understanding why and how P. vittata hyperaccumulates As is the core theoretical basis of As phytoremediation technology. In this review, we highlight the beneficial effects of As in P. vittata, including growth promotion, elemental defense, and other potential benefits. The stimulated growth of P. vittata induced by As can be defined as As hormesis, but differs from that in non-hyperaccumulators in some aspects. Furthermore, the As coping mechanisms of P. vittata, including As uptake, reduction, efflux, translocation, and sequestration/detoxification are discussed. We hypothesize that P. vittata has evolved strong As uptake and translocation capacities to obtain beneficial effects from As, which gradually leads to As accumulation. During this process, P. vittata has developed a strong As vacuolar sequestration ability to detoxify overloaded As, which enables it to accumulate extremely high As concentrations in its fronds. This review also provides insights into several important research gaps that need to be addressed to advance our understanding of As hyperaccumulation in P. vittata from the perspective of the benefits of As.

Effect of NaCl and EDDS on Heavy Metal Accumulation in Kosteletzkya pentacarpos in Polymetallic Polluted Soil.

The ability of plants to accumulate heavy metals is a crucial factor in phytoremediation. This study investigated the effect of NaCl and S,S-ethylenediaminesuccinic acid (EDDS) on heavy metal accumulation in Kosteletzkya pentacarpos in soil polluted with arsenic, cadmium, lead, and zinc. The addition of NaCl reduced the bioavailability of arsenic and cadmium, while EDDS increased the bioavailability of arsenic and zinc. The toxicity of the polymetallic pollutants inhibited plant growth and reproduction, but NaCl and EDDS had no significant positive effects. NaCl reduced the accumulation of all heavy metals in the roots, except for arsenic. In contrast, EDDS increased the accumulation of all heavy metals. NaCl reduced the accumulation of arsenic in both the main stem (MS) and lateral branch (LB), along with a decrease in cadmium in the leaves of the main stem (LMS) and zinc in the leaves of the lateral branch (LLB). Conversely, EDDS increased the accumulation of all four heavy metals in the LB, along with an increase in arsenic and cadmium in the LMS and LLB. Salinity significantly decreased the bioaccumulation factor (BF) of all four heavy metals, while EDDS significantly increased it. NaCl had different effects on heavy metals in terms of the translocation factor (TFc), increasing it for cadmium and decreasing it for arsenic and lead, with or without EDDS. EDDS reduced the accumulation of all heavy metals, except for zinc, in the presence of NaCl in polluted soil. The polymetallic pollutants also modified the cell wall constituents. NaCl increased the cellulose content in the MS and LB, whereas EDDS had little impact. In conclusion, salinity and EDDS have different effects on heavy metal bioaccumulation in K. pentacarpos, and this species has the potential to be a candidate for phytoremediation in saline environments.

Rootstock increases the physiological defence of tomato plants against Pseudomonas syringae pv. tomato infection.

Climate change has intensified the infection of tomato plants by pathogens such as Pseudomonas syringae pv. tomato (Pst). Rootstocks may increase plant tolerance to leaf phytopathogens. The aim of this study was to evaluate the effects of the tolerant Poncho Negro (R) tomato rootstock on physiological defence and the role of hydrogen sulfide (H2S) in susceptible Limachino (L) tomato plant responses to Pst attack. Ungrafted (L), self-grafted (L/L), and grafted (L/R) plants were infected with Pst. Rootstock increased the concentration of antioxidant compounds including ascorbate in the scion. Tolerant rootstock induced an increase of H2S in the scion, which correlated with enhanced expression of the SlAPX2 gene. A high accumulation of salicylic acid was observed in Pst-inoculated grafted L/L and L/R plants, but this was higher in L/R plants. The increase of H2S during Pst infection was associated with a reduction of ethylene in L/R plants. Our study indicates that the Poncho Negro rootstock reduced the symptoms of bacterial speck disease in the Limachino tomato plants, conferring tolerance to Pst infection. This study provides new knowledge about the impact of rootstock in the defence of tomato plants against leaf pathogens that could be used in sustainable management of tomato cultivation.

Metabolomic Analysis of Microcystis aeruginosa After Exposure to the Algicide L-Lysine.

The widespread occurrence of cyanobacteria blooms damages the water ecosystem and threatens the safety of potable water and human health. Exogenous L-lysine significantly inhibits the growth of a dominant cyanobacteria Microcystis aeruginosa in freshwater. However, the molecular mechanism of how lysine inhibits the growth of M. aeruginosa is unclear. In this study, both non-target and target metabolomic analysis were performed to investigate the effects of algicide L-lysine. The results showed that 8 mg L- 1 lysine most likely disrupts the metabolism of amino acids, especially the arginine and proline metabolism. According to targeted amino acid metabolomics analysis, only 3 amino acids (L-arginine, ornithine, and citrulline), which belong to the ornithine-ammonia cycle (OAC) in arginine metabolic pathway, showed elevated levels. The intracellular concentrations of ornithine, citrulline, and arginine increased by 115%, 124%, and 19.4%, respectively. These results indicate that L-lysine may affect arginine metabolism and OAC to inhibit the growth of M. aeruginosa.

Tandem reduction and trifluoroethylation of quinolines and quinoxalines with trifluoroacetic acid and trimethylamine borane.

A metal-free tandem reduction and N-trifluoroethylation of quinolines and quinoxalines has been developed. It provided a convenient route to access trifluoroethylated tetrahydroquinolines and tetrahydroquinoxalines. This one-pot method avoids the purification process of the intermediate. Mechanistically, the in situ-generated boryl acetal species reacted with tetrahydroquinolines to generate iminiums followed by reduction to give the target compounds.

Switchable Reductive N-Trifluoroethylation and N-Trifluoroacetylation of Indoles with Trifluoroacetic Acid and Trimethylamine Borane.

The metal-free reductive N-trifluoroethylation and N-trifluoroacetylation of indoles have been developed. Bench stable and inexpensive trimethylamine borane and trifluoroacetic acid (TFA) were utilized as the reductive and fluorinating reagents, respectively. These transformations were switchable on the basis of altering the loading of trimethylamine borane and TFA. Preliminary experiments indicated indoline was the common intermediate in these two transformations.

Metabolomic profiling for drug-induced liver injury with autoantibodies.

BACKGROUNDS: Drug induced liver injury (DILI) is sometimes similar to autoimmune hepatitis (AIH) in serology and histology. Clinicians empirically screened DILI with significant autoimmune characteristics to implement clinical intervention. We tried to characterize DILI with autoantibodies by metabolomics. METHODS: Untargeted metabolomics coupled with pattern recognition approaches were performed on sera samples including AIH (n = 59), DILI with autoantibodies (DILIAb+, n = 68), and DILI without autoantibodies (DILIAb-, n = 75). The differential metabolites and fingerprint metabolites between AIH and DILIAb- were screened by orthogonal partial least squares-discriminant analysis and hierarchical clustering respectively. RESULTS: Of the 388 annotated differential metabolites between AIH and DILIAb-, 74 fingerprint metabolites were screened. The eigenmetabolite compressed from the fingerprint possessed high discrimination efficacy (AUC:0.891; 95 %CI, 0.838-0.944). In the fingerprint-based PCA model, AIH and DILIAb- were separated into three regions: the "pure region" of AIH (Region 1), the "pure region" of DILIAb- (Region 3), the mixture region of AIH and DILIAb- (Region 2). After incorporated into the PCA model, DILIAb+ samples were distributed into the three regions, indicating that DILIAb+ samples had different etiological tendencies. Moreover, the fingerprint-based radar model verified the results of PCA model characterizing DILIAb+. Notably, the antibody titers of DILIAb+ in the three regions did not differ significantly, while the response rates for glucocorticoids were obviously different. The metabolic difference among DILIAb+ in different regions mainly lies in energy metabolism. CONCLUSIONS: In terms of metabolic signature, DILIAb+ may not be a community of same pathogenesis, including AIH-inclined parts. Which deserves further study.

Metabolomic Analysis Uncovers Lipid and Amino Acid Metabolism Disturbance During the Development of Ascites in Alcoholic Liver Disease.

Ascites is one of the most common complications of cirrhosis, and there is a dearth of knowledge about ascites-related pathologic metabolism. In this study, 122 alcoholic liver disease (ALD) patients, including 49 cases without ascites, 18 cases with mild-ascites, and 55 cases with large-ascites (1) were established according to the International Ascites Club (2), and untargeted metabolomics coupled with pattern recognition approaches were performed to profile and extract metabolite signatures. A total of 553 metabolites were uniquely discovered in patients with ascites, of which 136 metabolites had been annotated in the human metabolome database. Principal component analysis (PCA) analysis was used to further identify 21 ascites-related fingerprints. The eigenmetabolite calculated by reducing the dimensions of the 21 metabolites could be used to effectively identify those ALD patients with or without ascites. The eigenmetabolite showed a decreasing trend during ascites production and accumulation and was negatively related to the disease progress. These metabolic fingerprints mainly belong to the metabolites in lipid metabolism and the amino acid pathway. The results imply that lipid and amino acid metabolism disturbance may play a critical role in the development of ascites in ALD patients and could be a potent prognosis marker.

Metabolomic Profiling for Histologically Fibrotic Stage in Chronic Drug-Induced Liver Injury.

Background and aims: Chronic drug-induced liver injury (DILI) is a rare but under-researched adverse drug reaction-related disease, which is highly likely to progress into liver fibrosis and even cirrhosis. In this study, metabolomics was used to screen out characteristic metabolites related to the histological progression of fibrosis in chronic DILI and analyze the metabolic changes during the development of fibrosis to explain the underlying mechanism. Methods: Chronic DILI patients who underwent liver biopsy were divided into different fibrosis grades. Serum was analyzed by untargeted metabolomics to find serological characteristic metabolite fingerprints. The screened fingerprints were validated by the validation group patients, and the identification ability of fingerprints was compared using FibroScan. Results: A total of 31 metabolites associated with fibrosis and 11 metabolites associated with advanced fibrosis were identified. The validation group confirmed the accuracy of the two metabolite fingerprints [area under the curve (AUC) value 0.753 and 0.944]. In addition, the fingerprints showed the ability to distinguish the grades of fibrosis by comparing using FibroScan. The metabolite fingerprint pathway showed that bile acid synthesis is disturbed while lipid metabolism is extremely active, resulting in an overload of lipid metabolites in the occurrence and development of chronic DILI-associated fibrosis. Conclusions: Our metabolomic analysis reveals the unique metabolomic fingerprints associated with chronic DILI fibrosis, which have potential clinical diagnostic and prognostic significances. The metabolomic fingerprints suggest the disturbance of the lipid metabolites as the most important factor in the development of DILI fibrosis.

A global meta-analysis of heavy metal(loid)s pollution in soils near copper mines: Evaluation of pollution level and probabilistic health risks.

With the rapid development of the mining industry, the pollution of heavy metal(loid)s in soils near copper (Cu) mining sites is a significant concern worldwide. However, the pollution status and probabilistic health risks of heavy metal(loid)s of soils associated with Cu mines, have rarely been studied on a global scale. In this study, eight heavy metal(loid) concentrations in soil samples taken near 102 Cu mining sites worldwide were obtained through a literature review. Based on this database, the heavy metal(loid) pollution and ecological risk in soils near Cu mines were evaluated. Most of the study sites exceeded the moderately to heavily polluted levels of Cu and Cd; compared to other regions, higher pollution levels were observed at sites in Oman, China, Australia, and the United Kingdom. Soil pollution by Cd, Pb, and Zn at agricultural sites was higher than that in non-agricultural sites. In addition, these heavy metal(loid)s produced a high ecological risk to soils around Cu mining sites in which the contribution of Cd, Cu, and As reached up to 46.5%, 21.7%, and 18.4%, respectively. The mean hazard indices of the eight heavy metal(loid)s were 0.209 and 0.979 for adults and children, respectively. The Monte Carlo simulation further predicted that 1.40% and 29.9% of non-carcinogenic risk values for adults and children, respectively, exceeded the safe level of 1.0. Moreover, 84.5% and 91.0% of the total cancer risk values for adults and children, respectively, exceeded the threshold of 1E-04. Arsenic was the main contributor to non-carcinogenic risk, while Cu had the highest exceedance of carcinogenic risk. Our findings indicate that the control of Cu, Cd, and As should be prioritized because of their high incidence and significant risks in soils near Cu mines. These results provide valuable inputs for policymakers in designing effective strategies for reducing the exposure of heavy metal(loid)s in this area worldwide.

Metabolomics coupled with network pharmacology study on the protective effect of Keguan-1 granules in LPS-induced acute lung injury.

CONTEXT: Keguan-1 (KG-1) plays a vital role in enhancing the curative effects, improving quality of life, and reducing the development of acute lung injury (ALI). OBJECTIVE: To unravel the protective effect and underlying mechanism of KG-1 against ALI. MATERIALS AND METHODS: C57BL/6J mice were intratracheally instilled with lipopolysaccharide to establish the ALI model. Then, mice in the KG-1 group received a dose of 5.04 g/kg for 12 h. The levels of proinflammatory cytokines, chemokines, and pathological characteristics were determined to explore the effects of KG-1. Next, untargeted metabolomics was used to identify the differential metabolites and involved pathways for KG-1 anti-ALI. Network pharmacology was carried out to predict the putative active components and drug targets of KG-1 anti-ALI. RESULTS: KG-1 significantly improved the levels of TNF-α (from 2295.92 ± 529.87 pg/mL to 1167.64 ± 318.91 pg/mL), IL-6 (from 4688.80 ± 481.68 pg/mL to 3604.43 ± 382.00 pg/mL), CXCL1 (from 4361.76 ± 505.73 pg/mL to 2981.04 ± 526.18 pg/mL), CXCL2 (from 5034.09 ± 809.28 pg/mL to 2980.30 ± 747.63 pg/mL), and impaired lung histological damage. Untargeted metabolomics revealed that KG-1 significantly regulated 12 different metabolites, which mainly related to lipid, amino acid, and vitamin metabolism. Network pharmacology showed that KG-1 exhibited anti-ALI effects through 17 potentially active components acting on seven putative drug targets to regulate four metabolites. DISCUSSION AND CONCLUSIONS: This work elucidated the therapeutic effect and underlying mechanism by which KG-1 protects against ALI from the view of the metabolome, thus providing a scientific basis for the usage of KG-1.

The aryl hydrocarbon receptor: A predominant mediator for the toxicity of emerging dioxin-like compounds.

The aryl hydrocarbon receptor (AHR) is a member of the basic helix-loop-helix/Per-ARNT-Sim (bHLH-PAS) family of transcription factors and has broad biological functions. Early after the identification of the AHR, most studies focused on its roles in regulating the expression of drug-metabolizing enzymes and mediating the toxicity of dioxins and dioxin-like compounds (DLCs). Currently, more diverse functions of AHR have been identified, indicating that AHR is not just a dioxin receptor. Dioxins and DLCs occur ubiquitously and have diverse health/ecological risks. Additional research is required to identify both shared and compound-specific mechanisms, especially for emerging DLCs such as polyhalogenated carbazoles (PHCZs), polychlorinated diphenyl sulfides (PCDPSs), and others, of which only a few investigations have been performed at present. Many of the toxic effects of emerging DLCs were observed to be predominantly mediated by the AHR because of their structural similarity as dioxins, and the in vitro TCDD-relative potencies of certain emerging DLC congeners are comparable to or even greater than the WHO-TEFs of OctaCDD, OctaCDF, and most coplanar PCBs. Due to the close relationship between AHR biology and environmental science, this review begins by providing novel insights into AHR signaling (canonical and non-canonical), AHR's biochemical properties (AHR structure, AHR-ligand interaction, AHR-DNA binding), and the variations during AHR transactivation. Then, AHR ligand classification and the corresponding mechanisms are discussed, especially the shared and compound-specific, AHR-mediated effects and mechanisms of emerging DLCs. Accordingly, a series of in vivo and in vitro toxicity evaluation methods based on the AHR signaling pathway are reviewed. In light of current advances, future research on traditional and emerging DLCs will enhance our understanding of their mechanisms, toxicity, potency, and ecological impacts.