Metabolic landscape of human alveolar type II epithelial cells undergoing epithelial-mesenchymal transition induced directly by silica exposure.

Epithelial-mesenchymal transition (EMT) plays an irreplaceable role in the development of silicosis. However, molecular mechanisms of EMT induced by silica exposure still remain to be addressed. Herein, metabolic profiles of human alveolar type II epithelial cells (A549 cells) exposed directly to silica were characterized using non-targeted metabolomic approaches. A total of 84 differential metabolites (DMs) were identified in silica-treated A549 cells undergoing EMT, which were mainly enriched in metabolisms of amino acids (e.g., glutamate, alanine, aspartate), purine metabolism, glycolysis, etc. The number of DMs identified in the A549 cells obviously increased with the elevated exposure concentration of silica. Remarkably, glutamine catabolism was significantly promoted in the silica-treated A549 cells, and the levels of related metabolites (e.g., succinate) and enzymes (e.g., α-ketoglutarate (α-KG) dehydrogenase) were substantially up-regulated, with a preference to α-KG pathway. Supplementation of glutamine into the cell culture could substantially enhance the expression levels of both EMT-related markers and Snail (zinc finger transcription factor). Our results suggest that the EMT of human alveolar epithelial cells directly induced by silica can be essential to the development of silicosis.

Recent advances in the removal of psychoactive substances from aquatic environments: A review.

Psychoactive substances (PS) have become emerging contaminants in aquatic environments, characterized by their wide distribution, high persistence, bioaccumulation and toxicity. They are difficult to be completely removed in sewage treatment plants due to their high stability under different conditions. The incomplete removal of PS poses a threat to the aquatic animals and can also lead to human health problems through accumulation in the food chain. PS has become a huge burden on global health systems. Therefore, finding an effective technology to completely remove PS has become a "hot topic" for researchers. The methods for removal PS include physical techniques, chemical methods and biological approaches. However, there is still a lack of comprehensive and systematic exploration of these methods. This review aims to address this gap by providing a comprehensive overview of traditional strategies, highlighting recent advancements, and emphasizing the potential of natural aquatic plants in removing trace PS from water environments. Additionally, the degradation mechanisms that occur during the treatment process were discussed and an evaluation of the strengths and weaknesses associated with each method was provided. This work would help researchers in gaining a deeper understanding of the methodologies employed and serve as a reference point for future research endeavors and promoting the sustainable and large-scale application of PS elimination.

Effective strategies alleviate mitochondrial toxicity of perfluorooctanoic acid: Modification of functional head group and inhibition of toxic target.

Minimizing the detrimental impacts of perfluorooctanoic acid (PFOA) on human health is a daunting task. Here, we aimed to propose effective strategies for reducing PFOA-induced mitochondrial toxicity in human liver and intestinal cells. PFOA could occupy the fatty acid-binding pockets of human peroxisome proliferator-activated receptor alpha (hPPARα). PFOA not only could structurally interact with hPPARα, but also substantially upregulated the expression levels of PPARα and its downstream gene (i.e., pyruvate dehydrogenase kinase (PDK4)). The increased expression of PDK4 was associated with the mitochondrial toxicity of PFOA, and inhibition of PDK4 or knock-down of PDK4 could effectively attenuate the mitochondrial toxicity of PFOA. Moreover, modification of carboxyl group via an esterification of PFOA into methyl perfluorooctanoate (MePFOA) decreased the affinity to hPPARα, resulting in the loss of upregulated expressions of PPARα and PDK4. Lower mitochondrial toxicity and cytotoxicity were found in the MePFOA-treated cells compared to PFOA exposure. Our study supported that the carboxyl group of PFOA (as functional head group) was required for inducing its mitochondrial toxicity. Two strategies, including modification of functional head group and inhibition of toxic target of PFOA, are feasible to ameliorate mitochondrial toxicity of PFOA.

A quantitative method for aquaporin-1 protein using magnetic preconcentration and probe-based immunoassay coupling to inductively coupled plasma mass spectrometry in urine analysis.

BACKGROUND: Aquaporin-1 (AQP1) protein plays a crucial role in intracellular and extracellular water homeostasis and fluid transport in organs and tissues associated with diverse life activities and is extremely abundant in the kidney. Accurate detection of AQP1 in urine can be applied as screening of early-stage disease. Application of magnetic preconcentration and probe-based signal amplification strategy coupling to inductively coupled plasma mass spectrometry (ICP-MS) is a more accurate, sensitive and specific detection method for AQP1 in complex biological samples compared to conventional methods. RESULTS: We described an element-labelling strategy based on magnetic preconcentration and probe-based immunoassay coupling to ICP-MS detection. The magnetic beads (MBs) modified with epoxy groups were capable of enriching AQP1 proteins and separating them from complex matrices. The probe constructed by conjugating anti-AQP1 antibody molecules on the surface of gold nanoparticles could specifically recognize AQP1 proteins attached on MBs and be analyzed by ICP-MS. The concentration of AQP1 protein could be precisely quantified and amplified by 14,000 times through the corresponding signal of Au atoms. This assay for AQP1 protein quantification achieved a detection limit down to 0.023 ng mL-1, a broad linear calibration curve between 0.3 ng mL-1 and 30 ng mL-1, as well as outstanding specificity. SIGNIFICANCE: The proposed method was successfully applied to detect AQP1 protein in human urine samples, showing the potential for its applications concerning accurate AQP1 quantification. It can also screen a wide range of proteins provided the antibodies specific to these target proteins are available.

Effects of cable bacteria on vertical redox profile formation and phenanthrene biodegradation in intertidal sediment responded to tide.

Periodic oxygen permeation is critical for pollutant removal within intertidal sediments. However, tidal effects on the vertical redox profile associated with cable bacterial activity is not well understood. In this study, we simulated and quantified the effects of tidal flooding, exposing, and their periodic alternation on vertical redox reactions and phenanthrene removal driven by cable bacteria in the riverbank sediment. Results show that electrogenic sulfur oxidation (e-SOx) mediated by cable bacteria during exposing process drove the vertical permeation of oxidation potential characterized by a decrease in Fe(II) and sulfide concentrations. The sulfate produced was observed in deep sediment (5-10 mm) and served as an electron acceptor for anaerobic oxidation, thereby triggering the functional succession of microbial community. About 78.2 % and 80.8 % of phenanthrene was degraded in deep sediment where cable bacteria grew well under exposing and tidal conditions. Anaerobic processes during tidal flood were also found to be important for the survival of cable bacteria. Higher cable bacteria abundance (up to 1.5 %) was observed under tidal conditions compared to that under continuous exposing conditions and flooding conditions. This might be attributed to lower oxidation stress and sulfide replenishment via sulfate reduction while flooding. Under tidal conditions, the cable bacteria interacted with sulfate reduction bacteria (e.g. Desulfobacca spp. and Desulfatiglans spp.) and maintained the dynamic balance of HS- and SO42- in sediment profiles. This HS--SO42- cycle could serve as a "redox connector" that continuously delivers oxidation potential to deep sediments, resulting in the removal of organic pollutants. The findings provide preliminary evidence of the self-purification mechanisms within intertidal sediments and suggest a potential strategy for sediment remediation.

Nanospray Laser-Induced Plasma Ionization Mass Spectrometry for Sensitive and High-Coverage Analysis of Broad Polarity Organic Pollutants.

Accurate, sensitive, and high-coverage analysis of various organic pollutants in complex samples and single cells is significant in investigating their environmental behaviors and toxic effects. Here we proposed a nanospray laser-induced plasma ionization mass spectrometry (nLIPI-MS) method for sensitive and high-coverage analysis of broad polarity organic pollutants under ambient and open-air conditions. The nLIPI-MS method combines nanospray with laser-induced plasma ionization, enabling direct analysis without sophisticated sample pretreatment. For the analysis of nonpolar and very weakly polar organic pollutants such as polycyclic aromatic hydrocarbons (PAHs) and alkyl-PAHs, the nLIPI-MS method showed desirable analytical performance, with limits of detection of as low as the µg/L level. For moderately polar organic pollutants such as p-phenylenediamine quinones (PPD-Qs), nLIPI-MS displayed significant enhanced sensitivity by 1 to 2 orders of magnitude in comparison to nanoelectrospray ionization (nESI)-MS. For more polar organic pollutants such as per- and polyfluoroalkyl substances (PFASs), nLIPI-MS also showed good analytical performance, with a sensitivity improvement of 1.3- to 2.7-fold over that of nESI-MS. The sensitivity of nLIPI-MS for the analysis of PPD-Qs and PFASs reached as low as the ng/L level, enabling the analysis of ultratrace levels of these pollutants in complex samples and even single cells. Our experimental results demonstrated that nLIPI-MS was an extensive ambient MS method, showing desirable analytical performance for the analysis of organic pollutants with broad polarity ranges.

Biofluorescence imaging-guided spatial metabolic tracing: In vivo tracking of metabolic activity in circulating tumor cell-mediated multi-organ metastases.

Circulating tumor cells (CTC) are considered metastatic precursors that are shed from the primary or metastatic deposits and navigate the bloodstream before undergoing extravasation to establish distant metastases. Metabolic reprogramming appears to be a hallmark of metastatic progression, yet current methods for evaluating metabolic heterogeneity within organ-specific metastases in vivo are limited. To overcome this challenge, we present Biofluorescence Imaging-Guided Spatial Metabolic Tracing (BIGSMT), a novel approach integrating in vivo biofluorescence imaging, stable isotope tracing, stain-free laser capture microdissection, and liquid chromatography-mass spectrometry. This innovative technology obviates the need for staining or intricate sample preparation, mitigating metabolite loss, and substantially enhances detection sensitivity and accuracy through chemical derivatization of polar metabolites in central carbon pathways. Application of BIGSMT to a preclinical CTC-mediated metastasis mouse model revealed significant heterogeneity in the in vivo carbon flux from glucose into glycolysis and the tricarboxylic acid (TCA) cycle across distinct metastatic sites. Our analysis indicates that carbon predominantly enters the TCA cycle through the enzymatic reaction catalyzed by pyruvate dehydrogenase. Thus, our spatially resolved BIGSMT technology provides fresh insights into the metabolic heterogeneity and evolution during melanoma CTC-mediated metastatic progression and points to novel therapeutic opportunities.

One-Pot Tandem/Spirocyclization Reaction: Synthesis of Spiro[pyridine-thiazolidine] Ring Derivatives.

An efficient one-pot, three-component approach was devised to synthesize spiro[pyridine-thiazolidine] ring skeletons using thiazole salts, aldehydes, and enaminones. This method allows the assembly of structurally diverse spiroazepines through [3 + 1 + 2] tandem/spirocyclization reactions. This spirocyclization reaction offers several advantages, including transition metal-free conditions, high chemoselectivity, and the ability to construct structurally novel polycyclic compounds.

An Acid-Activatable Fluorescent Probe for Sulfur Dioxide in Traditional Chinese Medicines and Living cells.

Excessive sulfur dioxide (SO2) disturbs physiology of lysosomes causing diseases and threatening human health. A fluorescent probe has been regarded as one of the most attractive approaches, which is compatible with living cells and possesses high sensitivity. However, most of fluorescent probes' reaction sites are activated before they reach the destination. In this work, an acid-activatable fluorescent probe PT1 was synthesized, characterized, and used for SO2 detection. The introduction of oxazolines in PT1 enables the intelligent response of probe to release the activation stie for SO2 derivatives through Michael addition upon exposure to acid. In vitro studies showed a remarkable selectivity of PT1 to SO2 derivatives than other biothiols with a limit of detection as low as 62 nM. Precise spatiotemporal identification of lysosomal SO2 fluctuations has been successfully performed by PT1. Furthermore, PT1 can be applied for monitoring SO2 derivatives in traditional Chinese medicines.

Chlorophyll a acts as a natural photosensitizer to drive nitrate reduction in nonphotosynthetic microorganisms.

With the death and decomposition of widely distributed photosynthetic organisms, free natural pigments are often detected in surface water, sediment and soil. Whether free pigments can act as photosensitizers to drive biophotoelectrochemical metabolism in nonphotosynthetic microorganisms has not been reported. In this work, we provide direct evidence for the photoelectrophic relationship between extracellular chlorophyll a (Chl a) and nonphotosynthetic microorganisms. The results show that 10 µg of Chl a can produce significant photoelectrons (∼0.34 A/cm2) upon irradiation to drive nitrate reduction in Shewanella oneidensis. Chl a undergoes structural changes during the photoelectric process, thus the ability of Chl a to generate a photocurrent decreases gradually with increasing illumination time. These changes are greater in the presence of microorganisms than in the absence of microorganisms. Photoelectron transport from Chl a to S. oneidensis occurs through a direct pathway involving the cytochromes MtrA, MtrB, MtrC and CymA but not through an indirect pathway involving riboflavin. These findings reveal a novel photoelectrotrophic linkage between natural photosynthetic pigments and nonphototrophic microorganisms, which has important implications for the biogeochemical cycle of nitrogen in various natural environments where Chl a is distributed.

Chlorinated Anthracenes Induced Pulmonary Immunotoxicity in 3D Coculture Spheroids Simulating the Lung Microenvironment.

Chlorinated anthracenes (Cl-Ants), persistent organic pollutants, are widely detected in the environment, posing potential lung toxicity risks due to frequent respiratory exposure. However, direct evidence and a comprehensive understanding of their toxicity mechanisms are lacking. Building on our prior findings of Cl-Ants' immunotoxic risks, this study developed a three-dimensional coculture spheroid model mimicking the lung's immune microenvironment. The objective is to explore the pulmonary immunotoxicity and comprehend its mechanisms, taking into account the heightened immune reactivity and frequent lung exposure of Cl-Ants. The results demonstrated that Cl-Ants exposure led to reduced spheroid size, increased macrophage migration outward, lowered cell viability, elevated 8-OHdG levels, disturbed anti-infection balance, and altered cytokine production. Specifically, the chlorine substituent number correlates with the extent of disruption of spheroid indicators caused by Cl-Ants, with stronger immunotoxic effects observed in dichlorinated Ant compared to those in monochlorinated Ant. Furthermore, we identified critical regulatory genes associated with cell viability (ALDOC and ALDOA), bacterial response (TLR5 and MAP2K6), and GM-CSF production (CEBPB). Overall, this study offers initial in vitro evidence of low-dose Cl-PAHs' pulmonary immunotoxicity, advancing the understanding of Cl-Ants' structure-related toxicity and improving external toxicity assessment methods for environmental pollutants, which holds significance for future monitoring and evaluation.

Construction of 2D/2D ZnIn2S4/Nb2CTx (MXene) hybrid with hole transport highway and active facet exposure boost photocatalytic hydrogen evolution.

In this study, leveraging the tunable surface groups of MXene, the two-dimensional (2D) Nb2CTx with OH terminal (NC) was synthesized. 2D ZnIn2S4 (ZIS) nanosheets were prepared with the aid of sodium citrate, enhancing the exposure ratio of active (110) facet. On this basis, 2D/2D ZnIn2S4/Nb2CTx heterojunctions were fabricated to improve photocatalytic hydrogen evolution reaction (HER) performance. The optimized 6 wt%Nb2CTx/ZnIn2S4-450 (6NC/ZIS-450) photocatalyt exhibits a remarkable HER rate of 3603 µmol g-1h-1, which is 10 times superior to that of the original ZnIn2S4. Its apparent quantum efficiency (AQE) at 380 nm reaches 14.9 %. Meanwhile, even after 5 rounds of HER, the activity of 2D/2D ZnIn2S4/Nb2CTx heterojunction remained at 90 %, far superior to that of pure ZnIn2S4 (34 % and 31 %). Energy band structure analysis and density functional theory (DFT) calculation indicate that Nb2CTx adsorbed with OH exhibit a low work function. By serving as a hole cocatalyst, it effectively boosts the photocatalytic HER rate of ZnIn2S4/Nb2CTx heterojunction and inhibits the photocorrosion of ZnIn2S4. This unique insight, via hole transport highways and increased exposure of active facets, effectively enhances the activity and stability of sulfides photocatalysts.

Effect of oxidative stress induced by 2,3,7,8- tetrachlorodibenzo-p-dioxin on DNA damage.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a highly toxic persistent organic pollutant (POP) that can induce DNA damage within cells. Although oxidative stress is one of the primary mechanisms causing DNA damage, its role in the process of TCDD-induced DNA damage remains unclear. In this study, the TCDD-induced production of reactive oxygen species (ROS) and the occurrence of DNA damage at the AP site were monitored simultaneously. Further investigation revealed that TCDD impaired the activities of superoxide dismutase (SOD) and catalase (CAT), compromising the cellular antioxidant defense system. Consequently, this led to an increase in the production of O2.- and NO, thus inducing DNA damage at the AP site under oxidative stress. Our findings were further substantiated by the upregulation of key genes in the base excision repair (BER) pathway and the absence of DNA AP site damage after inhibiting O2.- and NO. In addition, transcriptome sequencing revealed that TCDD induces DNA damage by upregulating genes associated with oxidative stress in the mitogen-activated protein kinase (MAPK), cyclic adenosine monophosphate (cAMP), and breast cancer pathways. This study provides important insights into the toxicity mechanisms of TCDD.

Rapid and sensitive determination of legacy and emerging per- and poly-fluoroalkyl substances with solid-phase microextraction probe coupled with mass spectrometry.

This study was designed to develop a rapid and sensitive method for quantifying legacy and emerging per- and polyfluoroalkyl substances (PFASs) in environmental samples with solid-phase microextraction (SPME) coupled with mass spectrometry (MS). An innovative SPME probe was fabricated via in situ polymerization, and the probe coating was optimized with response surface methodology to maximize the fluorine-fluorine interactions and electrostatic properties and ensure high selectivity for the target PFASs with enrichment factors of 48-491. The coupled SPME and MS provided a rapid and sensitive method for analyses of PFASs, with excellent linearity (r ≥ 0.9962) over the concentration range 0.001-1 µg/L and remarkably low detection limits of 0.1-13.0 ng/L. This method was used to analyze trace PFASs in tap water, river water, and wastewater samples and proved to be a simple and efficient analytical method for selective enrichment and detection of contaminants in the environment.

Quantitative detecting low concentration polystyrene nanoplastics in aquatic environments via an Ag/Nb2CTx (MXene) SERS substrate.

In this study, the plasmonic Ag nanoparticles (Ag NPs) were uniformly anchored on the high conductivity Nb2CTx (MXene) nanosheets to construct an Ag/Nb2CTx substrate for surface-enhanced Raman spectroscopy (SERS) detection of polystyrene (PS) nanoplastics. The KI addition (0.15 mol/L), the volume ratio between substrate colloid and nanoplastic suspension (2:1), and the mass ratio of Nb2CTx in substrate (14%) on SERS performance were optimized. The EM hot spots of Ag/Nb2CTx are significantly enlarged and enhanced, elucidated by FDFD simulation. Then, the linear relationship between the PS nanoplastics concentration with three different sizes (50, 300, and 500 nm) and the SERS intensity was obtained (R2 > 0.976), wherein, the detection limit was as low as 10-4 mg/mL for PS nanoplastic. Owing to the fingerprint feature, the Ag/Nb2CTx-14% substrate successfully discerns the mixtures from two-component nanoplastics. Meanwhile, it exhibits excellent stability of PS nanoplastics on different detection sites. The recovery rates of PS nanoplastics with different sizes in lake water ranged from 94.74% to 107.29%, with the relative standard deviation (RSD) ranging from 2.88% to 8.30%. Based on this method, the expanded polystyrene (EPS) decomposition behavior was evaluated, and the PS concentrations in four water environments were analyzed. This work will pave the way for the accurate quantitative detection of low concentration of nanoplastics in aquatic environments.

In Situ Activation of Azaarenes and Terminal Alkynes to Construct Bridged Polycyclic Compounds Containing Isoquinolinones.

A copper-catalyzed [4+2] cyclization reaction of isoquinolines and alkynes is developed for the one-step construction of isoquinolinone derivatives with multisubstituted bridging rings. The unique feature of this three-component tandem cyclization reaction is the functionalization of the C1, N2, C3, and C4 positions of 3-haloisoquinolines via the construction of new C-N, C═O, and C-C bonds. This dearomatization strategy for the synthesis of structurally complex isoquinolinone-bridged cyclic compounds offers good chemoselectivity, broad functional group compatibility, greenness, and high step economy.

Environmentally relevant concentrations of 2,3,7,8-TCDD induced inhibition of multicellular alternative splicing and transcriptional dysregulation.

Alternative splicing (AS), found in approximately 95 % of human genes, significantly amplifies protein diversity and is implicated in disease pathogenesis when dysregulated. However, the precise involvement of AS in the toxic mechanisms induced by TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) remains incompletely elucidated. This study conducted a thorough global AS analysis in six human cell lines following TCDD exposure. Our findings revealed that environmentally relevant concentration (0.1 nM) of TCDD significantly suppressed AS events in all cell types, notably inhibiting diverse splicing events and reducing transcript diversity, potentially attributed to modifications in the splicing patterns of the inhibitory factor family, particularly hnRNP. And we identified 151 genes with substantial AS alterations shared among these cell types, particularly enriched in immune and metabolic pathways. Moreover, TCDD induced cell-specific changes in splicing patterns and transcript levels, with increased sensitivity notably in THP-1 monocyte, potentially linked to aberrant expression of pivotal genes within the spliceosome pathway (DDX5, EFTUD2, PUF60, RBM25, SRSF1, and CRNKL1). This study extends our understanding of disrupted alternative splicing and its relation to the multisystem toxicity of TCDD. It sheds light on how environmental toxins affect post-transcriptional regulatory processes, offering a fresh perspective for toxicology and disease etiology investigations.

Inner-Wall Coated Nanopipette Microextraction for Quantitative Analysis of Per- and Polyfluoroalkyl Substances in Single Cells Using Mass Spectrometry.

Per- and polyfluoroalkyl substances (PFASs) are a series of organic pollutants with potential cytotoxicity and biotoxicity. Accurate and sensitive detection of trace PFASs in single cells can provide insights into investigating their cytotoxicity, carcinogenicity, and mutagenicity. Here we report the development of an inner-wall coated nanopipette microextraction coupled with induced nanoelectrospray ionization mass spectrometry (InESI-MS) method and its application for rapid, sensitive, and accurate analysis of trace PFASs in single cells. A specially designed inner-wall coated nanopipette was prepared for sampling of the cytoplasm from a single cell, and the trace PFASs in the cytoplasm were selectively enriched into the coating via reversed-phase adsorption, ion bonding adsorption, and π-π interaction mechanisms. After the extraction, the cytoplasm was removed, and the enriched PFASs were then desorbed into some organic solvent, applying an alternating current (AC) voltage to the inner-wall coated nanopipette for InESI-MS analysis. The inner-wall coated nanopipette showed an exhaustive extraction to the trace PFASs in one single cell, and thus, the mass of each target analyte in the cytoplasm can be calculated via an internal standard calibration curve method, avoiding the measurement of ultrasmall volume cytoplasm for one single cell. By using the inner-wall coated nanopipette microextraction coupled with InESI-MS method, trace PFASs accumulated in the LO2 cells with pollutant exposure were successfully detected, and the accumulative behaviors and heterogeneities of PFASs in single cells were explored.

Di-2-ethylhexyl phthalate disrupts hepatic lipid metabolism in obese mice by activating the LXR/SREBP-1c and PPAR-α signaling pathways.

Di-2-ethylhexyl phthalate (DEHP), a widely utilized plasticizer, has been described as a potential obesogen based on in vivo disruption of hepatic lipid homeostasis and in vitro promotion of lipid accumulation. However, limited literature exists regarding the specific ramifications of DEHP exposure on obese individuals, and the precise mechanisms underlying the adverse effects of DEHP exposure remain unclear. This study aimed to assess the impact of DEHP on hepatic lipid metabolism in obese mice by comparing them to normal mice. Following a 10-week DEHP exposure period, the obese mice exhibited higher blood lipid levels, more severe hepatic steatosis, and more infiltrations of inflammatory cells in liver tissue than normal mice. Interestingly, the body weight of the mice exhibited no significant alteration. In addition, transcriptomic analyses revealed that both lipogenesis and fatty acid oxidation contributed to hepatic lipid metabolism dysregulation following DEHP exposure. More specifically, alterations in the transcription of genes associated with hepatic lipid metabolism were linked to the different responses to DEHP exposure observed in normal and obese mice. Additionally, the outcomes of in vitro experiments validated the in vivo findings and demonstrated that DEHP exposure could modify hepatic lipid metabolism in normal mice by activating the LXR/SREBP-1c signaling pathway to promote lipogenesis. At the same time, DEHP exposure led to inhibition of the Camkkß/AMPK pathway to suppress ß-fatty acid oxidation. Conversely, in obese mice, DEHP exposure was found to be associated with the stimulation of both lipogenesis and fatty acid oxidation via activation of the LXR/SREBP-1c and PPAR-α signaling pathways, respectively. The findings presented in this study first elucidate the contrasting mechanisms underlying DEHP-induced liver damage in obese and normal mice, thereby offering valuable insights into the pathogenesis of DEHP-induced liver damage in individuals with obesity.

Fe, N, S co-doped carbon network derived from acetate-modified Fe-ZIF-8 for oxygen reduction reaction.

In this work, potassium acetate (KAc) was added during the synthesis of a Zn-Fe based metal-organic framework (Fe-ZIF-8) to increase the fixed amount of Fe while simultaneously enhancing the number of pores. Electrospinning was utilized to embed KAc-modified Fe-ZIF-8 (Fe-ZIF-8-Ac) into the polyacrylonitrile nanofiber mesh, to obtain a network composite (Fe@NC-Ac) with hierarchical porous structure. Fe@NC-Ac was co-pyrolyzed with thiourea, resulting in Fe, N, S co-doped carbon electrocatalyst. The electrochemical tests indicated that the prepared catalyst displayed relatively remarkable oxygen reduction reaction (ORR) catalytic activity, with an onset potential (Eonset) of 1.08 V (vs. reversible hydrogen electrode, RHE) and a half-wave potential (E1/2) of 0.94 V, both higher than those of the commercial Pt/C (Eonset = 0.95 V and E1/2 = 0.84 V), respectively. Assembled into Zn-air batteries, the optimized catalyst exhibited higher open circuit voltage (1.698 V) and peak power density (90 mW cm-2) than those of the commercial 20 wt% Pt/C (1.402 V and 80 mW cm-2), respectively. This work provided a straightforward manufacturing strategy for the design of hierarchical porous carbon-based ORR catalysts with desirable performance.