Network pharmacology and in vivo experiment-based strategy for investigating the mechanism of chronic prostatitis/chronic pelvic pain syndrome in QianLieJinDan tablets.

Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common urinary system disease that is prone to recurrence. It typically leads to varying degrees of pelvic pain and discomfort, as well as symptoms related to the urinary system in affected patients. QianLieJinDan tablets (QLJD), a traditional Chinese medicine, have shown promising therapeutic effects on CP/CPPS in clinical practice, but the underlying mechanisms of QLJD in treating CP/CPPS have not been determined. Objective: To reveal the phytochemical characterization and multitarget mechanism of QLJD on CP/CPPS. Methods: The concentrations of the components of QLJD were determined using UHPLC-Q Exactive Orbitrap-MS. Utilizing network pharmacology approaches, the potential components, targets, and pathways involved in the treatment of CP/CPPS caused by QLJD were screened. Molecular docking calculations were employed to assess the affinity between the components of the QLJD and potential targets, revealing the optimal molecular conformation and binding site. Finally, the therapeutic efficacy and potential underlying mechanisms of QLJD were investigated through pharmacological experiments. Results: In this study, a total of 35 components targeting 29 CP-related genes were identified, among which quercetin, baicalin, icariin, luteolin, and gallic acid were the major constituents. Enrichment analysis revealed that the potential targets were involved mainly in the regulation of cytokines, cell proliferation and apoptosis, and the oxidative stress response and were primarily associated with the cytokine‒cytokine receptor interaction pathway, the IL-17 signaling pathway, the Th17 cell differentiation pathway, and the JAK-STAT signaling pathway. In vivo experiments demonstrated that QLJD effectively attenuated the infiltration of CD3+ T cells and the expression of ROS in a CP/CPPS model rat prostate tissue. Furthermore, through the inhibition of IL-6 and STAT3 expression, QLJD reduced the differentiation of Th17 cells, thereby ameliorating pathological injury and prostatic index in prostate tissue. Conclusion: The potential of QLJD as an anti-CP/CPPS agent lies in its ability to interfere with the expression of IL-6 and STAT3, inhibit Th17 cell differentiation, reduce inflammatory cell infiltration in rat prostate tissue, and alleviate oxidative stress damage through its multi-component, multi-target, and multi-pathway effects.

Acute exposure to tris(2,4-di-tert-butylphenyl)phosphate elicits cardiotoxicity in zebrafish (Danio rerio) larvae via inducing ferroptosis.

Tris(2,4-di-tert-butylphenyl)phosphate (AO168 =O), a novel organophosphate ester, is prevalent and abundant in the environment, posing great exposure risks to ecological and public health. Nevertheless, the toxicological effects of AO168 =O remain entirely unknown to date. The results in this study indicated that acute exposure to AO168 =O at 10 and 100 µg/L for 5 days obviously impaired cardiac morphology and function of zebrafish larvae, as proofed by decreased heartbeat, stroke volume, and cardiac output and the occurrence of pericardial edema and ventricular hypertrophy. Transcriptomics, polymerase chain reaction, and molecular docking revealed that the strong interaction of AO168 =O and transferrin receptor 1 activated the transportation of ferric iron into intracellular environment. The release of free ferrous ion to cytoplasmic iron pool also contributed to the iron overload in heart region, thus inducing ferroptosis in larvae via generation of excessive reactive oxygen species, glutathione peroxidase 4 inhibition, glutathione depletion and lipid peroxidation. Ferroptosis inhibitor (Fer-1) co-exposure effectively relieved the cardiac dysfunctions of zebrafish, verifying the dominant role of ferroptosis in the cardiotoxicity caused by AO168 =O. This research firstly reported the adverse impact and associated mechanisms of AO168 =O in cardiomyogenesis of vertebrates, underlining the urgency of concerning the health risks of AO168 =O.

Adverse effects of fenpropathrin on the intestine of common carp (Cyprinus carpio L.) and the mechanism involved.

Fenpropathrin (FEN), a pyrethroid pesticide, is frequently detected in natural water bodies, unavoidable pose adverse effects to aquatic organisms. However, the harmful effects and potential mechanisms of FEN on aquatic species are poorly understood. In this study, common carp were treatment with FEN at 0.45 and 1.35 µg/L for 14 d, and the toxic effects and underlying mechanisms of FEN on the intestine of carp were revealed. RNA-seq results showed that FEN exposure cause a wide range of transcriptional alterations in the intestine and the differentially expressed genes were mainly enrichment in the pathways related to immune and metabolism. Specifically, FEN exposure induced pathological damage and altered submicroscopic structure of the intestine, elevated the levels of Bacteroides fragilis enterotoxin, altered the contents of claudin-1, occludin, and zonula occluden-1 (ZO-1), and causing injury to the intestinal barrier. In addition, inflammation-related index TNF-α in the serum and IL-6 in the intestinal tissues were generally increased after FEN exposure. Moreover, FEN exposure promoted an increase in reactive oxygen species (ROS), altered the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), upregulated the contents of malondialdehyde (MDA) in the intestines. The apoptosis-related parameter cytochrome c, caspase-9, and caspase-3 were significantly altered, indicating that inflammation reaction, oxidative stress, and apoptosis may be involved in the toxic mechanism of FEN on carp. Moreover, FEN treatment also altered the intestinal flora community significantly, which may affect the intestinal normal physiological function and thus affect the growth of fish. Overall, the present study help to clarify the intestinal reaction mechanisms after FEN treatment, and provide a basis for the risk assessment of FEN.

Fenpropathrin disrupted the gills of common carp (Cyprinus carpio L.) through oxidative stress, inflammatory responses, apoptosis, and transcriptional alterations.

Fenpropathrin (FEN) is an extensively utilized synthetic pyrethroid insecticide frequently found in aquatic ecosystems. However, the adverse effects and potential mechanisms of FEN on aquatic species are poorly understood. In this work, common carp were treated with FEN at concentrations of 0.45 and 1.35 µg/L FEN for 14 days, after which the tissue structure, physiological alterations, and mRNA transcriptome of the gills were evaluated. Specifically, FEN exposure caused pathological damage to the gills of carp, downregulated the levels of claudin-1, occludin, and zonula occluden-1 (ZO-1), and inhibited Na+-K+-ATPase activity in the gills. In addition, FEN exposure promoted an increase in reactive oxygen species (ROS) levels and significantly upregulated the levels of malondialdehyde (MDA), 8-hydroxy-2 deoxyguanosine (8-OHdG), and protein carbonyl (PC) in the gills. Moreover, the inflammation-related indices (TNF-α, IL-1ß, and IFN-γ) and the apoptosis-related parameter caspase-3 were generally increased, especially in the 1.35 µg/L FEN group, and these indices were significantly greater than those in the control group. These findings suggest that FEN exposure can cause oxidative stress, the inflammatory response, and apoptosis in carp gills. Importantly, the results of RNA-seq analysis showed that 0.45 and 1.35 µg/L FEN could significantly interfere with multiple immune and metabolic pathways, including the phagosome, NOD-like receptor (NLR) signalling pathway, Toll-like receptor (TLR) signalling pathway, necroptosis, and arachidonic acid metabolism pathways, indicating that the effects of FEN on the gills of fish are intricate. In summary, our findings confirm the toxic effects of FEN on common carp gills and provide additional comprehensive information for evaluating the toxicity and underlying molecular mechanisms of FEN in aquatic organisms.

Fenpropathrin induces neurotoxic effects in common carp (Cyprinus carpio L.).

Fenpropathrin (FEN) is a synthetic pyrethroid that has been frequently detected in aquatic environments, yet the neurotoxic impacts and underlying mechanisms on nontarget organisms are lacking. In this experiment, common carp were exposed to 0.45 and 1.35 µg/L FEN for 14 d and exhibited abnormal locomotor behaviour. Biochemical and molecular analysis results indicated that FEN altered the contents of tight junction proteins (claudin-1, occludin, and ZO-1), disturbed Na+-K+-ATPase and AChE activities, caused abnormal expression of neurotransmitters (ACh, DA, GABA, 5-HT, and glutamate) and caused histological damage in the brain, suggesting that FEN may damage the blood-brain barrier and induce neurotoxicity in carp. Furthermore, FEN also promoted an increase in ROS, changed SOD and CAT activities, and generally upregulated the contents of MDA, 8-OHdG, and protein carbonyl in the brain, indicating that FEN can induce oxidative stress and cause damage to lipids, DNA, and proteins. Moreover, inflammation-related indicators (TNF-α, IL-1ß, IL-6, and IL-10), mitophagy-related genes (PINK1, parkin, ulk1, beclin1, LC3, p62, tfeb, and atg5), and apoptosis-related parameters (p53, bax, bcl-2, caspase-3, caspase-8, and caspase-9) were also significantly changed, suggesting that inflammation, mitophagy, and apoptosis may participate in FEN-induced neurotoxicity in carp. This study refines the understanding of the toxicity mechanism of FEN and thus provides data support for the risk assessment of FEN.

Photosynthesis of Benzonitriles on BiOBr Nanosheets Promoted by Vacancy Associates.

Photocatalytic organic functionalization reactions represent a green, cost-effective, and sustainable synthesis route for value-added chemicals. However, heterogeneous photocatalysis is inefficient in directly activating ammonia molecules for the production of high-value-added nitrogenous organic products when compared with oxygen activation in the formation of related oxygenated compounds. In this study, we report the heterogeneous photosynthesis of benzonitriles by the ammoxidation of benzyl alcohols (99 % conversion, 93 % selectivity) promoted using BiOBr nanosheets with surface vacancy associates. In contrast, the main reaction of catalysts with other types of vacancy sites is the oxidation of benzyl alcohol to benzaldehyde or benzoic acid. Experimental measurements and theoretical calculations have demonstrated a specificity of vacancy type with respect to product selectivity, which arises from the adsorption and activation of NH3 and O2 that is required to promote subsequent C-N coupling and oxidation to nitrile. This study provides a better understanding of the role of vacancies as catalytic sites in heterogeneous photocatalysis.

Environmental impacts of chlorpyrifos: Transgenerational toxic effects on aquatic organisms cannot be ignored.

Chlorpyrifos (CPF) has been extensively used in the world and frequently found in natural environments, might cause a range of environmental issues and pose a health risk to aquatic species. However, investigation of its toxic effects on offspring after parental exposure has been neglected, especially for aquatic organisms such as fish. In the current study, the effects of chronic CPF exposure (3 and 60 µg/L) on adult zebrafish (F0) was investigated to determine its influence on adult reproductive capacity and offspring (F1 and F2). The results showed the existence of CPF both in F0 ovaries and F1 embryos and larvae, indicating that CPF could be transferred directly from the F0 adult fish to F1 offspring. After 90 d exposure, we observed that F0 female fish showed increased proportion of perinucleolar oocyte in the ovaries, decreased proportion of mature oocyte, and decreased egg production, but not in F1 adult. The transcriptomic analysis revealed that the disruption of metabolism during oocyte maturation in the CPF treatment zebrafish might interfere with F0 oocytes development and quality and ultimately influence offspring survival. For the larvae, the parental CPF exposure distinctly inhibited heart rate at 72 and 120 hpf and increased the mortality of F1 but not F2 larvae. The changes of biochemical indicators confirmed a disturbance in the oxidative balance, induced inflammatory reaction and apoptosis in F1 larvae. Furthermore, the changing profiles of mRNA revealed by RNA-seq confirmed an increased susceptibility in F1 larvae and figured out potential disruptions of ROS metabolism, immune system, apoptosis, and metabolism pathways. Taken together, these results show that chronic CPF treatment can induce reproductive toxicity, and parental transfer of CPF occurs in fish, resulting in transgenerational alters in F1 generation survival and transcription that raising concerns on the ecological risk of CPF in the natural environment.

Single and Combined Effects of Chlorpyrifos and Glyphosate on the Brain of Common Carp: Based on Biochemical and Molecular Perspective.

Chlorpyrifos (CPF) and glyphosate (GLY) are the most widely used organophosphate insecticide and herbicide worldwide, respectively; co-occurrence of CPF and GLY in aquatic environments occurs where they inevitably have potential hazards to fish. However, the potential mechanisms of CPF and GLY to induce toxicity have not been fully explored. To identify the adverse impacts of CPF and GLY on fish, either alone or in combination (MIX), CPF (25 µg/L) and GLY (3.5 mg/L) were set up according to an environmentally relevant concentration to expose to common carp for 21 days. After exposure, CPF and GLY decreased the activities of acetylcholinesterase and Na+/K+-ATPase, altered monoamine oxidase levels, decreased antioxidant enzyme activities (superoxide dismutase, catalase, glutathione S-transferase and glutamic reductase), and induced the accumulation of malondialdehyde in the carp brain. The parameters in the MIX groups had a greater impact compared to that in the CPF or GLY group, suggesting that both single and combined exposure could affect neurological signaling systems and cause oxidative stress and lipid peroxidation damage in carp brains, and that MIX exposure increases the impact of each pollutant. RNA-seq results showed that single or combined exposure to CPF and GLY induced global transcriptomic changes in fish brains, and the number of differentially expressed genes in MIX-treated carp brains were globally increased compared to either the CPF or GLY groups, suggesting that the effects of co-exposure were greater than single exposure. Further analysis results revealed that the global transcriptomic changes participated in oxidative stress, immune dysfunction, and apoptosis of fish brains, and identified that the P13k-Akt signaling pathway participates in both single and combined exposure of CPF- and GLY-induced toxicity. Taken together, our results demonstrated that the interaction of CPF and GLY might be synergic and provided novel insights into the molecular mechanisms of fish brains coping with CPF and GLY.

Single-Atom-Mediated Spinel Octahedral Structures for Elevated Performances of Li-Oxygen Batteries.

Li-oxygen batteries have attracted much attention due to its ultra-high theoretical specific capacity, but the discharge product Li2 O2 is easy to accumulate, leading to low battery stability. Here, we demonstrate a series of high-efficiency cathode catalysts of Co3 O4 loaded with single-atomic metals (M=Ru, Pd, Pt, Au, Ir). The single-atomic metal could substitute the central Co atom in the octahedral coordination structure and maintain the structural stability; benefiting from the electron promoter effect, rendering more highly active Co3+ exposed, providing rich nucleation sites for Li2 O2 deposition. And the loaded M atoms could separate the active Co3+ centers, thereby regulating the dispersion of Li2 O2 to obtained a sheet-like morphology, which could facilitate its decomposition in the subsequent charge cycle. Our work found that the single atoms could effectively modulate the active metal oxide with which it is coordinated, thus collectively boosting the catalytic performance.

Heme oxygenase-1 protects against PM2.5 induced endothelial dysfunction through inhibition of HIF1α.

PM2.5 has been accepted as a strong risk factor for cardiovascular diseases. Activation of the renin-angiotensin system (RAS) has been proved to be a key factor in triggering vascular endothelial dysfunction upon PM2.5 exposure in our previous reports. In the current study, we observed the concurrent induction of hemoxygenase (HO)- 1 and RAS components (ANGII and AT1R) expression both in the vascular endothelial cell lines and in rat lung tissue after PM2.5 exposure. Furthermore, HO-1 inhibited RAS activation by suppressing the expression and activity of HIF1α, the upstream transcriptional activator of ANGII and AT1R. In addition, HO-1 blocked significantly increased the release of cell adhesion molecules and chemokines (VCAM-1, E-Selectin, P-Selectin, IL-8, MCP-1) that drive monocyte-endothelium adhesion, along with the enhanced the generation of oxidative stress response mediators in the vascular endothelium. These data together indicate that PM2.5 induced HO-1 upregulation functions as a self-defense response to antagonize endothelial dysfunction by inhibiting HIF1α-mediated RAS activation. Targeting endogenous protective pathway might be helpful to protect from PM2.5-induced cardiovascular injury.

Interfacial water engineering boosts neutral water reduction.

Hydrogen evolution reaction (HER) in neutral media is of great practical importance for sustainable hydrogen production, but generally suffers from low activities, the cause of which has been a puzzle yet to be solved. Herein, by investigating the synergy between Ru single atoms (RuNC) and RuSex cluster compounds (RuSex) for HER using ab initio molecular dynamics, operando X-ray absorption spectroscopy, and operando surface-enhanced infrared absorption spectroscopy, we establish that the interfacial water governs neutral HER. The rigid interfacial water layer in neutral media would inhibit the transport of H2O*/OH* at the electrode/electrolyte interface of RuNC, but the RuSex can promote H2O*/OH* transport to increase the number of available H2O* on RuNC by disordering the interfacial water network. With the synergy of RuSex and RuNC, the resulting neutral HER performance in terms of mass-specific activity is 6.7 times higher than that of 20 wt.% Pt/C at overpotential of 100 mV.

High-throughput transcriptome sequencing reveals the key stages of cardiovascular development in zebrafish embryos.

BACKGROUND: The cardiovascular developmental process is a tightly regulated network involving multiple genes. The current understanding of the molecular mechanism behind cardiovascular development is insufficient and requires further research. RESULTS: Transcriptome sequencing of three developmental stages in zebrafish embryos was performed and revealed three key cardiovascular developmental stages. Then, the differentially expressed genes (DEGs) involved in cardiovascular development were screened out. The three developmental stages were 18 (T1), 24 (T2), and 42 h post fertilization (hpf) (T3), and the three stages were confirmed by detecting differences in expression between cardiomyocyte and endothelial marker genes (cmlc2, fli1) using in situ hybridization, which represents the characteristics of cardiovascular development. Thousands of DEGs were identified using transcriptome analysis. Of them, 2605 DEGs were in T1-vs-T2, including 2003 up-regulated and 602 down-regulated genes, 6446 DEGs were in T1-vs-T3, consisting of 4608 up-regulated and 1838 down-regulated genes, and 3275 DEGs were in T2-vs-T3, including 2420 up-regulated and 855 down-regulated genes. There were 644 common DEGs and 167 common five-fold higher differentially expressed genes (HDEGs) identified, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID). Significant differences was observed in the levels of gene expression among different developmental stages in multiple GO terms and KEGG pathways, such as cell migration to the midline involved in heart development, cardiovascular system development, circulatory system process for biological processes of GO terms; and cardiac muscle contraction, adrenergic signaling in cardiomyocytes for KEGG pathways. These results demonstrated that these three stages were important period for the development of the cardiovascular system. Lastly, we used quantitative real-time PCR (qPCR) to validate the reliability of RNA-sequencing by selecting 21 DEGs. CONCLUSIONS: These results demonstrated that these three stages represented the important periods for cardiovascular system development of zebrafish and some candidate genes was obtained and provided a solid foundation for additional functional studies of the DEGs.

Effect of Acute Exposure to the Ionic Liquid 1-Methyl-3-octylimidazolium Chloride on the Embryonic Development and Larval Thyroid System of Zebrafish.

Previous studies have shown that ILs can induce toxicity in animals, plants, and cells. However, the effect of imidazolium-based ILs on the hypothalamus-pituitary-thyroid (HPT) axis of fish remains unknown. The present study aimed to evaluate the acute effect of [C8mim]Cl on the embryonic development and thyroid-controlled internal secretion system of zebrafish by determining the thyroid hormone level and the expression of HPT-related genes. The results obtained for embryonic developmental toxicity showed the survival rate, heart beats, and body length of fish had decreased 96 h after exposure to [C8mim]Cl, but the hatching rate had increased by the 48 h time point. The transcription levels of HTP-related genes showed that the genes dio3, tg, ttr, tsh, trhrα, trhrß, trhr2, and tpo were up-regulated, while the expression levels of dio1, trh, tshr, and nis were significantly suppressed. Furthermore, we found that exposure to [C8mim]Cl induced an alteration in the levels of thyroid hormones that increased the T3 but decreased the T4 content. In conclusion, our study indicated that acute exposure to [C8mim]Cl altered the expression of HTP-related genes and disturbed the thyroid hormone level, suggesting that the ionic liquid [C8mim]Cl might pose an aquatic environmental threat to fish.

Neurotoxicity of Chronic Co-Exposure of Lead and Ionic Liquid in Common Carp: Synergistic or Antagonistic?

Previous studies have indicated that the harmful heavy metal lead (Pb) contamination in aquatic systems has caused intelligence development disorders and nervous system function abnormalities in juveniles due to the increased permeability of the blood-brain barrier. Ionic liquids (ILs) are considered "green" organic solvents that can replace traditional organic solvents. Studies have found the presence of ILs in soil and water due to chemical applications or unintentional leakage. Therefore, what would happen if Pb interacted with ILs in a body of water? Could ILs enable Pb to more easily cross the blood-brain barrier? Therefore, we examined the combined exposure of Pb and ILs in common carp at low concentration (18.3 mg L-1 of Pb(CH3COO)2•3 H2O and 11 mg L-1 of the IL 1-methyl-3-octylimidazolium chloride, 5% of their LC50) for 28 days in the present study. The result of a neurobehavioral assay showed that chronic exposure of lead at lower concentrations significantly altered fish movement and neurobehaviors, indicating that lead exposure caused neurotoxicity in the carp. Increases in the neurotransmitter dopamine levels and injuries in the fish brain accounted for neurobehavioral abnormalities induced by lead exposure. Moreover, we also found that lead could easily cross the blood-brain barrier and caused significant bioaccumulation in the brain. Particularly, our study indicated that the ionic liquid could not synergistically promote blood-brain barrier permeability and hence failed to increase the absorption of lead in the fish brain, suggesting that the combined exposure of lead and ILs was not a synergistic effect but antagonism to the neurotoxicity. The results of this study suggested that ILs could recede the Pb induced neurotoxicity in fish.

Developmental toxicity of glyphosate on embryo-larval zebrafish (Danio rerio).

Glyphosate (GLY) induces developmental toxicity in fish, but research on the toxicity mechanism is limited. In this study, zebrafish embryos were exposed for 120 hpf to 0.7, 7, and 35 mg L-1 GLY. The results show that GLY treatment induced developmental toxicity in the fish, including premature hatching, reduced heartbeats, pericardial and yolk sac oedema, swim bladder deficiency, and shortened body length, which was possibly due to a significantly decreased triiodothyronine (T3)/thyroxine (T4) ratio and the abnormal expression patterns of hypothalamic-pituitary-thyroid (HPT) (crh, tshß, tr α, tr ß, and t tr ) and growth hormone/insulin-like growth factor (GH/IGF) axis-related genes (gh, ghrα, ghrß, igf1, igf1rα, and igf1rß) in larvae exposed to GLY. In addition, GLY exposure altered the levels of SOD and CAT, increased ROS, promoted malondialdehyde (MDA) content, and significantly altered the levels of endoplasmic reticulum (ER) stress signalling pathway factors (perk, eif2α, gadd34, atf4, ire1α, xbp1, atf6, hspa5, and chop), suggesting that GLY treatment induced oxidative injury and ER stress in the larvae. Further research showed that treatment with a higher concentration of GLY upregulated the levels of iNOS, IL-1ß, and TNF-α while inhibiting the expression of IL-10 and TGF-ß, suggesting that GLY causes an inflammatory reaction in the larvae. In addition, we also found that apoptosis was induced in the larvae, which was determined by acridine orange staining and abnormal expression of p53, caspase-3, -8, and -9. Taken together, our results demonstrate that GLY exposure altered the T3/T4 ratio, disturbed the expression patterns of HPT and GH/IGF axis-related genes, and induced oxidative and ER stress, inflammatory reactions, and apoptosis in the zebrafish larvae. This investigation contributes to improved understanding of the developmental toxicity mechanism of GLY in fish.

Distinct Crystal-Facet-Dependent Behaviors for Single-Atom Palladium-On-Ceria Catalysts: Enhanced Stabilization and Catalytic Properties.

High-performance, fully atomically dispersed single-atom catalysts (SACs) are promising candidates for next-generation industrial catalysts. However, it remains a great challenge to avoid the aggregation of isolated atoms into nanoparticles during the preparation and application of SACs. Here, the evolution of Pd species is investigated on different crystal facets of CeO2 , and vastly different behaviors on the single-atomic dispersion of surface Pd atoms are surprisingly discovered. In situ X-ray photoelectron spectroscopy (XPS), in situ near-ambient-pressure-XPS (NAP-XPS), in situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS), and X-ray absorption spectroscopy (XAS) reveal that, in a reducing atmosphere, more oxygen vacancies are generated on the (100) facet of CeO2 , and Pd atoms can be trapped and thus feature atomic dispersion; by contrast, on the CeO2 (111) facet, Pd atoms will readily aggregate into clusters (Pdn ). Furthermore, Pd1 /CeO2 (100) gives a high selectivity of 90.3% for the catalytic N-alkylation reaction, which is 2.8 times higher than that for Pdn /CeO2 (111). This direct evidence demonstrates the crucial role of crystal-facet effects in the preparation of metal-atom-on-metal-oxide SACs. This work thus opens an avenue for the rational design and targeted synthesis of ultrastable and sinter-resistant SACs.

Effects of polyvinyl chloride microplastics on reproduction, oxidative stress and reproduction and detoxification-related genes in Daphnia magna.

The drastic increase of microplastics (MPs) in aquatic environment has become a serious threat to marine and freshwater ecosystems. However, little information is available regarding the potential detrimental effects of polyvinyl chloride microplastics (PVC-MPs) on aquatic organisms. This study investigated the changes of reproduction parameters, oxidative stress and the expression of reproduction and detoxification-related genes in Daphnia magna after exposed to 2 ± 1 and 50 ± 10 µm PVC-MPs. The results showed that chronic exposure to 2 ± 1 µm PVC-MPs prolonged days to the first brood, increased total number of broods per female and frequency of molting per adult, decreased offspring number at first brood and total number of offspring per female in D. magna. Moreover, 2 ± 1 µm PVC-MPs also disturbed the activities of SOD and CAT, increased GSH and MDA levels. The expression of Vtg, SOD, CAT, CYP314 and CYP360A8 genes also exhibited different response patterns depending on exposure time. Furthermore, 50 ± 10 µm PVC-MPs decreased offspring at first brood and Vtg mRNA level, increased the transcription levels and activities of SOD and CAT. These results suggest that the presence of PVC-MPs in aquatic environment may cause reproduction toxicity by disrupting the reproduction and detoxification-related genes expression and inducing oxidative stress in D. magna.

Negative impacts of microcystin-LR and glyphosate on zebrafish intestine: Linked with gut microbiota and microRNAs?

Microcystin-LR (MC-LR) and glyphosate (GLY) have been classified as a Group 2B and Group 2A carcinogens for humans, respectively, and frequently found in aquatic ecosystems. However, data on the potential hazard of MC-LR and GLY exposure to the fish gut are relatively scarce. In the current study, a subacute toxicity test of zebrafish exposed to MC-LR (35 µg L-1) and GLY (3.5 mg L-1), either alone or in combination was performed for 21 d. The results showed that MC-LR or/and GLY treatment reduced the mRNA levels of tight junction genes (claudin-5, occludin, and zonula occludens-1) and altered the levels of diamine oxidase and D-lactic, indicating increased intestinal permeability in zebrafish. Furthermore, MC-LR and/or GLY treatment remarkably increased the levels of intestinal IL-1ß and IL-8 but decreased the levels of IL-10 and TGF-ß, indicating that MC-LR and/or GLY exposure induced an inflammatory response in the fish gut. MC-LR and/or GLY exposure also activated superoxide dismutase and catalase, generally upregulated the levels of p53, bax, bcl-2, caspase-3, and caspase-9, downregulated the levels of caspase-8 and caused notable histological injury in the fish gut. Moreover, MC-LR and/or GLY exposure also significantly altered the microbial community in the zebrafish gut and the expression of miRNAs (miR-146a, miR-155, miR-16, miR-21, and miR-223). Chronic exposure to MC-LR and/or GLY can induce intestinal damage in zebrafish, and this study is the first to demonstrate an altered gut microbiome and miRNAs in the zebrafish gut after MC-LR and GLY exposure.