Defect-Confinement Strategy for Constructing CuO Clusters on Carbon Nanotubes for Catalytic Oxidation of AsH3 at Room Temperature.

The efficient removal of the highly toxic arsine gas (AsH3) from industrial tail gases under mild conditions remains a formidable challenge. In this study, we utilized the confinement effect of defective carbon nanotubes to fabricate a CuO cluster catalyst (CuO/ACNT), which exhibited a capacity much higher than that of CuO supported on pristine multiwalled carbon nanotubes (MWCNT) (CuO/PCNT) for catalytically oxidizing AsH3 under ambient conditions. The experimental and theoretical results show that nitric acid steam treatment could induce MWCNT surface structural defects, which facilitated more stable anchoring of CuO and then improved the oxygen activation ability, therefore leading to excellent catalytic performance. Density functional theory (DFT) calculations revealed that the catalytic oxidation of AsH3 proceeded through stepwise dehydrogenation and subsequent recombination with oxygen to form As2O3 as the final product.

On the Working Mechanisms of Molecules-Based Van der Waals Dielectrics.

Sb2 O3 molecules offer unprecedented opportunities for the integration of a van der Waals (vdW) dielectric and a 2D vdW semiconductor. However, the working mechanisms underlying molecules-based vdW dielectrics remain unclear. Here, the working mechanisms of Sb2 O3 and two Sb2 O3 -like molecules (As2 O3 and Bi2 O3 ) as dielectrics are systematically investigated by combining first-principles calculations and gate leakage current theories. It is revealed that molecules-based vdW dielectrics have a considerable advantage over conventional dielectric materials: defects hardly affect their insulating properties. This shows that it is unnecessary to synthesize high-quality crystals in practical applications, which has been a long-standing challenge for conventional dielectric materials. Further analysis reveals that a large thermionic-emission current renders Sb2 O3 difficult to simultaneously satisfy the requirements of dielectric layers in p-MOS and n-MOS, which hinders its application for complementary metal-oxide-semiconductor (CMOS) devices. Remarkably, it is found that As2 O3 can serve as a dielectric for both p-MOS and n-MOS. This work not only lays a theoretical foundation for the application of molecules-based vdW dielectrics, but also offers an unprecedentedly competitive dielectric (i.e., As2 O3 ) for 2D vdW semiconductors-based CMOS devices, thus having profound implications for future semiconductor industry.

Intravenous As2O3 as a promising treatment for psoriasis - an experimental study in psoriasis-like mouse model.

OBJECTIVE: To evaluate the efficacy and mechanistic bases of the intravenous injection of arsenic trioxide at clinical-relevant doses for treating an imiquimod-induced psoriasis-like mouse model. METHODS: After inducing psoriasis-like skin lesions on the back of mice with imiquimod, mice in each group were injected with a clinical dose of arsenic trioxide through the tail vein. The changes in the gene expression, protein expression and distribution of relevant inflammatory factors were evaluated in the inflicted skin area, for mechanisms underlying the efficacy of intravenous As2O3 intervention. HaCaT cells were used to establish an in vitro psoriasis model and pcDNA3.1-NF-κB overexpression plasmid was transfected into cells to overexpress P65, which further confirmed the role of the NF-κB signaling pathway in the effectiveness of As2O3. RESULTS: Clinical dose of As2O3 can significantly improve abnormal symptoms and pathological changes in psoriasis-like skin lesions induced by IMQ in mice. While IMQ induced abnormal expression and distribution of inflammatory factors in the RIG-I pathway and the microRNA-31 (miR-31) pathway in psoriatic skin tissues, intravenous As2O3 can effectively regulate and restore the normality. The leading role of NF-κB signaling was evidenced in vivo and validated in vitro using the NF-κB-overexpressed HaCaT cell model. CONCLUSION: Clinical dosage of As2O3 may achieve effective treatment of IMQ-induced psoriatic skin lesions by modulating the NF-κB signaling pathway which regulates both the RIG-I and the miR-31 lines of action. Our data provided strong evidence supporting the claim that systemic As2O3 administration of clinical doses can be a promising treatment for psoriasis patients.

Effect of lycopene on As2O3 induced oxidative stress in SH-SY5Y cells.

It is known that oxidative stress may cause neuronal injury and several experimental models showed that As2O3 exposure causes oxidative stress. Lycopene, a carotenoid, has been shown to have protective effect in neurological disease models due to antioxidant activity, but its effect on As2O3-induced neurotoxicity is not identified yet. The aim of this study is to investigate the effects of lycopene on As2O3-induced neuronal damage and the related mechanisms. Cell viability was determined by the MTT assay. Lycopene was administrated with different concentrations (2, 4, 6 and 8 µM) one hour before 2 µM As2O3 exposure in SH-SY5Y human neuroblastoma cells. The anti-oxidant effect of lycopene was determined by measuring superoxide dismutase (SOD), catalase (CAT) hydrogen peroxide (H2O2), malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS). MTT results and LDH cytotoxicity analyses showed that pretreatment with 8 µM lycopene significantly improved the toxicity due to As2O3 exposure in SH­SY5Y neuroblastoma cells. Pretreatment with lycopene significantly increased the activities of anti­oxidative enzymes as well as total antioxidant status and decreased total oxidative status in As2O3 exposed cells. The results of this study indicate that lycopene may be a potent neuroprotective against oxidative stress and could be used to prevent neuronal injury or death in several neurological diseases.

BMP8A promotes survival and drug resistance via Nrf2/TRIM24 signaling pathway in clear cell renal cell carcinoma.

There is increasing evidence that bone morphogenetic proteins (BMP) are involved in the proliferation and drug tolerance of kidney cancer. However, the molecular mechanism of BMP8A in renal cell proliferation and drug tolerance is not clear. Here we showed that BMP8A was highly expressed in renal cell carcinoma, which suggests a poor prognosis of ccRCC. Promotion of cell proliferation and inhibition of apoptosis were detected by CCK-8 assay, Trypan Blue staining, flow cytometry and bioluminescence. BMP8A promoted resistance of As2 O3 by regulating Nrf2 and Wnt pathways in vitro and in vivo. Mechanistically, BMP8A enhanced phosphorylation of Nrf2, which, in turn, inhibited Keap1-mediated Nrf2 ubiquitination and, ultimately, promoted nuclear translocation and transcriptional activity of Nrf2. Nrf2 regulates the transcription of TRIM24 detected by ChIP-qPCR. BMP8A was highly expressed in ccRCC, which suggests a poor prognosis. BMP8A was expected to be an independent prognostic molecule for ccRCC. On the one hand, activated Nrf2 regulated reactive oxygen balance, and on the other hand, by regulating the transcription level of TRIM24, it was involved in the regulation of the Wnt pathway to promote the proliferation, invasion and metastasis of ccRCC and the resistance of As2 O3 . Taken together, our findings describe a regulatory axis where BMP8A promotes Nrf2 phosphorylation and activates TRIM24 to promote survival and drug resistance in ccRCC.

Preparation and anti-Raji lymphoma efficacy of a novel pH sensitive and magnetic targeting nanoparticles drug delivery system.

BACKGROUND: Non-Hodgkin's lymphoma (NHL) is a heterogeneous class of cancers that arises in lymph nodes or other lymphatic tissues, which causes many deaths worldwide and its incidence is increasing. METHODS: In this study, a pH-responsive DMSA-Fe3O4 magnetic nanoparticles (MNPs) covalently connect with ADM and As2O3 as a drug delivery system was invented to discuss the anticancer efficacy in non-Hodgkin's lymphoma (NHL) cell line--Raji. RESULTS: Detailedly, according to the chelation of ADM and Fe2+, the release rate of ADM was accelerated in acidic environment, and slowed down/blocked in neutral environment. The inhibitory effect to induce apoptosis of Fe3O4/As2O3+Doxil on Raji cells was obvious compared with that of single-drug group. Furthermore, the expression of Bcl-2 gene in Raji cells was suppressed under the action of MNPs. CONCLUSION: Taken together, the novel pH-responsive MNPs was proven to be a promising synergistic form of magnetic targeted drugs for clinical treatment of human Raji lymphoma.

Low dosage of arsenic trioxide (As2O3) inhibits angiogenesis in epithelial ovarian cancer without cell apoptosis.

Arsenic trioxide (As2O3) induces cell apoptosis and reduces the invasive and metastatic activities in various cancer types. However, the role of As2O3 in ovarian cancer angiogenesis remains unclear. In this study, we investigated the role of As2O3 in ovarian cancer angiogenesis and found that a low concentration of As2O3 causes no effects on epithelial ovarian cancer cell viability or apoptosis. Moreover, we found that As2O3-treated epithelial ovarian cancer cells demonstrate a reduced tube formation of endothelial cells in Matrigel. In addition, As2O3-treated epithelial ovarian cancer cells show a decreased VEGFA, VEGFR2 and CD31 mRNA expression. As per the underlying mechanisms involved in As2O3 treatment, we found that As2O3 inhibits VEGFA and VEGFR2 expression that thereby inhibits the VEGFA-VEGFR2-PI3K/ERK signaling pathway. This leads to a suppression in both VEGFA synthesis and angiogenesis-related gene expression. A decreased VEGFA synthesis and secretion also inhibits the VEGFA-VEGFR2-PI3K/ERK signaling pathway in human umbilical vein endothelial cells (HUVECs). In summary, our results may provide strategies for the use of As2O3 in the prevention of tumor angiogenesis.

Arsenic trioxide induces apoptosis and the formation of reactive oxygen species in rat glioma cells.

BACKGROUND: Arsenic trioxide (As2O3) has a dramatic therapeutic effect on acute promyelocytic leukemia (APL) patients. It can also cause apoptosis in various tumor cells. This study investigated whether As2O3 has an antitumor effect on glioma and explored the underlying mechanism. RESULTS: MTT and trypan blue assays showed that As2O3 remarkably inhibited growth of C6 and 9 L glioma cells. Cell viability decreased in glioma cells to a greater extent than in normal glia cells. The annexin V-FITC/PI and Hoechest/PI staining assays revealed a significant increase in apoptosis that correlated with the duration of As2O3 treatment and occurred in glioma cells to a greater extent than in normal glial cells. As2O3 treatment induced reactive oxygen species (ROS) production in C6 and 9 L cells in a time-dependent manner. Cells pretreated with the antioxidant N-acetylcysteine (NAC) showed significantly lower As2O3-induced ROS generation. As2O3 significantly inhibited the expression of the anti-apoptotic gene Bcl-2, and upregulated the proapoptotic gene Bax in both C6 and 9 L glioma cells in a time-dependent manner. CONCLUSIONS: As2O3 can significantly inhibit the growth of glioma cells and it can induce cell apoptosis in a time- and concentration-dependent manner. ROS were found to be responsible for apoptosis in glioma cells induced by As2O3. These results suggest As2O3 is a promising agent for the treatment of glioma.

A comprehensive analysis of Wnt/ß-catenin signaling pathway-related genes and crosstalk pathways in the treatment of As2O3 in renal cancer.

We aimed to investigate the effect of As2O3 treatment on Wnt/ß-catenin signaling pathway-related genes and pathways in renal cancer. Illumina-based RNA-seq of 786-O cells with or without As2O3 treatment was performed, and differentially expressed genes (DEGs) were identified using Cuffdiff software. TargetMine was utilized to perform Gene Ontology (GO) pathway and Disease Ontology enrichment analyses. Furthermore, TRANSFAC database and LPIA method were applied to select differentially expressed transcription factors (TFs) and pathways related to Wnt/ß-catenin signaling pathway, respectively. Additionally, transcriptional regulatory and pathway crosstalk networks were constructed. In total, 1684 DEGs and 69 TFs were screened out. The 821 up-regulated DEGs were mainly enriched in 67 pathways, 70 GO terms, and 46 disease pathways, while only 1 pathway and 5 GO terms were enriched for 863 down-regulated DEGs. A total of 18 DEGs (4 up-regulated and 14 down-regulated genes) were involved in the Wnt/ß-catenin signaling pathway. Among the 18 DEGs, 4 ones were TFs. Furthermore, 211 pathways were predicted to be linked to the Wnt/ß-catenin signaling pathway. In conclusion, As2O3 may have a significant effect on the Wnt/ß-catenin signaling pathway for renal cancer treatment. The potential key DEGs are expected to be used as therapeutic targets.

Arsenic Trioxide Suppressed Migration and Angiogenesis by Targeting FOXO3a in Gastric Cancer Cells.

Arsenic trioxide (As2O3), a traditional remedy in Chinese medicine, has been used in acute promyelocytic leukemia (APL) research and clinical treatment. Previous studies have shown that As2O3 exerts its potent antitumor effects in solid tumors by regulating cell proliferation and survival. The aim of this study was to investigate whether As2O3 inhibited gastric cancer cell migration and angiogenesis by regulating FOXO3a expression. We found that As2O3 reduced gastric cancer cell viability in a dose-dependent manner and also inhibited cell migration and angiogenesis in vitro. Western blotting and immunofluorescence showed that As2O3 downregulated the levels of p-AKT, upregulated FOXO3a expression in the nucleus, and attenuated downstream Vascular endothelial growth factor (VEGF) and Matrix metallopeptidase 9 (MMP9) expression. Moreover, we demonstrated that knockdown of FOXO3a significantly reversed the inhibition of As2O3 and promoted cell migration and angiogenesis in vitro. Further, As2O3 significantly inhibited xenograft tumor growth and angiogenesis by upregulating FOXO3a expression in vivo. However, knockdown of FOXO3a attenuated the inhibitory effect of As2O3 in xenograft tumors, and increased microvessel density (MVD) and VEGF expression. Our results demonstrated that As2O3 inhibited migration and angiogenesis of gastric cancer cells by enhancing FOXO3a expression.

(-)-Epicatechin rescues the As2 O3 -induced HERG K+ channel deficiency possibly through upregulating transcription factor SP1 expression.

(-)-Epicatechin (EPI) has beneficial effects on the cardiovascular disease. The human ether-a-go-go-related gene (HERG) potassium channel is crucial for repolarization of cardiac action potential. Dysfunction of the HERG channel can cause long QT syndrome type 2 (LQT2). Arsenic trioxide (As2 O3 ) has shown efficacy in the treatment of acute promyelocytic leukemia. However, As2 O3 can induce the deficiency of HERG channel and cause LQT2. In this study, we examined whether EPI could rescue the As2 O3 -induced HERG channel deficiency. We found that 3 µM EPI obviously increased protein expression and current of HERG channel. EPI was able to recover the protein expression and current of HERG channel disrupted by As2 O3 . EPI was able to increase the expression of SP1 protein and recover the expression of SP1 protein disrupted by As2 O3 . In addition, EPI significantly shortened action potential duration prolonged by As2 O3 . Our data suggest that EPI rescues As2 O3 -induced HERG channel deficiency through upregulating SP1 expression.

As2 O3 combined with leflunomide prolongs heart xenograft survival via suppressing the response of Th1, Th2, and B cells in a rat model.

Xenotransplantation remits the severe shortage of human organs and tissues for transplantation, which is a problem that severely limits the application of transplantation to the treatment of human disease. However, severe immune rejection significantly limits the efficacy of xenotransplantation. In this study, we systematically investigated the immunosuppressive effect and mechanism of action of As2 O3 and leflunomide using a hamster-to-rat heart xenotransplantation model. We initially examined heart xenograft survival following As2 O3 and leflunomide treatment alone or combined treatment. We found that treatment with As2 O3 combined with leflunomide can significantly prolong the survival of heart xenograft by inhibiting Th1 and Th2 differentiation and reducing the production of IgG and IgM. Interestingly, As2 O3 and leflunomide showed low toxicity to the organs of the recipient. Taken together, these observations indicate that treatment with As2 O3 combined with leflunomide may be a promising immunosuppressive schedule for xenotransplantation.

Cathepsin L silencing enhances arsenic trioxide mediated in vitro cytotoxicity and apoptosis in glioblastoma U87MG spheroids.

Despite improved treatment options, glioblastoma multiforme (GBM) remains the most aggressive brain tumour with the shortest post-diagnostic survival. Arsenite (As2O3) is already being used in the treatment of acute promyelocytic leukaemia (APL), yet its effects on GBM have not been evaluated in detail. In U87MG cell monolayers, we have previously shown that arsenite cytotoxicity significantly increases upon transient inhibition of lysosomal protease Cathepsin L (CatL). As multicellular spheroids more closely represent in vivo tumours, we aimed to evaluate the impact of permanent CatL silencing on arsenite treatment in U87MG spheroids. CatL was stably silenced using shRNA expression plasmid packed lentiviruses. By using metabolic- and cell viability assays, we demonstrated that long-term CatL silencing significantly increased arsenite cytotoxicity in U87MG spheroids. Silenced CatL also increased arsenite-mediated apoptosis in spheroids via elevated p53 expression, Bax/Bcl2 ratio and caspase 3/7 activity, though with lower efficacy than in monolayers. Arsenite cytotoxicity was enhanced by lower CatL activity, since similar cytotoxicity increase was also observed using the novel CatL inhibitor AT094. The results have significant translational impact, since stable CatL silencing would enable the application of lower systemic doses of arsenite to achieve the desired cytotoxic effects on GBMs in vivo.

FTIR microspectroscopic study of gastric cancer AGS cells apoptosis induced by As2O3.

As2O3 has shown significant anti-gastric cancer effects, but the mechanism is still unclear. Thus, biomacromolecular changes induced by As2O3 were investigated by using human gastric cancer AGS cells as the model. Flow cytometry results confirmed that As2O3 induced AGS cells apoptosis. Fourier transform infrared (FTIR) microspectroscopy detected biomacromolecular changes during As2O3-induced AGS cells apoptosis sensitively: IR spectra showed significant changes in the lipids content and the proteins and DNA structure. Peak-area ratios indicated obvious changes in the lipids and DNA content and the proteins structure, while also showing a relatively good linear relationship between A1733/A969 and the apoptosis rate. PCA exhibited significant alteration in nucleic acids while curve fitting further revealed the changes in nucleic acids and proteins. On the whole, our study explored As2O3-induced gastric cancer cells apoptosis in depth on the basis of analyzing biomacromolecular changes, in addition, it also suggested FTIR microspectroscopy to be possibly useful in the research of apoptosis.

Long-term prognosis of childhood acute promyelocytic leukaemia with arsenic trioxide administration in induction and consolidation chemotherapy phases: a single-centre experience.

OBJECTIVES: The efficacy of all-trans retinoic acid (ATRA) and arsenic trioxide (As2 O3 ) as induction therapy for adult acute promyelocytic leukaemia (APL) has been documented in several clinical trials. However, the role of ATRA/As2 O3 combination in induction and consolidation therapy in children remains unclear. Here, we report the efficacy of combined treatment with As2 O3 and ATRA as induction and consolidation chemotherapy to treat newly diagnosed childhood APL. METHODS: From 1998 to 2011, 43 children with newly diagnosed APL received induction and consolidation chemotherapy with ATRA and As2 O3 (Protocol B). Rates of complete remission (CR), event-free survival (EFS), disease-free survival (DFS), and overall survival (OS) and drug toxicity were compared between children treated with Protocol B and 25 others treated previously with ATRA alone as induction chemotherapy (Protocol A). RESULTS: Of 43 patients treated with Protocol B, 41 (95.4%) achieved CR (two died of intracranial haemorrhage on day 10 and 14). In contrast, only 20 (80%) of 25 patients treated with Protocol A achieved CR. Thus, the CR rate was significantly lower in patients receiving induction chemotherapy with Protocol A than in those treated with Protocol B (P = 0.045, χ(2) = 6.508). Of the 41 patients who achieved CR on induction therapy with Protocol B, 40 also received consolidation therapy. Molecular relapse, but no overt morphological relapse, occurred in one patient at 25 months after diagnosis; this patient regained CR status with As2 O3 treatment. With a median follow-up period of 75 months, estimated EFS, DFS and OS rates were 92.5 ± 4.2%, 97.1 ± 2.9% and 95.3 ± 3.2%, respectively, for Protocol B. In contrast, with a median follow-up of 127 months, the EFS, DFS and OS rates at 75 months were 70.4 ± 9.4%, 76.4 ± 9.2% and 70.4 ± 9.4%, respectively, for Protocol A. Thus, patients treated with Protocol A showed significantly lower EFS (P = 0.021) and OS (P = 0.007) rates than those treated with Protocol B. CONCLUSIONS: Application of As2 O3 and ATRA as induction and consolidation chemotherapy resulted in excellent outcomes and improved long-term prognosis in children with newly diagnosed APL.

Curcumin combined with arsenic trioxide in the treatment of acute myeloid leukemia: network pharmacology analysis and experimental validation.

PURPOSE: This study aimed to evaluate the effects of curcumin by co-administration of arsenic trioxide (As2O3) in acute myeloid leukemia (AML) treatment, using network pharmacology and experimental validation. METHODS: Using Pubchem database, Traditional Chinese Medicine Information Database (TCMID) database, and Swiss target prediction database to predict compound-related targets, AML-associated targets were determined using GeneCards and Online Mendelian Inheritance in Man (OMIM) databases. We identify overlapping common targets by comparing Compounds-related and AML-associated targets and using these targets to perform GO and KEGG functional enrichment analyses. Subsequently, these targets were input into the STRING database, and we used Cytoscape to construct protein-protein interaction (PPI) network. Finally, we used KG1-a cells and the AML mouse model to measure the anti-leukemia effects of curcumin and As2O3 and their combination. RESULTS: Compounds and targets screening hinted that 85 intersection targets were predicted in the curcumin treatment of AML, 75 targets in the As2O3 treatment of AML, and 48 targets in the curcumin combined with the As2O3 treatment of AML. GO and KEGG analyses indicated that the top 10 enriched biological processes and top 20 pathways implicated in the therapeutic effects of curcumin and As2O3 on AML, respectively. In addition, network pharmacology screening revealed STAT3, TP53, EP300, MAPK1, and PIK3CA as the top five genes in PPI network of curcumin treatment of AML and TP53, MAPK3, MAPK1, STAT3, and SRC as the top five genes in PPI network of As2O3 treatment of AML. Moreover, the in vitro experiment demonstrated that curcumin combined with As2O3 inhibited proliferation and induced apoptosis in KG1-a cells, and this effect is more substantial than curcumin or As2O3 alone. Mechanistically, the curcumin combined with As2O3 significantly down-regulated the protein expression of JAK2, STAT3, and Bcl-2, and up-regulated the levels of P53, P27, and Bax. In the mouse model, the survival time of mice in each administration group was drawn out to varying degrees, with the most significant prolongation in the curcumin combined with the As2O3 group. CONCLUSION: Our results suggested that curcumin and As2O3 combination therapy exerts more significant anti-leukemia effects in the treatment of AML than curcumin or As2O3 monotherapy by up-regulating p53 pathway and down-regulating the JAK2/STAT3 pathway.

MDM2-mediated Inhibitory Effect of Arsenic Trioxide on Small Cell Lung Cancer Cell Line by Degrading Mutant p53.

INTRODUCTION: Small cell lung cancer (SCLC) is featured by a high TP53 mutant rate. Our previous research found that arsenic trioxide (As2O3) could significantly inhibit the growth and metastasis of SCLC. Studies have shown that the degradation of mutant p53 mediated by murine double minute 2 (MDM2) can be induced by As2O3, which probably contributes to the inhibition of SCLC, but the detailed mechanism is still unclear. We aimed to testify that As2O3 can inhibit the growth of SCLC cells by degrading mutant p53 protein via binding to MDM2. METHODS: CCK-8 assay, cell cycle analysis, and western blot of apoptosis markers were used to evaluate the inhibitory effect of As2O3 on NCI-H446 cells (containing mutant p53) and NCI-H1299 cells (p53 null). The effects of As2O3 on p53 and its downstream proteins were identified by western blot using mut-p53-knockdown and overexpressed cell models. MDM2-knockdown cell models were constructed, and western blot, co-IP of mut-p53, and ubiquitin were carried out to explore the mediating effect of MDM2 in As2O3 induced mut-p53 degradation. RESULTS: As2O3 inhibited proliferation and induced cell cycle arrest and apoptosis of SCLC cells in a dose- and timedependent manner. After mut-p53 knockdown or overexpressed, the inhibitory effect of As2O3 was dampened or enhanced. Additionally, As2O3-induced mut-p53 ubiquitination was significantly weakened after MDM2 knockdown. CONCLUSION: As2O3 could inhibit SCLC cells by inhibiting proliferation and inducing cell cycle arrest and apoptosis. These inhibitory effects were achieved at least in part by upregulating MDM2, which, in turn, promotes ubiquitination and degradation of mut-p53.

Decoration of Poly-3-methyl Aniline with As(III) Oxide and Hydroxide as an Effective Photoelectrode for Electroanalytical Photon Sensing with Photodiode-like Behavior.

This study achieved the decoration of poly-3-methyl aniline (P3MA) with As2O3-As(OH)3 using K2S2O8 and NaAsO2 on the 3-methyl aniline monomer. This resulted in a highly porous nanocomposite polymer composite with wide absorption optical behavior, an average crystalline size of 22 nm, and a 1.73 eV bandgap. The photoelectrode exhibited a great electrical response for electroanalytical applications, such as photon sensing and photodiodes, with a Jph of 0.015 mA/cm2 and Jo of 0.004 mA/cm2. The variable Jph values ranged from 0.015 to 0.010 mA/cm2 under various monochromatic filters from 340 to 730 nm, which demonstrates high sensitivity to wavelengths. Effective photon numbers were calculated to be 8.0 × 1021 and 5.6 × 1021 photons/s for these wavelength values, and the photoresponsivity (R) values were 0.16 and 0.10 mA/W, respectively. These high sensitivities make the nanocomposite material a promising candidate for use in photodetectors and photodiodes, with potential for commercial applications in highly technological systems and devices. Additionally, the material opens up possibilities for the development of photodiodes using n- and p-type materials.

Unraveling the capture mechanism of gaseous As2O3 over H-ZSM-5 zeolite from coal-fired flue gas: Experimental and theoretical insights.

Gaseous As2O3 discharged from coal-fired power plants results in severe detriments to the ecological environment. It is of great urgency to develop highly efficient As2O3 capture technology for reducing atmospheric arsenic contamination. Utilizing solid sorbents for gaseous As2O3 capture is a promising treatment for As2O3 capture. The zeolite of H-ZSM-5 was applied for As2O3 capture at high temperatures of 500-900 °C. Special attention was paid to clarifying its capture mechanism and identifying the influence of flue gas components via density functional theory (DFT) calculations and ab initio molecular dynamics (AIMD) simulations. Results revealed that due to high thermal stability with large specific areas, H-ZSM-5 demonstrated excellent arsenic capture at 500-900 °C. The captured arsenic consisted of As3+ and As5+ speciations, ascribed to As2O3 adsorption and oxidation. Moreover, As3+ and As5+ compounds were both through physisorption or chemisorption at 500-600 °C while dominant chemisorption at 700-900 °C. In particular, As3+ compounds were much more steadily fixed in products at all operating temperatures. Combining the characterization analysis and DFT calculations, it further verified that both Si-OH-Al groups and external Al species of H-ZSM-5 could chemisorb As2O3, and the latter exhibited much stronger affinities via orbital hybridization and electron transfer. The introduced O2 could facilitate As2O3 oxidation and fixation in H-ZSM-5, especially at a lower concentration of 2%. Additionally, H-ZSM-5 possessed great acid gas resistance for As2O3 capture under the concentration of NO or SO2 less than 500 ppm. AIMD simulations further identified that compared to NO and SO2, As2O3 was far more competitive and occupied the active sites of the Si-OH-Al groups and external Al species of H-ZSM-5. Overall, it demonstrated that H-ZSM-5 is a promising sorbent for As2O3 capture from coal-fired flue gas.

Arsenic adsorption enhancement performances of Mn-modified γ-Al2O3 with flue gas constituents involved.

Some flue gas constituents have negative effects on As2O3 adsorption of γ-Al2O3 so promoting arsenic adsorption performances under complicated flue gas conditions is necessary based on previous studies. In this study, γ-Al2O3 is modified with manganous nitrate and then Mn-modified γ-Al2O3 is used as the adsorbents in experiments. Besides, molecular dynamics (MD) simulations and density functional theory (DFT) calculations are performed to explore mechanisms of how loadings of Mn enhance arsenic adsorption features of γ-Al2O3 when being affected by flue gas constituents in microscale and mesoscale, respectively. As for DFT calculations, it is uncovered that electron transfer/interaction among As2O3, flue gas constituents and Mn-modified γ-Al2O3 mostly influences arsenic adsorption. For MD simulations, it is expounded that the collision and aggregation of As2O3 and flue gas constituent molecules have most impact on arsenic adsorption. As far as experiments are concerned, they are conducted to show the macroscopic characterizations of arsenic adsorption performances, corresponding to results of DFT calculations and MD simulations. The understanding of these three different aspects could supply significant references for utilization of Mn-modified γ-Al2O3 in real industries to remove arsenic under complex flue gas conditions.