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Urothelial carcinoma (UC) is prevalent, especially in elderly males. The high rate of recurrence, treatment regime, and follow-up monitoring make UC a global health and economic burden. Arsenic is a ubiquitous toxicant that can be found in drinking water, and it is known that exposure to arsenic is associated with UC development. Around 25% of diagnosed UC cases are muscle-invasive (MIUC) which have poor prognosis and develop chemoresistance, especially if tumors are associated with squamous differentiation (SD). The immortalized UROtsa cell line is derived from normal human urothelium and our lab has malignantly transformed these cells using arsenite (As3+). These cells represent a basal subtype model of MIUC and the tumors derived from the As3+-transformed cells histologically and molecularly resemble clinical cases of the basal subtype of MIUC that have focal areas SD and expression of the basal keratins (KRT1, 5, 6, 14, and 16). Our previous data demonstrate that KRT6 protein expression correlates to areas of SD within the tumors. For this study, we performed a lentiviral knockdown of KRT6 in As3+-transformed UROtsa cells to evaluate the effects on morphology, gene/protein expression, growth, colony formation, and cisplatin sensitivity. The knockdown of KRT6 resulted in decreased expression of the basal keratins, decreased growth, decreased colony formation, and increased sensitivity to cisplatin, the standard treatment for MIUC. The results of this study suggest that KRT6 plays a role in UC cell growth and is an exploitable target to increase cisplatin sensitivity for MIUC tumors that may have developed resistance to cisplatin treatment. [ABSTRACT FROM AUTHOR]

Stress granules (SGs) are non-membranous organelles composed of mRNA and proteins that assemble in the cytosol when the cell is under stress. Although the composition of mammalian SGs is both cell-type and stress-dependent, they consistently contain core components, such as Ras GTPase activating protein SH3 domain binding protein 1 (G3BP1). Upon stress, living cells rapidly assemble micrometric SGs, sometimes within a few minutes, suggesting that SG components may be actively transported by the microtubule and/or actin cytoskeleton. Indeed, SG assembly has been shown to depend on the microtubule cytoskeleton and the associated motor proteins. However, the role of the actin cytoskeleton and associated myosin motor proteins remains controversial. Here, we identified G3BP1 as a novel binding protein of unconventional myosin-5a (Myo5a). G3BP1 uses its C-terminal RNA-binding domain to interact with the middle portion of Myo5a tail domain (Myo5a-MTD). Suppressing Myo5a function in mammalian cells, either by overexpressing Myo5a-MTD, eliminating Myo5a gene expression, or treatment with myosin-5 inhibitor, inhibits the arsenite-induced formation of both small and large SGs. This is different from the effect of microtubule disruption, which abolishes the formation of large SGs but enhances the formation of small SGs under stress conditions. We therefore propose that, under stress conditions, Myo5a facilitates the formation of SGs at an earlier stage than the microtubule-dependent process. [ABSTRACT FROM AUTHOR]

A growing body of evidence suggests that long-term arsenic exposure can induce liver injury. Our previous studies have demonstrated that liver injury occurs in arsenic-poisoning patients and arsenic-exposed rats. However, therapeutic targets are still unclear, and there is a lack of effective drugs. This study aimed to investigate the effects of sodium arsenite (arsenite) exposure on hepatocyte senescence and the intervention effect of ginkgo biloba extract in rats. In this study, 24 male Sprague–Dawley rats (weighing 180–200 g) were randomized into three groups. The control group received a normal diet, and the arsenic-exposed group was given 10 mg/L arsenite for 3 months by free drinking along with a normal diet. The ginkgo biloba extract treatment group was consecutively administered EGb761 (10 mg/kg, by gavage) for 1 month following 2 months of arsenite exposure. Our results showed that exposure to 10 mg/L arsenite induced narrowing of the hepatic sinus space, enlargement of hepatocytes, and increased multinucleated hepatocytes and inflammatory cell infiltration in rat liver tissue compared with the normal control group. Moreover, 10 mg/L arsenite also caused abnormal expression of inflammation-related indices (IL1-β, IL-6, TNF-α), oxidative damage-related indices (SOD, MDA, GPx), and senescence-related proteins (p16, p-p53, E2F1). EGb761 could effectively reduce the pathological damage of liver tissue and antagonize the abnormal expression of liver tissue inflammation and oxidative damage-related indices as well as cellular senescence-related proteins caused by arsenite exposure. Notably, EGb761 reduced the accumulation of arsenic in rat liver tissues. These results suggested that EGb761 could effectively alleviate subchronic arsenic exposure-induced senescence of hepatocytes, which may be achieved partially through inhibiting inflammation and oxidative damage in rats. This study may provide a new therapeutic target for arsenic-induced liver injury. [ABSTRACT FROM AUTHOR]

The ex-situ treatment of arsenic is widely adopted; however, there are emerging concerns related to system maintenance, material replacement, and waste generation. There is a scope to explore in-situ arsenite [As (III)] remediation in the aquifers. The main objective of this study is to evaluate the performance of in-situ synthesised FeS in immobilising As (III) in the natural groundwater when transported through a three-dimensional (3-D) porous media system. In this study, a 3-D tank of 0.50 m × 0.30 m × 0.30 m (L × W × H) was packed with natural sand to represent the subsurface porous media system. The homogeneous packing and uniform flow were ensured before synthesising FeS in-situ, where a total of 1.5 pore volumes (PVs) of 20 mM sodium sulfide (Na2S) and 20 mM ferrous sulfate (FeSO4) reagent solutions were injected alternatively into the pre-saturated porous media. Finally, 300 ± 15 μg/L of As (III) spiked natural groundwater was passed through the porous media, and the samples were collected through several sampling ports for analysing for total As and Fe. The result suggests that the concentration of As (III) reaches below 11 μg/L within 644 min (4 PVs) of injection of reagents. Furthermore, almost 88.4% of As (III) get immobilised after passing 31 PVs of contaminated water. In brief, almost 406 L of As contaminated groundwater can be treated by injecting 21 L of reagents with a reagent-to-treated water ratio of 1:20. [ABSTRACT FROM AUTHOR]

Various stress conditions, such as heat stress (HS) and oxidative stress, can cause biomolecular condensates represented by stress granules (SGs) via liquid-liquid phase separation. We have previously shown that Hsp90 forms aggregates in response to HS and that Hsp90 aggregates transiently co-localize with SGs as visualized by Pabp. Here, we showed that arsenite, one of the well-described SG-inducing stimuli, induces Hsp90 aggregates distinct from conventional SGs in fission yeast. Arsenite induced Hsp90 granules in a dose-dependent manner, and these granules were significantly diminished by the co-treatment with a ROS scavenger N-acetyl cysteine (NAC), indicating that ROS are required for the formation of Hsp90 granules upon arsenite stress. Notably, Hsp90 granules induced by arsenite do not overlap with conventional SGs as represented by eIF4G or Pabp, while HS-induced Hsp90 granules co-localize with SGs. Nrd1, an RNA-binding protein known as a HS-induced SG component, was recruited into Hsp90 aggregates but not to the conventional SGs upon arsenite stress. The non-phosphorylatable eIF2α mutants significantly delayed the Hsp90 granule formation upon arsenite treatment. Importantly, inhibition of Hsp90 by geldanamycin impaired the Hsp90 granule formation and reduced the arsenite tolerance. Collectively, arsenite stimulates two types of distinct aggregates, namely conventional SGs and a novel type of aggregates containing Hsp90 and Nrd1, wherein Hsp90 plays a role as a center for aggregation, and stress-specific compartmentalization of biomolecular condensates.

In this study, two chemosensors, N5R1 and N5R2, based on 5‐(4‐nitrophenyl)‐2‐furaldehyde, with varying electron‐withdrawing groups, were synthesized and effectively employed for the colorimetric selective detection of arsenite anions in a DMSO/H2O solvent mixture (8 : 2, v/v). Chemosensors N5R1 and N5R2 exhibited a distinct color change upon binding with arsenite, accompanied by a spectral shift toward the near‐infrared region (Δλmax exceeding 200 nm). These chemosensors established stability between a pH range 6–12. Among them, N5R2 displayed the lowest detection limit of 17.63 ppb with a high binding constant of 2.6163×105 M−1 for arsenite. The binding mechanism involved initial hydrogen bonding between the NH binding site and the arsenite anion, followed by deprotonation and an intramolecular charge transfer (ICT) mechanism. The mechanism was confirmed through UV and 1H NMR titrations, cyclic voltammetric studies, and theoretical calculations. The interactions between the sensor and arsenite anions were further analyzed using global reactivity parameters (GRPs). Practical applications were demonstrated through the utilization of test strips and molecular logic gates. Real water samples, honey, and milk samples were successfully analyzed by both chemosensors for the sensing of arsenite. [ABSTRACT FROM AUTHOR]

Heavy metal poisoning is the most prevalent health hazard at hazardous waste sites, affecting a large population on daily basis, with arsenite poisoning ranking third in terms of prevalence and severity. Therefore, the main objective of this study is to develop a novel, highly efficient sensor for detecting trace amounts of arsenite (AsIII) in human serum by utilising reduced graphene oxide/gold nanoparticles (rGO/AuNPs) based nanocomposite structure. In this work, a screen-printed carbon electrode (SPE) was modified using rGO/AuNPs nanocomposite to detect AsIII in human serum. The detection data were recorded and analysed using Cyclic Voltammetry (CV) and Differential Pulse Voltammetry (DPV), whereas transmission electron microscope (TEM), scanning electron microscope (SEM) as well as Fourier transform infrared (FTIR) spectroscopy were used to determine the surface morphological features and the presence of significant elements/groups in the prepared nanocomposite structure. Under the optimised conditions, the linear regression coefficient (R2) for the DPV response of the fabricated electrode (rGO/AuNPs@SPE) was observed to be 0.98. The rGO/AuNPs@SPE demonstrated remarkable sensor response for AsIII with detection limits of 10 ppb via DPV in standard samples, due to the synergistic effect of rGO and AuNPs based nanocomposite. The sensitivity of the sensor was found to be 0.0142 Appb−1cm−2 for 100–1000 ppb concentration range of AsIII. The rGO/AuNPs@SPE sensor also displayed good stability and reproducibility when used in AsIII spiked human serum samples in which the limit of detection was observed at 100ppb. The porous structure of rGO on the sensing interface efficiently improves the electrode's adsorption and conductivity, while citrate capped AuNPs offer the functional groups required for maximum adsorption of AsIII. Hence, the developed electrochemical sensor (rGO/AuNPs@SPE) can be used very precisely and reliably in various applications for trace level detection of AsIII in human serum. [ABSTRACT FROM AUTHOR]

Arsenic poisoning of groundwater is one of the most critical environmental hazards on Earth. Therefore, the practical and proper treatment of arsenic in water requires more attention to ensure safe drinking water. The World Health Organization (WHO) sets guidelines for 10 μg/L of arsenic in drinking water, and direct long-term exposure to arsenic in drinking water beyond this value causes severe health hazards to individuals. Numerous studies have confirmed the adverse effects of arsenic after long-term consumption of arsenic-contaminated water. Here, technologies for the remediation of arsenic from water are highlighted for the purpose of understanding the need for a single-point solution for the treatment of As(III)-contaminated water. As(III) species are neutral at neutral pH; the solution requires transformation technology for its complete removal. In this critical review, emphasis was placed on single-step technologies with multiple functions to remediate arsenic from water. [ABSTRACT FROM AUTHOR]

Present study deals with the role of gamma irradiation in modulating arsenic bioremediation of Pseudomonas sp. AK1 and AK9 strains The bacterial strains AK1 and AK9 of Pseudomonas sp. were irradiated at different doses (5 Gy, 10 Gy, 15 Gy and 20 Gy) of gamma irradiation. The effect of γ-irradiation on the growth and arsenic modulating ability of AK1 and AK9 strains was determined in the presence and absence of arsenic along with non-irradiated strains. Further, a comparative study of non-irradiated and irradiated strains by protein profiling in absence and presence of arsenic was carried out to confirm of the increased expression ofarsenite oxidase. Both strains were able to transform AsIII to AsV. Both strains AK1 and AK9 decrease the arsenic concentration by 626.68 ppb (13.36%) and 686.40 ppb (14.71%) after an incubation period of 96 h in presence of arsenic. Gamma irradiated AK9 strains showed doubled growth in presence of arsenic as compared to non-irradiated strains at 10 Gy treatment whereas no changes in growth was observed in irradiated AK1 strains. Gamma irradiated AK9 strain decrease 378.65 ppb (7.27%) more arsenic concentration from natural water sample supplemented with AsIII than non-irradiated AK9 strain. Further, in the protein profile, increased expression of arsenite oxidase (∼85 kDa) was observed in irradiated AK9 strains in presence of arsenic. Overall, the results suggested that the gamma irradiated AK9 strain having potential for arsenic accumulation and increased arsenite tolerance may play a great role in the bioremediation of the arsenite at arsenic contaminated sites. [ABSTRACT FROM AUTHOR]

The leaching of contaminants is a complex, pivotal process for understanding how biochar can immobilize them effectively. In this study, we investigated the impact of biochar, produced at different temperatures, on the behavior of arsenic (As) and lead (Pb) in leached sediments. Before leaching, we combined biochar with sediment, allowing it to naturally age for 365 days. The biochar derived from sugarcane straw was pyrolyzed at 350 °C (BC350), 550 °C (BC550), and 750 °C (BC750). Using UV–Vis spectroscopy, we assessed changes in dissolved organic carbon quality and examined geochemical alterations employing high-performance liquid chromatography–inductively coupled plasma mass spectrometry (HPLC–ICP-MS). The addition of biochar decreased Pb mobility while increasing As mobility. The extent of immobilization varied depending on the pyrolysis temperature: BC750 notably reduced Pb leaching by 54%, whereas BC350 enhanced As mobility by 2.5 times. Although no leaching of monomethylarsonic or dimethylarsinic acids occurred, both BC350 and BC750 amplified As3+ leaching by 2.5 times. In summary, biochar addition at different temperatures altered the environmental fate of As and Pb. Higher pyrolysis temperatures, as seen with BC750, were more effective in mitigating Pb mobility, reducing sediment leaching by 54%. Interestingly, exogenous dissolved organic carbon and phosphorus promoted As leaching.Highlights: Biochar temp influenced As/Pb mobility in sediment. 750 °C pyrolysis notably reduced Pb leaching by 54%. Lower temperature (350 °C) increased As mobility 2.5 times. External carbon/phosphorus boosted As leaching. 550 °C biochar was more effective against As3+ leaching. [ABSTRACT FROM AUTHOR]

Inorganic arsenic is a well-known environmental toxicant, and exposure to this metalloid is strongly linked with severe and extensive toxic effects in various organs including the lungs. In the present study, we aimed to investigate the acute and chronic effects of arsenite exposure on pulmonary tissue in young and adult mice. In brief, young and adult female Balb/C mice were exposed to 3 and 30 ppm arsenite daily via drinking water for 30 and 90 days. Subsequently, the animals were sacrificed and various histological and immunohistochemistry (IHC) analyses were performed using lung tissues. Our findings showed arsenite was found to cause dose-dependent pathological changes such as thickening of the alveolar septum, inflammatory cell infiltrations and lung fibrosis in young and adult mice. In addition, arsenite exposure significantly increased the expression of inflammatory markers NF-κB and TNF-α, indicating that arsenite-exposed mice suffered from severe lung inflammation. Moreover, the IHC analysis of fibrotic proteins demonstrated an increased expression of TGF-β1, α-SMA, vimentin and collagen-I in the arsenite-exposed mice compared to the control mice. This was accompanied by apoptosis, which was indicated by the upregulated expression of caspase-3 in arsenite-exposed mice compared to the control. Adult mice were generally found to be more prone to arsenite toxicity during chronic exposure relative to their younger counterparts. Overall, our findings suggest that arsenite in drinking water may induce dose-dependent and age-dependent structural and functional impairment in the lungs through elevating inflammation and fibrotic proteins. [ABSTRACT FROM AUTHOR]

Arsenic is a widespread carcinogen and an important etiological factor for lung cancer. Dysregulated miRNAs have been implicated in arsenic carcinogenesis and the mechanisms of arsenic-induced dysregulated miRNAs have not been fully elucidated. N6-methyladenosine (m6A) modification is known to modulate pri-miRNA processing. However, whether m6A-mediated pri-miRNA processing is involved in arsenic carcinogenesis is poorly understood. Here, we found that m6A modification was significantly increased in arsenite-transformed human bronchial epithelial BEAS-2B cells (0.5 µM arsenite, 16 weeks). Meanwhile, METTL3 was significantly upregulated at week 12 and 16 during cell transformation. The proliferation, migration, invasion, and anchorage-independent growth of arsenite-transformed cells were inhibited by the reduction of m6A levels through METTL3 knockdown. Further experiments suggest that the oncogene miR-106b-5p is a potentially essential m6A target mediating arsenic-induced lung cancer. miR-106b-5p was observed to be upregulated after exposure to arsenite for 12 and 16 weeks, and the reduction of m6A levels caused by METTL3 knockdown inhibited miR-106b-5p maturation in arsenite-transformed cells. What’s more, miR-106b-5p overexpression successfully rescued METTL3 knockdown-induced inhibition of the neoplastic phenotypes of transformed cells. Additionally, Basonuclin 2 (BNC2) was uncovered as a potential target of miR-106b-5p and downregulated by METTL3 via enhancing miR-106b-5p maturation. Additionally, the METTL3 inhibitor STM2457 suppressed neoplastic phenotypes of arsenite-transformed BEAS-2B cells by blocking pri-miR-106b methylation. These results demonstrate that m6A modification promotes the neoplastic phenotypes of arsenite-transformed BEAS-2B cells through METTL3/miR-106b-5p/BNC2 pathway, providing a new prospective for understanding arsenic carcinogenesis.

Chronic arsenic exposure is considered to increase the risk of breast cancer. p62 is a multifunctional adaptor protein that controls myriad cellular processes and is overexpressed in breast cancer tissues. Although previous studies have indicated the involvement of p62 accumulation in arsenic tumorigenesis, the underlying mechanism remains obscure. Here, we found that 0.1 µM or 0.5 µM arsenite exposure for 24 weeks induced oncogenic phenotypes in human mammary epithelial cells. Elevated aerobic glycolysis, cell proliferation capacity, and activation of p62-mTOR pathway, as indicated by increased protein levels of p62, phosphorylated-mTOR (p-mTOR) and hypoxia-inducible factor 1α (HIF1α), were observed in chronically arsenite-exposed cells, and of note in advance of the onset of oncogenic phenotypes. Moreover, p62 silencing inhibited acquisition of oncogenic phenotypes in arsenite-exposed cells. The protein levels of p-mTOR and HIF1α, as well as aerobic glycolysis and cell proliferation, were suppressed by p62 knockdown. In addition, re-activation of p‑mTOR reversed the inhibitory effects of p62 knockdown. Collectively, our data suggest that p62 exerts an oncogenic role via mTORC1 activation and acts as a key player in glucose metabolism during arsenite-induced malignant transformation, which provides a new mechanistic clue for the arsenite carcinogenesis. [ABSTRACT FROM AUTHOR]

The use of probiotic lactobacilli has been proposed as a strategy to mitigate damage associated with exposure to toxic metals. Their protective effect against cationic metal ions, such as those of mercury or lead, is believed to stem from their chelating and accumulating potential. However, their retention of anionic toxic metalloids, such as inorganic arsenic, is generally low. Through the construction of mutants in phosphate transporter genes (pst) in Lactiplantibacillus plantarum and Lacticaseibacillus paracasei strains, coupled with arsenate [As(V)] uptake and toxicity assays, we determined that the incorporation of As(V), which structurally resembles phosphate, is likely facilitated by phosphate transporters. Surprisingly, inactivation in Lc. paracasei of PhoP, the transcriptional regulator of the two-component system PhoPR, a signal transducer involved in phosphate sensing, led to an increased resistance to arsenite [As(III)]. In comparison to the wild type, the phoP strain exhibited no differences in the ability to retain As(III), and there were no observed changes in the oxidation of As(III) to the less toxic As(V). These results reinforce the idea that specific transport, and not unspecific cell retention, plays a role in As(V) biosorption by lactobacilli, while they reveal an unexpected phenotype for the lack of the pleiotropic regulator PhoP. [ABSTRACT FROM AUTHOR]

As a notable toxic substance, metalloid arsenic (As) widely exists in water body and drinking As-contaminated water for an extended period of time can result in serious health concerns. Here, the performance of nanoscale zero-valent iron (nZVI) modified N-doped biochar (NBC) composites (nZVI@NBC) activated peroxydisulfate (PDS) for As(III) removal was investigated. The removal efficiencies of As(III) with initial concentration ranging from 50 to 1000 μg/L were above 99% (the residual total arsenic below 10 μg/L, satisfying the contaminant limit for arsenic in drinking water) within 10 min by nZVI@NBC (0.2 g/L)/PDS (100 μM). As(III) removal efficiency influenced by reaction time, PDS dosage, initial concentration, pH, co-existing ions, and natural organic matter in nZVI@NBC/PDS system were investigated. The nZVI@NBC composite is magnetic and could be conveniently collected from aqueous solutions. In practical applications, nZVI@NBC/PDS has more than 99% As(III) removal efficiency in various water bodies (such as deionized water, piped water, river water, and lake water) under optimized operation parameters. Radical quenching and EPR analysis revealed that SO4·− and ·OH play important roles in nZVI@NBC/PDS system, and the possible reaction mechanism was further proposed. These results suggest that nZVI@NBC activated peroxydisulfate may be an efficient and fast approach for the removal of water contaminated with As(III). [ABSTRACT FROM AUTHOR]

Arsenic in drinking water threatens public health worldwide. Phytoremediation has brought new vitality to solve this problem. The aim of this work was to study the role of emergent macrophyte sweet flag (Acorus calamus L.) in phytoremediation of arsenate [As(V)] and arsenite [As(III)] from polluted water. For that, the methods of analytic chemistry and physiology were used. The results showed that As(III) could be removed by A. calamus more efficiently than As(V). The removal efficiencies of As(V) and As(III) both reached more than 95%. In As(V)- and As(III)-exposed A. calamus, the arsenic contents were much higher in root than in stem and leaf. The translocation factors of As(V) and As(III) were no more than 0.152. Both As(V) and As(III) were found in the whole plant, whereas dimethylarsinic acid (DMA, 0.06‒0.13 mg kg‒1) was only present in the aboveground part. As(V) was the main species in the As(V)-exposed plants (45.86–70.21%). As(III) was the main species in stem and leaf of As(III)-exposed plants (55.76–85.52%), while As(V) was still dominant in root. A. calamus could keep its green leaves during the 31 days of inorganic arsenic (iAs) exposure. However, iAs had a little inhibitory effect on biomass accumulation, and high-concentration iAs was beneficial to promote root growth. The concentrations of malondialdehyde (MDA) and hydrogen peroxide (H2O2), as well as the activity of catalase (CAT) were significantly higher in root than those in stem and leaf. The oxidative stress response of A. calamus to As(III) was more than that to As(V). The findings of this study indicated that A. calamus was regarded as a promising material for the phytoremediation of arsenic from water.Highlights: calamus L. exhibited high tolerance to As(III) and As(V). As(III) can be methylated to DMA in the aboveground part of A. calamus L. Most of arsenic was accumulated in the roots. High-concentration iAs was beneficial to promote root growth. [ABSTRACT FROM AUTHOR]

In the present study, activated carbon decorated with zirconia nanoparticle composite (ZrO2/AC) have been prepared using hydrothermal method and then utilized as an adsorbent for the removal of arsenite from aqueous solution. The composite is composed of highly agglomerated ZrO2 particles on AC surface. The high surface area of the synthesized adsorbent results in its high adsorption capacity toward arsenite. Adsorption isotherm and kinetic data of arsenite adsorption process can be well fitted to the Langmuir isotherm with maximum monolayer adsorption capacity of 64.00 mg.g-1. The experimental results suggest that the adsorption process of arsenite onto ZrO2/AC material involves the formation of both outer-sphere and inner-sphere complexes between arsenite and adsorbent. The high adsorption ability toward arsenite as well as the high recyclable nature of this material makes it a potential alternative material for the removal of toxic heavy metals from wastewater. [ABSTRACT FROM AUTHOR]

The arsenic adsorption performance of silicon (Si), iron (Fe), and magnesium (Mg) mixed hydrous oxide containing a Si: Fe: Mg metal composition ratio of 0.05:0.9:0.05 (SFM05905) was investigated. SFM05905 was synthesized by the co-precipitation method. Batch experiments on arsenic adsorption were conducted at various temperatures and concentrations. Adsorption isotherms models were represented by a linearized equations and were insensitive to temperature change. The anion selectivity of SFM05905 at single component was high for arsenite (III), arsenate (V), and phosphate (PO4), indicating that PO4 inhibits arsenic adsorption. The adsorption amount of As (III), As (V), and PO4 were compared using a column packed with granular SFM05905, and an aqueous solution was passed by a combination of several anions that are single, binary, and ternary adsorbate systems. As (III) had the highest adsorption amount; however, As (III) and PO4 were affected by each other under the ternary mixing condition. Although the adsorption amount of As (V) was smaller than that of As (III), it was not affected by other adsorbates in the column experiments. Finally, although the adsorption of both arsenic continued, the adsorbed PO4 gradually desorbed. [ABSTRACT FROM AUTHOR]

Simple Summary: This study explores the potential use of retinoic acid in treating a severe form of bladder cancer, known as basal muscle-invasive bladder cancer (MIBC), which is among the deadliest cancers in the United States of America. All-trans retinoic acid (tretinoin), commonly used in the differentiation therapy of blood cancer, is investigated in this study for its efficacy against MIBC. By treating bladder cancer cells with tretinoin, the study aimed to determine whether it could diminish the aggressive behavior of these cells. The findings show promising results, suggesting that tretinoin can indeed make the basal muscle cancer cells less aggressive by reducing cell proliferation and increasing differentiation markers. This research could lead to new treatment approaches that improve survival chances for patients with basal muscle-invasive bladder cancer. Bladder cancer (BC) is the eighth most common cause of cancer death in the United States of America. BC is classified into non-muscle-invasive bladder cancer (NMIBC) and muscle-invasive bladder cancer (MIBC). Genetically, MIBCs are categorized into the more aggressive basal subtype or less aggressive luminal subtype. All-trans retinoic acid (tretinoin), the ligand for the RAR-RXR retinoic acid receptor, is clinically used as a differentiation therapy in hematological malignancies. This study aims to determine the effects of retinoic acid on arsenite-transformed malignant urothelial cells (UROtsa As), serving as a model for basal muscle-invasive bladder cancer. We treated three independent isolates of arsenite-transformed malignant human urothelial UROtsa cells (UROtsa As) with tretinoin for 48 h. Cell viability, proliferation, and apoptosis were analyzed using crystal violet staining and flow cytometry. mRNA and protein level analyses were performed using RT-qPCR and the Simple Western™ platform, respectively. Tretinoin was found to reduce cell proliferation and urosphere formation, as well as decrease the expression of basal markers (KRT1, KRT5, KRT6, EGFR) and increase the expression of luminal differentiation markers (GATA3, FOXA1). Mechanistically, the antiproliferative effect of tretinoin was attributed to the downregulation of c-myc. Our results suggest that targeting the retinoic acid pathway can diminish the aggressive behavior of basal muscle-invasive urothelial cancer and may enhance patient survival. [ABSTRACT FROM AUTHOR]

Arsenic is a well‐known environmental toxicant and emerging evidence suggests that arsenic exposure has potential skeletal muscle toxicity; however, the underlying mechanism has not yet been clarified. The aim of this study was to investigate the correlation among adverse effects of subchronic and chronic environmental arsenic exposure on skeletal muscle as well as specific myokines secretion and angiotensin II (AngII)–melatonin (MT) axis in rats. Four‐week‐old rats were exposed to arsenite (iAs) in drinking water at environmental relevant concentration of 10 ppm for 3 or 9 months. Results indicated that the gastrocnemius muscle had atrophied and its mass was decreased in rats exposed to arsenite for 9 months, whereas, they had no significant changes in rats exposed to arsenite for 3 months. The levels of serum‐specific myokine irisin and gastrocnemius muscle insulin‐like growth factor‐1 (IGF‐1) were increased in 3‐month exposure group and decreased in 9‐month exposure group, while serum myostatin (MSTN) was increased significantly in 9‐month exposure group. In addition, serum AngII level increased both in 3‐ and 9‐month exposure groups, while serum MT level increased in 3‐month exposure group and decreased in 9‐month exposure group. Importantly, the ratio of AngII to MT level in serum increased gradually with the prolongation of arsenite exposure. It showed a certain correlation between AngII–MT axis and gastrocnemius muscle mass, gastrocnemius muscle level of IGF‐1 or serum levels of irisin and MSTN. In conclusion, the disruption of AngII–MT axis balance may be a significant factor for skeletal muscle atrophy induced by chronic environmental arsenic exposure. [ABSTRACT FROM AUTHOR]

Arsenic (As) is a highly toxic metalloid that can be found in insufficiently purified drinking water and exerts adverse effects on the physiology of living organisms that can negatively affect human health after subchronic exposure, causing several diseases, such as liver damage. A high‐fat diet, which is increasing in frequency worldwide, can aggravate hepatic pathology. However, the mechanisms behind liver injury caused by the combinatory effects of As exposure and a high‐fat diet remain unclear. In this study, we investigated such underlying mechanisms by focusing on three different aspects: As biotransformation, pathological liver damage, and differential expression of signaling pathway components. We employed mice that were fed a regular diet or a high‐fat diet and exposed them to a range of arsenite concentrations (As(III), 0.05–50 mg/L) for 12 weeks. Our results showed that a high‐fat diet increased the absorption of As into the liver and enhanced liver toxicity, which became progressively more severe as the As concentration increased. Co‐exposure to a high‐fat diet and As(III) activated PI3K/AKT and PPAR signaling as well as fatty acid metabolism pathways. In addition, the expression of proteins related to lipid cell function, lipid metabolism, and the regulation of body weight was also affected. Our study provides insights into the mechanisms that contribute to liver injury from subchronic combinatory exposure to As and a high‐fat diet and showcases the importance of a healthy lifestyle, which may be of particular benefit to people living in areas with high As(III) concentrations, as a means to reduce or prevent aggravated liver damage. [ABSTRACT FROM AUTHOR]

Efficient removal of extremely mobile and toxic As(III) from water is a challenging but critical task. Herein, we developed a functionalized sorbent of chitosan nanofiber with iron–manganese (Fe-Mn@CS NF) using a one-step hybrid electrospinning approach to remove trace As(III) from water. Batch adsorption studies were performed to determine the adsorption efficiency under a variety of conditions, including contact time, starting concentration of As(III), ionic strength, and the presence of competing anions. The experimental results demonstrated that the concentration of As(III) dropped from 550 to less than 1.2 µg/L when using 0.5 g/L Fe-Mn@CS NF. This demonstrates the exceptional adsorption efficiency (99.8%) of Fe-Mn@CS NF for removing As(III) at pH 6.5. The kinetic tests revealed that the adsorption equilibrium was reached in 2.6 h, indicating a quick uptake of As(III). The ionic strength effect analysis showed that the adsorbed As(III) formed inner-sphere surface complexes with Fe-Mn@CS NF. The presence of SO42− or F− had a negligible impact on As(III) uptake, while the presence of PO43− impeded As(III) absorption by competing for adsorption sites. The exhausted sorbent could be effectively regenerated with a dilute NaOH solution. Even after 10 cycles of regenerating Fe-Mn@CS NF, the adsorption efficiency of As(III) in natural groundwater was maintained over 65%. XPS and FTIR analyses show that the presence of M–OH and C–O groups on the sorbent surface is essential for removing As(III) from water. Overall, our study highlights the significant potential of Fe-Mn@CS NF for the efficient and quick elimination of As(III) from water. [ABSTRACT FROM AUTHOR]

YTH N6-methyladenosine RNA binding protein 2 (YTHDF2) undergoes phase separation in response to the stimulation of high concentration of arsenite, suggesting that oxidative stress, the major mechanism of arsenite toxicity, may play a role in YTHDF2 phase separation. However, whether arsenite-induced oxidative stress is involved in phase separation of YTHDF2 has yet to be established. To explore the effect of arsenite-induced oxidative stress on YTHDF2 phase separation, the levels of oxidative stress, YTHDF2 phase separation, and N6-methyladenosine (m6A) in human keratinocytes were detected after exposure to various concentrations of sodium arsenite (0-500 µM; 1 h) and antioxidant N-acetylcysteine (0–10 mM; 2 h). We found that arsenite promoted oxidative stress and YTHDF2 phase separation in a concentration-dependent manner. In contrast, pretreatment with N-acetylcysteine significantly relieved arsenate-induced oxidative stress and inhibited YTHDF2 phase separation. As one of the key factors to YTHDF2 phase separation, N6-methyladenosine (m6A) levels in human keratinocytes were significantly increased after arsenite exposure, accompanied by upregulation of m6A methylesterase levels and downregulation of m6A demethylases levels. On the contrary, N-acetylcysteine mitigated the arsenite-induced increase of m6A and m6A methylesterase and the arsenite-induced decrease in m6A demethylase. Collectively, our study firstly revealed that oxidative stress induced by arsenite plays an important role in YTHDF2 phase separation driven by m6A modification, which provides new insights into the arsenite toxicity from the phase-separation perspective. [ABSTRACT FROM AUTHOR]

Sorption on minerals significantly influences the fate and transport of arsenic (As) in subsurface environmental systems. In the study, goethite is widely utilized to remove both arsenate (As(V)) and arsenite (As(III)) species, was the focus. The objectives were to investigate the mechanism and reactions governing the transport of As(III) from the solution to the goethite surface and to evaluate the effects of different pH levels (4, 7, and 10) on its sorption. The sorption experiment evaluated various As(III) concentrations at different pH levels to determine the equilibrium time, while the kinetic experiment involved observing As sorption on goethite at these pH levels until equilibrium was reached. Physiochemical parameters, including pH, contact time, and initial As(III) concentration sorption capacity, were analyzed using Langmuir and Freundlich isotherms, along with pseudo-first and pseudo-second sorption kinetic models. Results showed that the maximum sorption capacity for As(III) was 2.17 mg/g at pH 7. The data fitted better with the Freundlich isotherm than with the Langmuir isotherm model across all pH levels (R2 = 0.99 at pH 7). Although the separation factor (RL) of the Langmuir model was between 0 and 1, indicating favorable sorption. The optimum contact time for As(III) was observed to be 360 mins at all tested pH levels. Kinetic data from As(III) sorption fitted well with the pseudo-second-order model (R2 = 0.99), with the equilibrium rates (k2) being 8.63, 6.08 and 6.48 g/mg⋅min−1 for pH levels 4, 7, and 10, respectively. In conclusion, this study revealed that a pH level of 7 is optimum for the sorption of As(III) from aqueous systems, positioning goethite as a viable As(III) sorbent for further investigation in acidic or alkaline environments.

Urothelial carcinoma (UC) is prevalent, especially in elderly males. The high rate of recurrence, treatment regime, and follow-up monitoring make UC a global health and economic burden. Arsenic is a ubiquitous toxicant that can be found in drinking water, and it is known that exposure to arsenic is associated with UC development. Around 25% of diagnosed UC cases are muscle-invasive (MIUC) which have poor prognosis and develop chemoresistance, especially if tumors are associated with squamous differentiation (SD). The immortalized UROtsa cell line is derived from normal human urothelium and our lab has malignantly transformed these cells using arsenite (As3+). These cells represent a basal subtype model of MIUC and the tumors derived from the As3+-transformed cells histologically and molecularly resemble clinical cases of the basal subtype of MIUC that have focal areas SD and expression of the basal keratins (KRT1, 5, 6, 14, and 16). Our previous data demonstrate that KRT6 protein expression correlates to areas of SD within the tumors. For this study, we performed a lentiviral knockdown of KRT6 in As3+-transformed UROtsa cells to evaluate the effects on morphology, gene/protein expression, growth, colony formation, and cisplatin sensitivity. The knockdown of KRT6 resulted in decreased expression of the basal keratins, decreased growth, decreased colony formation, and increased sensitivity to cisplatin, the standard treatment for MIUC. The results of this study suggest that KRT6 plays a role in UC cell growth and is an exploitable target to increase cisplatin sensitivity for MIUC tumors that may have developed resistance to cisplatin treatment.

The goethite (α-FeOOH) nanoparticles were wrapped on the reduced graphene oxide (rGO) to synthesize the α-FeOOH/rGO nanocomposites. The nanocomposites (NCs) were initially examined for their optical, structural, and morphological properties. The XRD data obtained the crystallite size of the α-FeOOH, showed that the average crystal size for pristine α-FeOOH and α-FeOOH/rGO nanocomposites were about 85 and 90 nm, respectively. The transmission electron microscope confirmed the nanoparticles (NPs) were evenly distributed throughout the reduced graphene oxide sheets. The nanocomposites improved glassy carbon electrodes (GCE), making them efficient sensors for detecting the arsenic(III) (As+3) in a pH 5 phosphate buffer solution with an Ag/AgCl reference electrode. The detection limit for As+3 was 0.07 μgL−1 and the resulting sensitivity was 0.39 μA−1 μgL−1 in the linear dynamic range of 0.1–10 μgL−1. The α-FeOOH/rGO/GCE was more sensitive than its original and showed a synergistic effect due to the influence of α-FeOOH on the properties of rGO. The α-FeOOH/rGO NCs-modified GCE electrode performed as a promising sensor, by separating the common interfering ions. Moreover, the modified electrode exhibited remarkable stability, repeatability, and potential real-time application towards the detection of arsenic(III). Additionally, the proposed approach has been successfully applied to the detection of As+3 in the real water sample. [ABSTRACT FROM AUTHOR]

Arsenic (As) toxicity hinders plant growth and productivity and poses human health concerns. However, silicon (Si) nutrition can help improve plant tolerance to abiotic stresses. This study evaluated the influence of Si application on plant growth and As accumulation in an As hyperaccumulator plant, Isatis (Isatis cappadocica Desv.) under As stress. Isatis seedlings were exposed to 0, 5, 25, 125, and 625 μM Na2HAsO4.7H2O (AsV) and NaAsO2 (AsIII) and then Si was applied as Na2SiO3 (1 and 2 mM). Plant exposure to As(V: 650 μM) and As(III: 125 µM) caused significant reduction in plant fresh weight by 31 and 42%, and photosynthetic pigments by 47 and 62%, respectively. The same treatments caused 37- and 4.2-fold increase in levels of reactive oxygen species. However, exogenous application of Si effectively mitigated As stress, and caused a decrease in shoot As concentration up to 15% and 21% in As(V) and As(III) treated plants, respectively. In this regard, Si application at 1 mM level was more effective. The Si-induced tolerance against As in Isatis was attributed to the activation of antioxidant defense system (increase in the activities of gluthatione-S-transferase and guaiacol peroxidase, carotenoids, proline and anthocyanin contents). In conclusion, Si application improved the As tolerance in Isatis plants by modulating plant growth, decreasing As accumulation and activating the antioxidant defense system. [ABSTRACT FROM AUTHOR]

Long-term exposure to arsenic has been linked to a variety of cancers, among which skin cancer is the most prevalent form. However, the mechanism underlying arsenic carcinogenesis is unclear, and there is still limited information on the role of miRNAs in arsenic-induced skin cancer. This study aims to explore the role of miR-96-5p in the arsenite-induced proliferation and malignant transformation of human HaCaT keratinocytes. The GEO database (accession numbers GSE97303, GSE97305, and GSE97306) was used to extract mRNA and miRNA expression profiles of HaCaT cells treated with or without 0.1 μmol/L sodium arsenite for 3 and 7 weeks. In this paper, according to the CCK8 assay result, HaCaT cells exposed to 0.1 μmol/L sodium arsenite for 48 h were finalized. CCK8, MTT, EdU incorporation, and colony formation assays were used to determine the viability and proliferation of HaCaT cells and transformed HaCaT (T-HaCaT) cells. The subcellular localization and relative expression levels of DTL, as well as miR-96-5p in HaCaT cells induced by arsenite, were determined via immunofluorescence, RT-qPCR, and Western blot. Dual-luciferase reporter assay was performed to identify miR-96-5p bound directly to DTL. Transfection of miR-96-5p mimics or DTL siRNA was conducted to verify the arsenite-induced viability of HaCaT cells and T-HaCaT cells. T-HaCaT cells and nude mice were used to construct arsenite-induced malignant transformation and an in vivo xenograft model to demonstrate the over-expressed effect of miR-96-5p. The results showed that DTL was the target gene of miR-96-5p. Meanwhile, we also found that 0.1 μmol/L sodium arsenite upregulated DTL by decreasing the miR-96-5p level, leading to the proliferation and malignant transformation of HaCaT cells. MiR-96-5p agomir treatment slowed the growth of transplanted HaCaT cells transformed by arsenite in a manner associated with DTL downregulation in the nude mice xenograft model. Taken together, we confirmed that miR-96-5p, as a potent regulator of DTL, suppressed arsenite-induced HaCaT cell proliferation and malignant transformation, which might provide a novel therapeutic target for the treatment of arsenic-induced skin cancer. [ABSTRACT FROM AUTHOR]

ABSTRACTAnaerobic microbes play crucial roles in environmental processes, industry, and human health. Traditional methods for monitoring the growth of anaerobes, including plate counts or subsampling broth cultures for optical density measurements, are time and resource-intensive. The advent of microplate readers revolutionized bacterial growth studies by enabling high-throughput and real-time monitoring of microbial growth kinetics. Yet, their use in anaerobic microbiology has remained limited. Here, we present a workflow for using small-footprint microplate readers and the Growthcurver R package to analyze the kinetic growth metrics of anaerobic bacteria. We benchmarked the small-footprint Cerillo Stratus microplate reader against a BioTek Synergy HTX microplate reader in aerobic conditions using Escherichia coli DSM 28618 cultures. The growth rates and carrying capacities obtained from the two readers were statistically indistinguishable. However, the area under the logistic curve was significantly higher in cultures monitored by the Stratus reader. We used the Stratus to quantify the growth responses of anaerobically grown E. coli and Clostridium bolteae DSM 29485 to different doses of the toxin sodium arsenite. The growth of E. coli and C. bolteae was sensitive to arsenite doses of 1.3 µM and 0.4 µM, respectively. Complete inhibition of growth was achieved at 38 µM arsenite for C. bolteae and 338 µM in E. coli. These results show that the Stratus performs similarly to a leading brand of microplate reader and can be reliably used in anaerobic conditions. We discuss the advantages of the small format microplate readers and our experiences with the Stratus.IMPORTANCEWe present a workflow that facilitates the production and analysis of growth curves for anaerobic microbes using small-footprint microplate readers and an R script. This workflow is a cost and space-effective solution to most high-throughput solutions for collecting growth data from anaerobic microbes. This technology can be used for applications where high throughput would advance discovery, including microbial isolation, bioprospecting, co-culturing, host-microbe interactions, and drug/toxin-microbial interactions.

Rice is a worldwide cultivated crop that serves as an important source of food for the human population, but it is also the simplest route for arsenic (As) contamination of the food chain. The As inorganic forms, arsenate [As(V)] and arsenite [As(III)], are the highly toxic As species found in the soil and the most easily absorbed by the roots. The absorption of As(V) prevails in aerobic soils while that of As(III) is favored in anaerobic soils. As(V) is converted to As(III) in the roots, although small amounts of As(V) also remain in the plant organs. The root system is the first target of the action of both As forms. The mechanisms of action of As(V) and As(III) are still widely unknown. Understanding them is essential for selecting rice genotypes with a lower capacity of As uptake and transport to the caryopses, thus improving food safety. Auxin is the phytohormone necessary for the development and plasticity of the root system, and its action is modulated by endogenous/exogenous brassinosteroids (BRs), mainly under stress conditions. The research aim was to deepen the knowledge of the mechanisms triggered by As(III) or As(V) in rice roots with particular attention to the role played by the interaction between auxin transport and BRs. We show that As(III) is the main As species present in rice roots regardless of the As(III) or As(V) forms supplied to the growing medium. Arsenic alters auxin distribution in both adventitious and lateral roots, but strongly in the latter ones. The application of an exogenous BR, the 24-epibrassinolide (eBL), combined with As(III) or As(V) strongly increases the expression of the OsPIN2 and OsAUX1 genes involved in auxin transport, thus contributing to restore the correct auxin distribution altered by As, and mainly by As(III), with higher effects on the LRs. Moreover, eBL increases the antioxidant activity in the roots in the presence of As, but only when combined with As(V).

Inorganic trivalent arsenic (iAsⅢ) at environmentally relevant levels has been found to cause developmental toxicity. Maternal exposure to iAsⅢ leads to enduring hepatic lipid deposition in later adult life. However, the exact mechanism in iAsⅢ induced hepatic developmental hazards is still unclear. In this study, we initially found that gestational exposure to iAsⅢ at an environmentally relevant concentration disturbs lipid metabolism and reduces levels of alpha-ketoglutaric acid (α-KG), an important mitochondrial metabolite during the citric acid cycle, in fetal livers. Further, gestational supplementation of α-KG alleviated hepatic lipid deposition caused by early-life exposure to iAsⅢ. This beneficial effect was particularly pronounced in female offspring. α-KG partially restored the β-oxidation process in hepatic tissues by hydroxymethylation modifications of carnitine palmitoyltransferase 1a (Cpt1a) gene during fetal development. Insufficient β-oxidation capacities probably play a crucial role in hepatic lipid deposition in adulthood following in utero arsenite exposure, which can be efficiently counterbalanced by replenishing α-KG. These results suggest that gestational administration of α-KG can ameliorate hepatic lipid deposition caused by iAsⅢ in female adult offspring partially through epigenetic reprogramming of the β-oxidation pathway. Furthermore, α-KG shows potential as an interventive target to mitigate the harmful effects of arsenic-induced hepatic developmental toxicity.

Shubin Li, Xingna Dong, Limeng Xu, Zhenli Wu Department of Geriatric Medical Center, Inner Mongolia People’s Hospital, Hohhot, 010021, People’s Republic of ChinaCorrespondence: Zhenli Wu, Email zhenliwu@126.comIntroduction: The potential effects of selenium nanoparticles (SeNPs) administration on arsenic exposure-mediated nephrotoxicity by alleviating fibrosis, inflammation, oxidative stress-related damage, and apoptosis remains more detailed investigations.Methods: After the synthesis of selenium nanoparticles (SeNPs) by sodium selenite (Na2SeO3) through a versatile and green procedure, the biosafety of SeNPs was assessed by assaying renal functions and inflammation in mice. Subsequently, nephroprotective effects of SeNPs against sodium arsenite (NaAsO2)-induced damages were confirmed by biochemical, molecular, and histopathological assays, including renal function, histological lesion, fibrosis, inflammation, oxidative stress-related damage, and apoptosis in mice renal tissues and renal tubular duct epithelial cells (HK2 cells).Results: The excellent biocompatibility and safety of SeNPs prepared in this study were confirmed by the non-significant differences in the renal functions and inflammation levels in mice between the negative control (NC) and 1 mg/kg SeNPs groups (p> 0.05). The results of biochemical, molecular, and histopathological assays confirmed that daily administration of 1 mg/kg SeNPs for 4 weeks not only ameliorated renal dysfunctions and injuries caused by NaAsO2 exposure but also inhibited the fibrosis, inflammation, oxidative stress-related damage, and apoptosis in the renal tissues of NaAsO2-exposed mice. In addition, altered viability, inflammation, oxidative stress-related damage, and apoptosis in the NaAsO2-exposed HK2 cells were effectively reversed after 100 μg/mL SeNPs supplementation.Conclusion: Our findings authentically confirmed the biosafety and nephroprotective effects of SeNPs against NaAsO2 exposure-induced damages by alleviating inflammation, oxidative stress-related damage, and apoptosis.Keywords: selenium nanoparticles, arsenite, nephroprotective, inflammation, oxidative stress, apoptosis

Electrochemical sensing is considered as one of the most promising approaches for quick, reliable, and on-site detection and monitoring of arsenic (As) levels in water. However, the unavailability of stable, selective, and affordable electrode materials hampers the development of portable, cost-effective, reliable, and practically applicable arsenic-sensing electrochemical devices. In this article, we describe a straightforward biphasic synthesis method for the crafting of sulfur-doped reduced graphene oxide (S-rGO)-supported Prussian blue (PB) nanodeposits (S-rGO/PB), a nanocomposite with exceptional stability and activity for selective and sensitive electrochemical sensing of As. The S-rGO/PB is demonstrated to selectively and sensitively electrocatalyze the As(0)/As-(III) and As-(III)/As-(V) charge transfer processes via the participation of the Fe-(II)/Fe-(III) cycle as revealed by X-ray photoelectron spectroscopy, thereby ensuring accurate and sensitive electrochemical sensing of As in water samples. We demonstrate that with the S-rGO/PB electrode, As-(III) can be sensed via differential pulse voltammetry (DPV) with sensitivity values of 1.79 (As(0)–As-(III)) and 10.69 μA ppb–1 cm–2 (As-(III)–As-(V)) and limits of detection as low as 0.0104 and 0.0536 ppb, respectively. Alongside real-time applicability, the S-rGO/PB is demonstrated to exhibit excellent stability and specificity toward arsenic sensing even in the presence of other interferents. Importantly, the As-(III) estimates obtained for real water samples using DPV over S-rGO/PB closely match the estimates obtained with atomic absorption spectrometry, a highly expensive and sophisticated state-of-the-art technique known for its accuracy in estimation of the sub-ppb traces of heavy metals. The presented results suggest that the S-rGO/PB composite is a promising electrode material that can facilitate the design and development of portable, affordable, reliable, and practically applicable electrochemical setups for on-site sensing and electrodetoxification of As-(III) in water samples. The availability and accessibility of such setups are a must for the worldwide success of arsenic mitigation initiatives, particularly in underdeveloped and impoverished nations. [ABSTRACT FROM AUTHOR]

There are many areas in the world where ground water has been contaminated by arsenic. MnO2 is one of the most inexpensive materials which can both adsorb arsenic and oxide arsenite [As(III)] to arsenate [As(V)]. In this study, the Ultra-long α-MnO2 nanowires with the (1 1 0) surface are used to remove As(III) and As(V) from solutions under different conditions. The adsorption kinetics for both As(III) and As(V) fit well with the pseudo-second-order kinetic model. For example, the pseudo-second-order adsorption kinetic constants are 0.076 × 103 and 0.077 × 103 g μg−1 min−1 at pH 7 for As(III) and As(V), respectively. At the same time, compared to the Freundlich model the Langmuir model better describes the adsorption equilibrium isotherms. For example, the maximum adsorption capacity values of the α-MnO2 nanowires obtained from the Langmuir model are 1.012 × 103 and 1.158 × 103 μg g−1 at pH 7 for As(III) and As(V), respectively. The adsorption capacities of α-MnO2 nanowires are affected by the pH value and increase with the initial arsenic concentration. Furthermore, the As(III) oxidation rate can be denoted by the pseudo-zero-order kinetic model and is related to O2 concentration, the light source used, the initial concentration of As(III), and the pH value. For example, the pseudo-zero-order kinetic equation is y = −0.90x + 163.6 with 4 L min−1 of O2, dark condition, 0.2 × 103 μg L−1 of As(III) and at pH 7. Finally, the oxidation mechanism is investigated and the oxidant in this reaction should be related with O2 not Mn(II). Besides its special structure and easy separation ability, it is a promising material to remove arsenic from water. [ABSTRACT FROM AUTHOR]

A novel arsenite resistant bacterial strain SSBW5 was isolated from the battery waste site of Corlim, Goa, India. This strain interestingly exhibited rapid arsenite oxidation with an accumulation of 5 mM arsenate within 24 h and a minimum inhibitory concentration (MIC) of 18 mM. The strain SSBW5 was identified as Paenarthrobacter nicotinovorans using 16S rDNA sequence analysis. Fourier-transformed infrared (FTIR) spectroscopy of arsenite-exposed cells revealed the interaction of arsenite with several important functional groups present on the cell surface, possibly involved in the resistance mechanism. Interestingly, the whole genome sequence analysis also clearly elucidated the presence of genes, such as GlpF, aioAB and aioE encoding transporter, arsenite oxidase and oxidoreductase enzyme, respectively, conferring their role in arsenite resistance. Furthermore, this strain also revealed the presence of several other genes conferring resistance to various metals, drugs, antibiotics and disinfectants. Further suggesting the probable direct or indirect involvement of these genes in the detoxification of arsenite thereby increasing its tolerance limit. In addition, clumping of bacterial cells was observed through microscopic analysis which could also be a strategy to reduce arsenite toxicity thus indicating the existence of multiple resistance mechanisms in strain SSBW5. In the present communication, we are reporting for the first time the potential of P. nicotinovorans strain SSBW5 to be used in the bioremediation of arsenite via arsenite oxidation along with other toxic metals and metalloids. [ABSTRACT FROM AUTHOR]

Arsenite is both more harmful and challenging to get out of water than arsenate. For enhanced As (III) removal, a ternary oxide nanoparticle (FCCTO) mainly composed of iron(Fe), with a small proportion of cerium(Ce) and copper(Cu) was created using a coprecipitation–calcination process. FCCTO was found to be effective in removing As (III) from water, with factors such as adsorbent dose, pH, temperature, and coexisting anions influencing its efficiency. The surface area of FCCTO reached 180.2 m2/g and the doping significantly increased its pore volume and diameter. The adsorption process on FCCTO was endothermic and spontaneous. Ce and Cu in FCCTO were able to efficiently oxidize 81.3% As (III) to As(V). Abundant sites were provided by surface hydroxyl groups for arsenic adsorption. The maximal As(III) adsorption capacity of this adsorbent under the synergistic impact of oxidation and adsorption was 101.5 mg/g. After five cycles, the FCCTO's As(III) adsorption rate dropped to 60% as a result of tetravalent Ce consumption. Surface complexation, redox, and adsorption all had a significant impact on the adsorption process. Overall, FCCTO was an excellent adsorbent with benefits of being facile fabrication, environmentally, recyclable, and having a high As(III) adsorption capacity. [ABSTRACT FROM AUTHOR]

BRCA1 is a key player in maintaining genomic integrity with multiple functions in DNA damage response (DDR) mechanisms. Due to its thiol-rich zinc-complexing domain, the protein may also be a potential target for redox-active and/or thiol-reactive (semi)metal compounds. The latter includes trivalent inorganic arsenic, which is indirectly genotoxic via induction of oxidative stress and inhibition of DNA repair pathways. In the present study, we investigated the effect of NaAsO2 on the transcriptional and functional DDR. Particular attention was paid to the potential impairment of BRCA1-mediated DDR mechanisms by arsenite by comparing BRCA1-deficient and -proficient cells. At the transcriptional level, arsenite itself activated several DDR mechanisms, including a pronounced oxidative stress and DNA damage response, mostly independent of BRCA1 status. However, at the functional level, a clear BRCA1 dependency was observed in both cell cycle regulation and cell death mechanisms after arsenite exposure. Furthermore, in the absence of arsenite, the lack of functional BRCA1 impaired the largely error-free homologous recombination (HR), leading to a shift towards the error-prone non-homologous end-joining (NHEJ). Arsenic treatment also induced this shift in BRCA1-proficient cells, indicating BRCA1 inactivation. Although BRCA1 bound to DNA DSBs induced via ionizing radiation, its dissociation was impaired, similarly to the downstream proteins RAD51 and RAD54. A shift from HR to NHEJ by arsenite was further supported by corresponding reporter gene assays. Taken together, arsenite appears to negatively affect HR via functional inactivation of BRCA1, possibly by interacting with its RING finger structure, which may compromise genomic stability. [ABSTRACT FROM AUTHOR]

We report copper(II) arsenite-encapsulated ferritin nanoparticles (CuAS-FNs) as oxidative stress-amplifying anticancer agents. The CuAS-FNs were fabricated through CuAS mineralization in the cavity of the FNs. The formation of crystalline CuAS complex minerals in the FNs was systematically identified using various analytical tools, including X-ray photoelectron spectroscopy (XPS) and transmission electron microscopy (TEM)-associated energy-dispersive X-ray spectroscopy (TEM-EDS). The CuAS-FNs showed pH-dependent release behavior, in which the CuAS mineral was effectively retained at physiological pH, in contrast, at lysosomal pH, the CuAS complex was dissociated to release arsenite and Cu2+ ions. At lysosomal pH, the release rate of arsenite (HAsO 3 2−) and Cu2+ ions from the CuAS-FNs more accelerated than at physiological pH. Upon transferrin receptor-1-mediated endocytosis, the CuAS-FNs simultaneously released arsenite and Cu2+ ions in cells. The released arsenite ions can increase the intracellular concentration of hydrogen peroxide (H 2 O 2), with which the Cu2+ ions can elevate the level of hydroxyl radicals (·OH) via Fenton-like reaction. Thus, the CuAS-FNs could target cancer cell through the recognizing ability of FNs and kill cancer cells by amplifying the ·OH level through the synergistic activity of Cu2+ and arsenic ions. Importantly, MCF-7 tumors were effectively suppressed by CuAS-FNs without systemic in vivo toxicity. Therefore, the CuAS-FNs is a promising class of Fenton-like catalytic nanosystem for cancer treatment. Copper(II) arsenite-encapsulated ferritin nanoparticles (CuAS-FNs) were developed as targeted and oxidative stress-amplifying anticancer agents. The CuAS-FNs were rationally designed by combining the TfR-1-mediated endocytosis of the FNs and the oxidative stress amplification of the CuAS. This study paves a way for a wide range of novel cancer-specific therapeutics by systematically modulating the oxidative stress in cancer cells. [Display omitted] [ABSTRACT FROM AUTHOR]

The use of probiotic lactobacilli has been proposed as a strategy to mitigate damage associated with exposure to toxic metals. Their protective effect against cationic metal ions, such as those of mercury or lead, is believed to stem from their chelating and accumulating potential. However, their retention of anionic toxic metalloids, such as inorganic arsenic, is generally low. Through the construction of mutants in phosphate transporter genes (pst) in Lactiplantibacillus plantarum and Lacticaseibacillus paracasei strains, coupled with arsenate [As(V)] uptake and toxicity assays, we determined that the incorporation of As(V), which structurally resembles phosphate, is likely facilitated by phosphate transporters. Surprisingly, inactivation in Lc. paracasei of PhoP, the transcriptional regulator of the two-component system PhoPR, a signal transducer involved in phosphate sensing, led to an increased resistance to arsenite [As(III)]. In comparison to the wild type, the phoP strain exhibited no differences in the ability to retain As(III), and there were no observed changes in the oxidation of As(III) to the less toxic As(V). These results reinforce the idea that specific transport, and not unspecific cell retention, plays a role in As(V) biosorption by lactobacilli, while they reveal an unexpected phenotype for the lack of the pleiotropic regulator PhoP.

The arsenic adsorption performance of silicon (Si), iron (Fe), and magnesium (Mg) mixed hydrous oxide containing a Si: Fe: Mg metal composition ratio of 0.05:0.9:0.05 (SFM05905) was investigated. SFM05905 was synthesized by the co-precipitation method. Batch experiments on arsenic adsorption were conducted at various temperatures and concentrations. Adsorption isotherms models were represented by a linearized equations and were insensitive to temperature change. The anion selectivity of SFM05905 at single component was high for arsenite (III), arsenate (V), and phosphate (PO4), indicating that PO4 inhibits arsenic adsorption. The adsorption amount of As (III), As (V), and PO4 were compared using a column packed with granular SFM05905, and an aqueous solution was passed by a combination of several anions that are single, binary, and ternary adsorbate systems. As (III) had the highest adsorption amount; however, As (III) and PO4 were affected by each other under the ternary mixing condition. Although the adsorption amount of As (V) was smaller than that of As (III), it was not affected by other adsorbates in the column experiments. Finally, although the adsorption of both arsenic continued, the adsorbed PO4 gradually desorbed.