Arsenic activated GLUT1-mTORC1/HIF-1α-PKM2 positive feedback networks promote proliferation and migration of bladder epithelial cells.

Arsenic (As) is recognized as a potent environmental contaminant associated with bladder carcinogenesis. However, its molecular mechanism remains unclear. Metabolic reprogramming is one of the hallmarks of cancer and is as a central feature of malignancy. Here, we performed the study of cross-talk between the mammalian target of rapamycin complex 1 (mTORC1)/ Hypoxia-inducible factor 1 alpha (HIF-1α) pathway and aerobic glycolysis in promoting the proliferation and migration of bladder epithelial cells treated by arsenic in vivo and in vitro. We demonstrated that arsenite promoted N-methyl-N-nitrosourea (MNU)-induced tumor formation in the bladder of rats and the malignant behavior of human ureteral epithelial (SV-HUC-1) cell. We found that arsenite positively regulated the mTORC1/HIF-1α pathway through glucose transporter protein 1 (GLUT1), which involved in the malignant progression of bladder epithelial cells relying on glycolysis. In addition, pyruvate kinase M2 (PKM2) increased by arsenite reduced the protein expressions of succinate dehydrogenase (SDH) and fumarate hydratase (FH), leading to the accumulation of tumor metabolites of succinate and fumarate. Moreover, heat shock protein (HSP)90, functioning as a chaperone protein, stabilized PKM2 and thereby regulated the proliferation and aerobic glycolysis in arsenite treated SV-HUC-1 cells. Taken together, these results provide new insights into mTORC1/HIF-1α and PKM2 networks as critical molecular targets that contribute to the arsenic-induced malignant progression of bladder epithelial cells.

Arsenite tolerance and removal potential of the indigenous halophilic bacterium, Halomonas elongata SEK2.

The indigenous halophilic arsenite-resistant bacterium Halomonas elongata strain SEK2 isolated from the high saline soil of Malek Mohammad hole, Lut Desert, Iran, could tolerate high concentrations of arsenate (As5+) and arsenite (As3+) up to 800 and 40 mM in the SW-10 agar medium, respectively. The isolated strain was able to tolerate considerable concentrations of other toxic heavy metals and oxyanions, including Cadmium (Cd2+), Chromate (Cr6+), lead (Pb2+), and selenite (Se4+), regarding the high salinity of the culture media (with a total salt concentration of 10% (w/v)), the tolerance potential of the isolate SEK2 was unprecedented. The bioremoval potential of the isolate SEK2 was examined through the Silver diethyldithiocarbamate (SDDC) method and demonstrated that the strain SEK2 could remove 60% of arsenite from arsenite-containing growth medium after 48 h of incubation without converting it to arsenate. The arsenite adsorption or uptake by the halophilic bacterium was investigated and substantiated through Fourier-transform infrared spectroscopy (FTIR), Scanning Electron Microscope (SEM), and Energy Dispersive X-ray (EDX) analyses. Furthermore, Transmission electron microscope (TEM) analysis revealed ultra-structural alterations in the presence of arsenite that could be attributed to intracellular accumulation of arsenite by the bacterial cell. Genome sequencing analysis revealed the presence of arsenite resistance as well as other heavy metals/oxyanion resistance genes in the genome of this bacterial strain. Therefore, Halomonas elongata strain SEK2 was identified as an arsenite-resistant halophilic bacterium for the first time that could be used for arsenite bioremediation in saline arsenite-polluted environments.

Phase transformation of schwertmannite in paddy soil under different water management regimes and its impact on the migration of arsenic in soil.

Schwertmannite (Sch) holds a great promise as an iron material for remediating Arsenic (As)-contaminated paddy soils, due to its extremely high immobilization capacities for both arsenate [As(V)] and arsenite [As(III)]. However, there is still limited knowledge on the mineral phase transformation of this metastable iron-oxyhydroxysulfate mineral in paddy soils, particularly under different water management regimes including aerobic, intermittent flooding, and continuous flooding, and how its phase transformation impacts the migration of As in paddy soils. In this study, a membrane coated with schwertmannite was first developed to directly reflect the phase transformation of bulk schwertmannite applied to paddy soils. A soil incubation experiment was then conducted to investigate the mineral phase transformation of schwertmannite in paddy soils under different water management regimes and its impact on the migration of As in paddy soil. Our findings revealed that schwertmannite can persist in the paddy soil for 90 days in the aerobic group, whereas in the continuous flooding and intermittent flooding groups, schwertmannite transformed into goethite, with the degree or rate of mineral phase transformation being 5% Sch >1% Sch > control. These results indicated that water management practices and the amount of schwertmannite applied were the primary factors determining the occurrence and degree of mineral transformation of schwertmannite in paddy soil. Moreover, despite undergoing phase transformation, schwertmannite still significantly reduced the porewater As (As(III) and As(V)), and facilitated the transfer of non-specifically adsorbed As (F1) and specifically adsorbed As (F2) to amorphous iron oxide-bound As (F3), effectively reducing the bioavailability of soil As. These findings contribute to a better understanding of the mineralogical transformation of schwertmannite in paddy soils and the impact of mineral phase transformation on the retention of As in soil, which carry important implications for the application of schwertmannite in remediating As-contaminated paddy soils.

Protective Effects of Lactoferrin Treatment Against Sodium Arsenite Exposure-Induced Nephrotoxicity.

It is said that a wide range of renal functions are at risk from arsenic exposure. We examined how lactoferrin administration may mitigate inflammation, apoptosis, redox imbalance, and fibrosis in order to counteract arsenic-induced nephrotoxicity. Accordingly, male C57BL/6 mice (6 weeks) were divided into six experimental groups with six mice in each group. The first and second groups were intragastrically administered normal saline and sodium arsenite (NaAsO2) at 5 mg/kg body weight concentrations as the negative control (NC) and NaAsO2 groups. The third, fourth, and fifth groups were intragastrically administered lactoferrin at concentrations of 100, 200, and 400 mg/kg body weight in addition to NaAsO2 at concentrations of 5 mg/kg body weight. The sixth group was intragastrically administered lactoferrin at a concentration of 200 mg/kg body weight with the experimental group set as the lactoferrin group. After daily drug administration for 4 weeks, the lactoferrin concentrations were optimized based on the results of renal index and renal function. Histopathological, biochemical, and gene expression analyses were performed to evaluate the status of renal tissue architecture, redox imbalance, inflammation, apoptosis, and fibrosis to confirm the alleviative effect of lactoferrin treatment against the NaAsO2 exposure-induced nephrotoxicity. The results confirmed that the 200 mg/kg lactoferrin treatment mitigated these arsenic effects and maintained the normal renal frameworks. Conclusively, disrupting the renal redox balance and triggering inflammation, apoptosis, along with fibrosis is a milieu that arsenic, robustly exerts its nephrotoxic effect. Lactoferrin, probably by its direct and indirect control mechanism on these said pathways, can mitigate the nephrotoxicity and preserve the normal renal health.

Untying arsenite tolerance mechanisms in contrasting maize genotypes attributed to NIPs-mediated controlled influx and root-to-shoot translocation, redox homeostasis and phytochelatin-mediated detoxification pathway.

Contamination of ground water and soil with toxic metalloids like arsenic (As) poses a serious hazard to the global agricultural food production. One of the best ways to restrict entry of As into the food chain is selection of germplasms which accrue extremely low level of As in grains. Here, we screened diverse maize genotypes under high arsenite (100 µM AsIII) stress and identified PMI-PV-9 and PMI-PV-3 as AsIII-tolerant and -sensitive maize genotype respectively. Expression of genes associated with As uptake, vacuolar sequestration, biosynthesis of phytochelatins, root-to-shoot translocation, in vivo ROS generation, fine tuning of antioxidant defense system, DNA and membrane damage, H2O2 and superoxide anion (O2•-) levels were compared among the selected genotypes. PMI-PV-9 plants performed much better than PMI-PV-3 in terms of plant growth with no visible symptom of As toxicity. Susceptibility of PMI-PV-3 to AsIII stress may be attributed to comparatively low expression of genes involved in phytochelatins (PCs) biosynthesis. Concomitant decrease in ABCC1 expression might be another key factor for futile sequestration of AsIII into root vacuoles. Moreover, up-regulation of ZmNIP3;1 might contribute in high root-to-leaf As translocation. Substantial spike in H2O2, O2•- and MDA levels indicates that PMI-PV-3 plants have experienced more oxidative stress than PMI-PV-9 plants. Appearance of prominent deep brown and dark blue spots/stripes on leaves as revealed after DAB and NBT staining respectively suggest severe oxidative burst in PMI-PV-3 plants. Marked reduction in DHAR and MDAR activity rendered PMI-PV-3 cells to recycle ascorbate pool ineffectively, which might have exacerbated their susceptibility to AsIII stress. In a nutshell, incompetent PCs mediated detoxification system and disruption of cellular redox homeostasis owing to feeble antioxidant defence system resulting oxidative burst might be the prime reasons behind reduced performance of PMI-PV-3 plants under AsIII stress.

Arsenite oxidation and adsorptive arsenic removal from contaminated water: a review.

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.

Hepatoprotective effects of zingerone on sodium arsenite-induced hepatotoxicity in rats: Modulating the levels of caspase-3/Bax/Bcl-2, NLRP3/NF-κB/TNF-α and ATF6/IRE1/PERK/GRP78 signaling pathways.

OBJECTIVE: Long-term exposure to arsenic has been linked to several illnesses, including hypertension, diabetes, hepatic and renal diseases and cardiovascular malfunction. The aim of the current investigation was to determine whether zingerone (ZN) could shield rats against the hepatotoxicity that sodium arsenite (SA) causes. METHODS: The following five groups of thirty-five male Sprague Dawley rats were created: I) Control; received normal saline, II) ZN; received ZN, III) SA; received SA, IV) SA + ZN 25; received 10 mg/kg body weight SA + 25 mg/kg body weight ZN, and V) SA + ZN 50; received 10 mg/kg body weight SA + 50 mg/kg body weight ZN. The experiment lasted 14 days, and the rats were sacrificed on the 15th day. While oxidative stress parameters were studied by spectrophotometric method, apoptosis, inflammation and endoplasmic reticulum stress parameters were measured by RT-PCR method. RESULTS: The SA disrupted the histological architecture and integrity of the liver and enhanced oxidative damage by lowering antioxidant enzyme activity, such as those of glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) level and increasing malondialdehyde (MDA) level in the liver tissue. Additionally, SA increased the mRNA transcript levels of Bcl2 associated x (Bax), caspases (-3, -6, -9), apoptotic protease-activating factor 1 (Apaf-1), p53, tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), c-Jun NH2-terminal kinase (JNK), mitogen-activated protein kinase 14 (MAPK14), MAPK15, receptor for advanced glycation endproducts (RAGE) and nod-like receptor family pyrin domain-containing 3 (NLRP3) in the liver tissue. Also produced endoplasmic reticulum stress by raising the mRNA transcript levels of activating transcription factor 6 (ATF-6), protein kinase RNA-like ER kinase (PERK), inositol-requiring enzyme 1 (IRE1), and glucose-regulated protein 78 (GRP-78). These factors together led to inflammation, apoptosis, and endoplasmic reticulum stress. On the other hand, liver tissue treated with ZN at doses of 25 and 50 mg/kg showed significant improvement in oxidative stress, inflammation, apoptosis and endoplasmic reticulum stress. CONCLUSIONS: Overall, the study's data suggest that administering ZN may be able to lessen the liver damage caused by SA toxicity.

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

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

Subchronic intake of arsenic at environmentally relevant concentrations causes histological lesions and oxidative stress in the prostate of adult Wistar rats.

The prostate gland is one of the main sites of hyperplasia and cancer in elderly men. Numerous factors have been demonstrated to disrupt prostate homeostasis, including exposure to environmental pollutants. Arsenic is a metalloid found ubiquitously in soil, air, and water, which favors human poisoning through the involuntary intake of contaminated drinking water and food and has harmful effects by increasing the oxidative stress response. This study aimed to investigate the effects of prolonged exposure to arsenic at environmentally relevant concentrations on the prostate biology of adult Wistar rats. Thirty 80-day-old male rats were divided into three experimental groups. Rats from the control group received filtered water, whereas animals from the arsenic groups ingested 1 mg L-1 and 10 mg L-1 of arsenic, in the form of sodium arsenite, daily. The arsenic solutions were provided ad libitum in the drinking water for eight weeks. Our results showed that 1 mg L-1 and 10 mg L-1 of arsenic made the prostate susceptible to evolving benign and premalignant histopathological changes. While the ingestion of 1 mg L-1 of arsenic reduced SOD activity only, 10 mg L-1 diminished SOD and CAT activity in the prostate tissue, culminating in high MDA production. These doses, however, did not affect the intraprostatic levels of DHT and estradiol. In conclusion, exposure to arsenic at environmentally relevant concentrations through drinking water induces histological and oxidative stress-related changes in the prostate of adult rats, strengthening the between arsenic exposure and prostate disorders.

Phosphate Uptake and Its Relation to Arsenic Toxicity in Lactobacilli.

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.

Sodium arsenite induces hepatic stellate cells activation by m6A modification of TGF-ß1 during liver fibrosis.

The compound known as Sodium arsenite (NaAsO2), which is a prevalent type of inorganic arsenic found in the environment, has been strongly associated with liver fibrosis (LF), a key characteristic of nonalcoholic fatty liver disease (NAFLD), which has been demonstrated in our previous study. Our previous research has shown that exposure to NaAsO2 triggers the activation of hepatic stellate cells (HSCs), a crucial event in the development of LF. However, the molecular mechanism is still unknown. N6-methyladenosine (m6A) modification is the most crucial post-transcriptional modification in liver disease. Nevertheless, the precise function of m6A alteration in triggering HSCs and initiating LF caused by NaAsO2 remains unknown. Here, we found that NaAsO2 induced LF and HSCs activation through TGF-ß/Smad signaling, which could be reversed by TGF-ß1 knockdown. Furthermore, NaAsO2 treatment enhanced the m6A modification level both in vivo and in vitro. Significantly, NaAsO2 promoted the specific interaction of METTL14 and IGF2BP2 with TGF-ß1 and enhanced the TGF-ß1 mRNA stability. Notably, NaAsO2-induced TGF-ß/Smad pathway and HSC-t6 cells activation might be avoided by limiting METTL14/IGF2BP2-mediated m6A modification. Our findings showed that the NaAsO2-induced activation of HSCs and LF is made possible by the METTL14/IGF2BP2-mediated m6A methylation of TGF-ß1, which may open up new therapeutic options for LF brought on by environmental hazards.

Rcn1, the fission yeast homolog of human DSCR1, regulates arsenite tolerance independently from calcineurin.

Calcineurin (CN) is a conserved Ca2+/calmodulin-dependent phosphoprotein phosphatase that plays a key role in Ca2+ signaling. Regulator of calcineurin 1 (RCAN1), also known as Down syndrome critical region gene 1 (DSCR1), interacts with calcineurin and inhibits calcineurin-dependent signaling in various organisms. Ppb1, the fission yeast calcineurin regulates Cl--homeostasis, and Ppb1 deletion induces MgCl2 hypersensitivity. Here, we characterize the conserved and novel roles of the fission yeast RCAN1 homolog rcn1+. Consistent with its role as an endogenous calcineurin inhibitor, Rcn1 overproduction reproduced the calcineurin-null phenotypes, including MgCl2 hypersensitivity and inhibition of calcineurin signaling upon extracellular Ca2+ stimuli as evaluated by the nuclear translocation and transcriptional activation of the calcineurin substrate Prz1. Notably, overexpression of rcn1+ causes hypersensitivity to arsenite, whereas calcineurin deletion induces arsenite tolerance, showing a phenotypic discrepancy between Rcn1 overexpression and calcineurin deletion. Importantly, although Rcn1 deletion induces modest sensitivities to arsenite and MgCl2 in wild-type cells, the arsenite tolerance, but not MgCl2 sensitivity, associated with Ppb1 deletion was markedly suppressed by Rcn1 deletion. Collectively, our findings reveal a previously unrecognized functional collaboration between Rcn1 and calcineurin, wherein Rcn1 not only negatively regulates calcineurin in the Cl- homeostasis, but also Rcn1 mediates calcineurin signaling to modulate arsenite cytotoxicity.

Nod-like receptor protein 3 inflammasome-mediated pyroptosis contributes to chronic NaAsO2 exposure-induced fibrotic changes and dysfunction in the liver of SD rats.

The metalloid arsenic, known for its toxic properties, is widespread presence in the environment. Our previous research has confirmed that prolonged exposure to arsenic can lead to liver fibrosis injury in rats, while the precise pathogenic mechanism still requires further investigation. In the past few years, the Nod-like receptor protein 3 (NLRP3) inflammasome has been found to play a pivotal role in the occurrence and development of liver injury. In this study, we administered varying doses of sodium arsenite (NaAsO2) and 10 mg/kg.bw MCC950 (a particular tiny molecular inhibitor targeting NLRP3) to Sprague-Dawley (SD) rats for 36 weeks to explore the involvement of NLRP3 inflammasome in NaAsO2-induced liver injury. The findings suggested that prolonged exposure to NaAsO2 resulted in pyroptosis in liver tissue of SD rats, accompanied by the fibrotic injury, extracellular matrix (ECM) deposition and liver dysfunction. Moreover, long-term NaAsO2 exposure activated NLRP3 inflammasome, leading to the release of pro-inflammatory cytokines in liver tissue. After treatment with MCC950, the induction of NLRP3-mediated pyroptosis and release of pro-inflammatory cytokines were significantly attenuated, leading to a decrease in the severity of liver fibrosis and an improvement in liver function. To summarize, those results clearly indicate that hepatic fibrosis and liver dysfunction induced by NaAsO2 occur through the activation of NLRP3 inflammasome-mediated pyroptosis, shedding new light on the potential mechanisms underlying arsenic-induced liver damage.

Influence of Phosphate on Arsenic Adsorption Behavior of Si-Fe-Mg Mixed Hydrous Oxide.

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.

mTORC1 - TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells.

The mechanistic target of rapamycin (RAPA) complex 1 (mTORC1) - transcription factor EB (TFEB) pathway plays a crucial role in response to nutritional status, energy and environmental stress for maintaining cellular homeostasis. But there is few reports on its role in the toxic effects of arsenic exposure and the related mechanisms. Here, we show that the exposure of bronchial epithelial cells (BEAS-2B) to sodium arsenite promoted the activation of mTORC1 (p-mTORC1) and the inactivation of TFEB (p-TFEB), the number and activity of lysosomes decreased, the content of reduced glutathione (GSH) and superoxide dismutase (SOD) decreased, the content of malondialdehyde (MDA) increased, the DNA and chromosome damage elevated. Further, when mTORC1 was inhibited with RAPA, p-mTORC1 and p-TFEB down-regulated, GSH and SOD increased, MDA decreased, the DNA and chromosome damage reduced significantly, as compared with the control group. Our data revealed for the first time that mTORC1 - TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells, and it may be a potential intervention target for the toxic effects of arsenic.

Bacteria associated with Comamonadaceae are key arsenite oxidizer associated with Pteris vittata root.

Pteris vittata (P. vittata), an arsenic (As) hyperaccumulator commonly used in the phytoremediation of As-contaminated soils, contains root-associated bacteria (RAB) including those that colonize the root rhizosphere and endosphere, which can adapt to As contamination and improve plant health. As(III)-oxidizing RAB can convert the more toxic arsenite (As(III)) to less toxic arsenate (As(V)) under As-rich conditions, which may promote plant survial. Previous studies have shown that microbial As(III) oxidation occurs in the rhizospheres and endospheres of P. vittata. However, knowledge of RAB of P. vittata responsible for As(III) oxidation remained limited. In this study, members of the Comamonadaceae family were identified as putative As(III) oxidizers, and the core microbiome associated with P. vittata roots using DNA-stable isotope probing (SIP), amplicon sequencing and metagenomic analysis. Metagenomic binning revealed that metagenome assembled genomes (MAGs) associated with Comamonadaceae contained several functional genes related to carbon fixation, arsenic resistance, plant growth promotion and bacterial colonization. As(III) oxidation and plant growth promotion may be key features of RAB in promoting P. vittata growth. These results extend the current knowledge of the diversity of As(III)-oxidizing RAB and provide new insights into improving the efficiency of arsenic phytoremediation.

Arsenic-Hyperaccumulator Pteris vittata Effectively Uses Sparingly-Soluble Phosphate Rock: Rhizosphere Solubilization, Nutrient Improvement, and Arsenic Accumulation.

Sparingly-soluble phosphate rock (PR), a raw material for P-fertilizer production, can be effectively utilized by the As-hyperaccumulator Pteris vittata but not most plants. In this study, we investigated the associated mechanisms by measuring dissolved organic carbon (DOC) and acid phosphatase in the rhizosphere, and nutrient uptake and gene expression related to the As metabolism in P. vittata. The plants were grown in a soil containing 200 mg kg-1 As and/or 1.5% PR for 30 days. Compared to the As treatment, the P. vittata biomass was increased by 33% to 4.6 g plant-1 in the As+PR treatment, corresponding to 27% decrease in its frond oxidative stress as measured by malondialdehyde. Due to PR-enhanced DOC production in the rhizosphere, the Ca, P, and As contents in P. vittata fronds were increased by 17% to 9.7 g kg-1, 29% to 5.0 g kg-1, and 57% to 1045 mg kg-1 in the As+PR treatment, thereby supporting its better growth. Besides, PR-induced rhizosphere pH increase from 5.0 to 6.9 promoted greater P uptake by P. vittata probably via upregulating low-affinity P transporters PvPTB1;1/1;2 by 3.7-4.1 folds. Consequently, 29% lower available-P induced the 3.3-fold upregulation of high-affinity P transporter PvPht1;3 in the As+PR treatment, which was probably responsible for the 58% decrease in available-As content in the rhizosphere. Consistent with the enhanced As translocation and sequestration, arsenite antiporters PvACR3/3;3 were upregulated by 1.8-4.4 folds in the As+PR than As treatment. In short, sparingly-soluble PR enhanced the Ca, P, and As availability in P. vittata rhizosphere and improved their uptake via upregulating genes related to As metabolism, suggesting its potential application for improving phytoremediation in As-contaminated soils.

Fast and efficient As(III) removal from water by bifunctional nZVI@NBC.

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).

Transporters and phytohormones analysis reveals differential regulation of ryegrass (Lolium perenne L.) in response to cadmium and arsenic stresses.

Cadmium (Cd) and arsenic (As) are two highly toxic heavy metals and metalloids that coexist in many situations posing severe threats to plants. Our investigation was conducted to explore the different regulatory mechanisms of ryegrass (Lolium perenne L.) responding to individual and combined Cd and As stresses in hydroponics. Results showed that the ryegrass well-growth phenotype was not affected by Cd stress of 10 mg·L-1. However, As of 10 mg·L-1 caused rapid water loss, proline surge, and chlorosis in shoots, suggesting that ryegrass was highly sensitive to As. Transcriptomic analysis revealed that the transcription factor LpIRO2 mediated the upregulation of ZIP1 and YSL6 that played an important role in Cd tolerance. We found that the presence of As caused the overexpression of LpSWT12, a process potentially regulated by bHLH14, to mitigate hyperosmolarity. Indoleacetic acid (IAA) and abscisic acid (ABA) contents and expression of their signaling-related genes were significantly affected by As stress rather than Cd. We predict a regulatory network to illustrate the interaction between transporters, transcription factors, and signaling transduction, and explain the antagonism of Cd and As toxicity. This present work provides a research basis for plant protection from Cd and As pollution.

Effects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways.

Objectives: This study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA). Materials and Methods: In the study, five groups were formed (n=7) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG 25 group, and SA+ZNG 50 group. While SA was administered orally to rats at 10 mg/kg/bw, ZNG was given to rats orally at 25 and 50 mg/kg/bw doses for 14 days. Results: As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-κB, TNF-α, IL-1ß, and IL-6 were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP3, and JAK-2/STAT3 gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-6, PERK, IRE1, and GRP78 genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-3 expressions and inhibiting Bcl-2 expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality. Conclusion: ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles.