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The fern Pteris vittata is an arsenic hyperaccumulator. The genes involved in arsenite (As(III)) transport are not yet clear. Here, we describe the isolation and characterization of a new P. vittata aquaporin gene, PvTIP4;1, which may mediate As(III) uptake. PvTIP4;1 was identified from yeast functional complement cDNA library of P. vittata. Arsenic toxicity and accumulating activities of PvTIP4;1 were analyzed in Saccharomyces cerevisiae and Arabidopsis. Subcellular localization of PvTIP4;1–GFP fusion protein in P. vittata protoplast and callus was conducted. The tissue expression of PvTIP4;1 was investigated by quantitative real‐time PCR. Site‐directed mutagenesis of the PvTIP4;1 aromatic/arginine (Ar/R) domain was studied. Heterologous expression in yeast demonstrates that PvTIP4;1 was able to facilitate As(III) diffusion. Transgenic Arabidopsis showed that PvTIP4;1 increases arsenic accumulation and induces arsenic sensitivity. Images and FM4‐64 staining suggest that PvTIP4;1 localizes to the plasma membrane in P. vittata cells. A tissue location study shows that PvTIP4;1 transcripts are mainly expressed in roots. Site‐directed mutation in yeast further proved that the cysteine at the LE1 position of PvTIP4;1 Ar/R domain is a functional site. PvTIP4;1 is a new represented tonoplast intrinsic protein (TIP) aquaporin from P. vittata and the function and location results imply that PvTIP4;1 may be involved in As(III) uptake.

Summary • When supplied with arsenate (As(V)), plant roots extrude a substantial amount of arsenite (As(III)) to the external medium through as yet unidentified pathways. The rice (Oryza sativa) silicon transporter Lsi1 (OsNIP2;1, an aquaporin channel) is the major entry route of arsenite into rice roots. Whether Lsi1 also mediates arsenite efflux was investigated. • Expression of Lsi1 in Xenopus laevis oocytes enhanced arsenite efflux, indicating that Lsi1 facilitates arsenite transport bidirectionally. • Arsenite was the predominant arsenic species in arsenate‐exposed rice plants. During 24‐h exposure to 5 μm arsenate, rice roots extruded arsenite to the external medium rapidly, accounting for 60–90% of the arsenate uptake. A rice mutant defective in Lsi1 (lsi1) extruded significantly less arsenite than the wild‐type rice and, as a result, accumulated more arsenite in the roots. By contrast, Lsi2 mutation had little effect on arsenite efflux to the external medium. • We conclude that Lsi1 plays a role in arsenite efflux in rice roots exposed to arsenate. However, this pathway accounts for only 15–20% of the total efflux, suggesting the existence of other efflux transporters.

Arsenic poisoning affects millions of people worldwide. Human arsenic intake from rice consumption can be substantial because rice is particularly efficient in assimilating arsenic from paddy soils, although the mechanism has not been elucidated. Here we report that two different types of transporters mediate transport of arsenite, the predominant form of arsenic in paddy soil, from the external medium to the xylem. Transporters belonging to the NIP subfamily of aquaporins in rice are permeable to arsenite but not to arsenate. Mutation in OsNIP2;1 (Lsi1, a silicon influx transporter) significantly decreases arsenite uptake. Furthermore, in the rice mutants defective in the silicon efflux transporter Lsi2, arsenite transport to the xylem and accumulation in shoots and grain decreased greatly. Mutation in Lsi2 had a much greater impact on arsenic accumulation in shoots and grain in field-grown rice than Lsi1. Arsenite transport in rice roots therefore shares the same highly efficient pathway as silicon, which explains why rice is efficient in arsenic accumulation. Our results provide insight into the uptake mechanism of arsenite in rice and strategies for reducing arsenic accumulation in grain for enhanced food safety.

Rice is a major dietary source of the toxic metalloid arsenic. Reducing arsenic accumulation in rice grain is important for food safety. We generated transgenic rice overexpressing two aquaporin genes, OsNIP1;1 and OsNIP3;3, under the control of a maize ubiquitin promoter or the rice OsLsi1 promoter, and tested the effect on arsenite uptake and translocation. OsNIP1;1 and OsNIP3;3 were highly permeable to arsenite in Xenopus oocyte assays. Both transporters were localized at the plasma membrane. Knockout of either gene had little effect on arsenite uptake or translocation. Overexpression of OsNIP1;1 or OsNIP3;3 in rice did not affect arsenite uptake but decreased root-to-shoot translocation of arsenite and shoot arsenic concentration markedly. The overexpressed OsNIP1;1 and OsNIP3;3 proteins were localized in all root cells without polarity. Expression of OsNIP1;1 driven by the OsLsi1 promoter produced similar effects. When grown in two arsenic-contaminated paddy soils, overexpressing lines contained significantly lower arsenic concentration in rice grain than the wild-type without compromising plant growth or the accumulation of essential nutrients. Overexpression of OsNIP1;1 or OsNIP3;3 provides a route for arsenite to leak out of the stele, thus restricting arsenite loading into the xylem. This strategy is effective in reducing arsenic accumulation in rice grain.

A bioreductive capacity of a plant, Terminalia arjuna leaf extract, was utilized for preparation of selenium nanoparticles. The leaf extract worked as good capping as well as stabilizing agent and facilitated the formation of stable colloidal nanoparticles. Resulting nanoparticles were characterized using UV–Vis spectrophotometer, transmission electron microscopy (TEM), energy dispersive X-ray analysis (EDAX), Fourier transform infrared spectroscopy (FT-IR), and X-ray diffraction analysis (XRD), respectively. The colloidal solution showed the absorption maximum at 390 nm while TEM and selected area electron diffraction (SAED) indicated the formation of polydispersed, crystalline selenium nanoparticles of size raging from 10 to 80 nm. FT-IR analysis suggested the involvement of O–H, N–H, C=O, and C–O functional group of the leaf extract in particle formation while EDAX analysis indicated the presence of selenium in synthesized nanoparticles. The effect of nanoparticles on human lymphocytes treated with arsenite, As(III), has been studied. Studies on cell viability using MTT assay and DNA damage using comet assay revealed that synthesized selenium nanoparticles showed protective effect against As(III)-induced cell death and DNA damage. Chronic ingestion of arsenic infested groundwater, and prevalence of arsenicosis is a serious public health issue. The synthesized benign nanoselenium can be a promising agent to check the chronic toxicity caused due to arsenic exposure.

Although the toxicity of arsenic depends on its chemical forms, few studies have taken into account the ambiguous phenomenon that sodium arsenite (NaAsO 2 ) acts as a potent carcinogen while arsenic trioxide (ATO, As 2 O 3 ) serves as an effective therapeutic agent in lymphoma, suggesting that NaAsO 2 and As 2 O 3 may act via paradoxical ways to either promote or inhibit cancer pathogenesis. Here, we compared the cellular response of the two arsenical compounds, NaAsO 2 and As 2 O 3 , on the Burkitt lymphoma cell model, the Epstein Barr Virus (EBV)-positive P3HR1 cells. Using flow cytometry and biochemistry analyses, we showed that a NaAsO 2 treatment induces P3HR1 cell death, combined with drastic drops in ΔΨm, NAD(P)H and ATP levels. In contrast, As 2 O 3 -treated cells resist to cell death, with a moderate reduction of ΔΨm, NAD(P)H and ATP. While both compounds block cells in G2/M and affect their protein carbonylation and lipid peroxidation, As 2 O 3 induces a milder increase in superoxide anions and H 2 O 2 than NaAsO 2 , associated to a milder inhibition of antioxidant defenses. By electron microscopy, RT-qPCR and image cytometry analyses, we showed that As 2 O 3 -treated cells display an overall autophagic response, combined with mitophagy and an unfolded protein response, characteristics that were not observed following a NaAsO 2 treatment. As previous works showed that As 2 O 3 reactivates EBV in P3HR1 cells, we treated the EBV - Ramos-1 cells and showed that autophagy was not induced in these EBV - cells upon As 2 O 3 treatment suggesting that the boost of autophagy observed in As 2 O 3 -treated P3HR1 cells could be due to the presence of EBV in these cells. Overall, our results suggest that As 2 O 3 is an autophagic inducer which action is enhanced when EBV is present in the cells, in contrast to NaAsO 2 , which induces cell death. That’s why As 2 O 3 is combined with other chemicals, as all-trans retinoic acid, to better target cancer cells in therapeutic treatments.

Arsenic (As) is a hazardous pollutant that negatively impacts the physiological functions of alga. So far, a detailed understanding of algal response to As stress is still lacking. In this study, a transcriptome analysis was performed to illustrate the toxicity response of Caulerpa lentillifera J. Agardh, an edible algae with rich nutrition, to arsenite [As(III)], a toxic form of As. Totally, 1913 differentially expressed genes (DEGs) were screened, of which 642 were up- and 1271 were downregulated in C. lentillifera under As(III) stress (30 mg·L –1 ) compared with control. As(III) stress promoted the growth of C. lentillifera at low concentration (0.1 mg·L –1 ) and inhibited the growth at high concentration (≥ 0.5 mg·L –1 ). Multiple DEGs involved in oxidoreductase activities were significantly affected by As(III), and several DEGs related to antioxidant enzyme activity were downregulated, resulting in suffering from oxidative stress in C. lentillifera . Results also showed that As(III) stress inhibited chlorophyll and carotenoid synthesis, destroyed the integrity of chloroplasts, and interfered with the absorption of light energy, thereby inhibiting photosynthesis in C. lentillifera . The highly enriched ABC transporter-related genes involved in the detoxification process were upregulated under As(III) stress, indicating their critical role in the resistance to As stress in C. lentillifera . The gene expressions for 10 selected DEGs were confirmed by qRT-PCR, showing the reliability of the data revealed by RNA sequencing. Our novel work illustrated the toxicity of C. lentillifera under As(III) stress at the molecular level, serving as a basis for future investigations on the prevention and treatment of such pollutants.

Complexation of arsenite [As(III)] with phytochelatins (PCs) is an important mechanism employed by plants to detoxify As; how this complexation affects As mobility was little known. We used high-resolution inductively coupled plasma-mass spectrometry and accurate mass electrospray ionization-mass spectrometry coupled to HPLC to identify and quantify As(III)-thiol complexes and free thiol compounds in Arabidopsis (Arabidopsis thaliana) exposed to arsenate [As(V)]. As(V) was efficiently reduced to As(III) in roots. In wild-type roots, 69% of As was complexed as As(III)-PC₄, As(III)-PC₃, and As(III)-(PC₂)₂. Both the glutathione (GSH)-deficient mutant cad2-1 and the PC-deficient mutant cad1-3 were approximately 20 times more sensitive to As(V) than the wild type. In cad1-3 roots, only 8% of As was complexed with GSH as As(III)-(GS)₃ and no As(III)-PCs were detected, while in cad2-1 roots, As(III)-PCs accounted for only 25% of the total As. The two mutants had a greater As mobility, with a significantly higher accumulation of As(III) in shoots and 4.5 to 12 times higher shoot-to-root As concentration ratio than the wild type. Roots also effluxed a substantial proportion of the As(V) taken up as As(III) to the external medium, and this efflux was larger in the two mutants. Furthermore, when wild-type plants were exposed to L-buthionine sulfoximine or deprived of sulfur, both As(III) efflux and root-to-shoot translocation were enhanced. The results indicate that complexation of As(III) with PCs in Arabidopsis roots decreases its mobility for both efflux to the external medium and for root-to-shoot translocation. Enhancing PC synthesis in roots may be an effective strategy to reduce As translocation to the edible organs of food crops.

BackgroundArsR-based whole-cell biosensors offer sensitive colorimetric detection of arsenite [As(III)], yet their broad reactivity toward Group 15 metalloids—especially antimonite [Sb(III)]—limits field specificity. The recently identified ant operon from Comamonas testosteroni JL40 confers Sb(III)-selective resistance via the efflux ATPase AntA, the metallochaperone AntC, and the regulator AntR, providing genetic parts to suppress Sb(III) cross-talk.ResultsWe systematically introduced antA, antC, and three antR homologs into an ArsR regulator coupled with a deoxyviolacein reporter chassis (pJ23119-K12). Co-expression of AntA and AntC under a moderate constitutive promoter (PceuR) shifted the Sb(III) limit of detection (LOD) from 0.073 µM to 0.586 µM, with a modest increase in the As(III) LOD to 0.018 µM. Subsequent integration of AntR1 not only maintained the As(III) LOD at 0.018 µM but also unexpectedly amplified the As(III) signal, extending the linear range to 36 nM–37.5 µM (R² = 0.991). It suggests that AntR1 may modulate the transcriptional circuitry via cross-regulation, warranting further mechanistic inquiry. The modified biosensor TOP10/pJ23119-antACR1 exhibited high selectivity for As(III) over divalent metals (Cd, Pb, Cu, Hg, Mn, Mg) and tolerated Sb(III) up to 1 µM. Performance was retained in 90% freshwater and 50% seawater matrices, enabling accurate quantification of 0–2.5 µM As(III) in deionized, tap, surface, and marine samples.ConclusionBy coupling Sb(III)-specific ant efflux/sequestration components with an ArsR-based sensing module, we developed a portable, low-cost biosensor that overcomes longstanding As(III)/Sb(III) cross-reactivity and performs robustly in complex environmental waters.Graphic abstract

Equilibrium sorption studies of anionic species of arsenite, As(III) ions and arsenate As(V) ions onto two biosorbents, namely, chitosan and nanochitosan, have been investigated and compared. The results and trends in the sorption behavior are novel, and we have observed during the sorption process of the As(III) and As(V) on chitosan, a slow process of desorption occurred after an initial maximum adsorption capacity was achieved, before reaching a final but lower equilibrium adsorption capacity. The same desorption trend, however, is not observed on nanochitosan. The gradual desorption of As(III) and As(V) in the equilibrium sorption on chitosan is attributed to the different fractions of the dissociated forms of arsenic on the adsorbent surface and in solution and the extent of protonation of chitosan with the changing of solution pH during sorption. The change of solution pH during the sorption of arsenite ions on chitosan was also influenced by the interaction between the buffering effect of the arsenite species in the aqueous medium and the physical properties of chitosan. The final equilibrium adsorption capacity of chitosan for As(III) and As(V) was found to be around 500 and 8000 μg/g, respectively, whereas the capacities on nanochitosan are 6100 and 13,000 μg/g, respectively.