Journal of Hazardous Materials

Metal(loid) salts have been used to treat infectious diseases due to their exceptional biocidal properties at low concentrations. However, the mechanism of their toxicity has yet to be fully elucidated. The production of reactive oxygen species (ROS) has been linked to the toxicity of soft metal(loid)s such as Ag(I), Au(III), As(III), Cd(II), Hg(II), and Te(IV). Nevertheless, few reports have described the direct, or ROS-independent, effects of some of these soft-metal(loid)s on bacteria, including the dismantling of iron-sulphur clusters [4Fe-4S] and the accumulation of porphyrin IX. Here, we used genome-wide genetic, proteomic, and biochemical approaches under anaerobic conditions to evaluate the direct mechanisms of toxicity of these metal(loid)s in Escherichia coli. We found that certain soft-metal(loid)s promote protein aggregation in a ROS-independent manner. This aggregation occurs during translation in the presence of Ag(I), Au(III), Hg(II), or Te(IV) and post-translationally in cells exposed to Cd(II) or As(III). We determined that aggregated proteins were involved in several essential biological processes that could lead to cell death. For instance, several enzymes involved in amino acid biosynthesis were aggregated after soft-metal(loid) exposure, disrupting intracellular amino acid concentration. We also propose a possible mechanism to explain how soft-metal(loid)s act as proteotoxic agents.

Per- and polyfluoroalkyl substances (PFAS) are highly resistant to enzymatic C-F bond cleavage, and hydrolytic defluorination of long-chain PFAS has rarely been demonstrated. Here, we report selective hydrolytic defluorination of branched perfluorooctanoic acid (PFOA) isomers by a haloacid dehalogenase (4A) from Delftia acidovorans strain D4B. A fluoride-specific riboswitch biosensor was used for initial substrate screening, followed by scaled-up assays in which fluoride release was quantified using a fluoride ion-selective electrode. Defluorination products were subsequently identified by liquid chromatography-mass spectrometry (LC-MS). Although purified 4A (10 M) readily catalyzed hydrolytic defluorination of fluoroacetic acid, incubation of PFOA (0.5 mM) with purified 4A resulted in a statistically significant increase in fluoride release at elevated enzyme loading (500 M). High-resolution LC-MS/MS analysis revealed that defluorination products originated from minor branched PFOA isomers rather than linear PFOA. Molecular docking analyses supported catalytically plausible binding geometries for branched PFOA isomers, positioning the substrate -carbon within [~]4 [A] of the catalytic aspartate residue. These findings demonstrate previously unrecognized hydrolytic reactivity of a haloacid dehalogenase toward branched PFAS isomers and expand the known catalytic scope of the haloacid dehalogenase family. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=109 SRC="FIGDIR/small/719434v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@16da75dorg.highwire.dtl.DTLVardef@6f575org.highwire.dtl.DTLVardef@dcf737org.highwire.dtl.DTLVardef@ea4ec9_HPS_FORMAT_FIGEXP M_FIG C_FIG SYNOPSISEnzymatic defluorination of PFAS is rarely observed in environmental systems. This study identifies hydrolytic defluorination of branched PFOA isomers, improving understanding of PFAS defluorination at the enzyme level.

Per- and polyfluoroalkyl substances (PFAS) are widespread environmental contaminants with documented toxic effects, yet their multi- and transgenerational impacts on neurodevelopment and underlying mechanisms remain poorly understood. Here, we present a comprehensive study delineating the effects of developmental exposure to environmentally relevant concentrations of PFOS and PFBS on behavior, transcriptome, and genome-wide DNA methylation patterns in the directly exposed generation (F0) and their unexposed offspring (F1 and F2) in zebrafish. Both PFOS and PFBS altered larval behavior, linked to transcriptomic and DNA methylation changes in neuro-related pathways, even in the unexposed offspring. Importantly, specific DNA methylation changes in F0 were associated with behavioral outcomes in F2 animals, suggesting that these alterations could underlie transgenerational effects. Pathways associated with differentially methylated genes were prominently enriched for response to light and circadian regulation. Our findings demonstrate that developmental exposure to PFAS causes transgenerational behavioral effects in zebrafish and suggest that epigenetic changes induced by direct exposure may serve as markers for predicting outcomes in subsequent, unexposed generations. TEASERPFAS induce circadian-related epigenetic changes in zebrafish associated with behavioral impacts in unexposed offspring.

Microbial arsenic methylation is established as a detoxification process under aerobic conditions (converting arsenite to monomethylated arsenate) but proposed to be a microbial warfare strategy under anoxic conditions due to the toxicity of its main product monomethylarsonous acid (MMAs(III)). Here, we leveraged a paddy soil-derived anaerobic arsenic methylator, Paraclostridium bifermentans strain EML, to gain insights into this process. Strain EML was inoculated into a series of media involving systematic dilutions of Reinforced Clostridial Broth (RCB) with 25 M arsenite to assess the impact of growth substrate concentration on arsenic methylation. Growth curves evidenced the sensitivity of strain EML to arsenite, and As speciation analysis revealed the production of MMAs(III). Concentrations of MMAs(III) and arsenic methylation gene (arsM) transcription were found to be positively correlated with the RCB dilution, suggesting that substrate limitation enhances arsM gene expression and associated anaerobic arsenic methylation. We propose that growth substrate competition between microorganisms may also lead to an increase in anaerobic As methylation. This hypothesis was further evaluated in an anaerobic co-couture mode of strain EML with either wild-type Escherichia coli K-12 MG1655 (WT) or E. coli expressing the MMAs(III)-resistance gene (arsP), (ArsP E. coli). We found increased MMAs(III) production in the presence of E. coli than its absence and growth inhibition of WT E. coli to a greater extent than ArsP E. coli, presumably due to MMAs(III) produced by strain EML. Taken together, our findings point to an ecological role for anaerobic arsenic methylation, highlighting the role of microbe-microbe competition/interaction in this process. IMPORTANCEAnaerobic arsenic methylation is enhanced in rice paddy soils under flooding conditions than that under drying conditions, leading to increased methylated arsenic accumulation in rice grains. Unlike the known detoxification role for aerobic arsenic methylation, the ecological role of anaerobic arsenic methylation remains elusive and is proposed to be an antibiotic-producing process involving in microbial warfare. In this study, we interrogated a rice paddy soil-derived anaerobic arsenic-methylating bacterium (Paraclostridium bifermentans strain EML) to investigate the effect of growth substrate limitation on arsenic methylation by strain EML in the context of the microbial warfare hypothesis. We provide direct evidence for the role of growth substrate competition in anaerobic arsenic methylation by strain EML. Furthermore, we evidence a feedback loop, by which a bacterium resistant to MMAs(III) enhances its production, presumably through enhanced arsM expression resulting from substrate limitation. Our work uncovers complex interactions between an anaerobic arsenic methylator and potential competitors.

Extensive mineral weathering and formation of large amounts of Fe-rich secondary mineral gels have been identified as precursors critical to forming massive hardpan caps in the surface layers of sulfidic tailings. However, how to initiate and accelerate these precursor processes remains to be established before developing this hardpan-based novel method to rehabilitate sulfidic tailings landscapes. In a 5-month microcosm experiment, the present study has demonstrated the concept of bio-engineering sulfidic tailings by inoculating Fe/S-oxidizing bacterial consortium to accelerate the weathering of sulfides and other Si-rich minerals for mineral gels formation. Synchrotron-based X-ray absorption fine structure spectroscopy (XAFS) demonstrated that the weathering of pyrite and biotite-like minerals was rapidly accelerated by the presence of Fe/S-oxidizing bacterial consortium. The microbial process and associated mineral transformation led to the formation of critical precursor mineral gels, i.e., jarosite-like minerals, as indicators of the onset of hardpan formation. In the meantime, the labile Zn liberated in the weathering was encapsulated in the jarosite-like minerals as revealed by X-ray fluorescence microscopy (XFM). This concept-proven bio-engineering process is ready to be scaled up in further studies under field conditions to develop an alternative hardpan-based method to cover and rehabilitate sulfidic tailing landscapes. TOC Art O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC="FIGDIR/small/285858v1_ufig1.gif" ALT="Figure 1"> View larger version (83K): org.highwire.dtl.DTLVardef@fc0292org.highwire.dtl.DTLVardef@10ce8c7org.highwire.dtl.DTLVardef@868a63org.highwire.dtl.DTLVardef@e77d57_HPS_FORMAT_FIGEXP M_FIG C_FIG

Mesoporous nanoparticles (NPs) are an interesting drug delivery system that has generated considerable attention in the biomedical sector. Despite recent attempts to conduct safety assessments using traditional methods based on phenotypic data, our understanding of the underlying molecular processes produced by mesoporous NPs is still in its infancy. In the present study, RNA sequencing was used to assess the biological perturbations and the pathways induced in response to early exposure of two different mesoporous NPs; mesoporous silica NPs (MSN) and mesoporous carbon NPs (MCN) in human liver hepatocellular carcinoma cells. In order to better understand the risks associated with NPs, it is required to consider the initial low-dose exposure effects that mimic the real exposure scenario. No overt toxicity was detected in the MTT assay when performed at 6 hours at low concentrations (MCN 25 g/ml and MSN 15 g/ml) of NPs; thus, we have selected this dose for RNA sequencing analysis. Our transcriptomics analysis showed significant differences in the expression of many genes after exposure to both NPs. Surprisingly, both NPs frequently deregulated 52.9 percent of upregulated and 42 percent of downregulated genes. Gene ontology categories, in particular, revealed comparable perturbations of biological reactions in the cellular system. HepG2 cells reacted to mesoporous NPs by allowing alterations in genes involved in cytoskeleton reorganisation (ATAT1, DMTN, PTK2 and PFN2). Exposure to mesoporous NPs increased transcripts expressing ubiquitin ligase (RNF187, ARIH2, VHL, and RAB40C), transferase (FBXO3 and WDSUB1), conjugating (UBE2J2), and also proteasomal subunits (PSMD2, PSMD13) enzymes, indicating that protein turnover rates are altered in response to environmental damage. In addition, DNA damage and DNA damage checkpoint genes were upregulated, indicating that NPs induced stress in the cells. These finding showed low dosage acute exposure have comparable responses between mesoporous NPs. These results may add further knowledge in conceptualization of Safer-by-Design strategy of NPs in biomedical field.

Organic germanium, particularly carboxyethyl germanium sesquioxide (Ge-132), has been investigated for decades in relation to diverse biological effects, with a strong emphasis on its antioxidant properties. However, the available literature remains dispersed, encompassing heterogeneous experimental models and endpoints that limit mechanistic interpretation. While antiglycative activity has been described at the biochemical level, its downstream gene regulatory consequences under glycative stress remain inconsistently characterized. Here, we combined systematic review of the literature of experimental studies with targeted molecular analysis in a standardized cellular model. The literature mapping was used to guide pathway selection rather than to establish quantitative associations. Based on patterns emerging from literature, we focused on pathways associated with glycative stress responses, including carbonyl stress, inflammatory signaling, and autophagy regulation. Gene expression analysis revealed a limited and selective modulation of regulatory pathways under glycative stress conditions, consistent with a context-dependent effect rather than broad transcriptional reprogramming. In parallel, protein analysis showed reduced intracellular accumulation of advanced glycation end products (AGEs) in Ge-132-treated cells under glycative stress conditions. Importantly, these findings support a dissociation between glycative damage reduction and cellular stress-response pathways. This combined approach helps interpretation of previously fragmented observations across the literature and highlights gene regulation under glycative stress as a relevant but still unresolved aspect of organogermanium biology.

Depleted uranium (DU) is an environmental contaminant with a 30 g/L (ppb; parts per billion) EPA maximum contaminant level (MCL) for drinking water. The mining of uranium and use of DU in modern weapons underly human exposure that disproportionally impacts military and tribal communities in the United States. Uranium's radiotoxic characteristics are understood, but its chemical hazards much less so. In zebrafish (Danio rerio) and human cell cultures we test the hypothesis that exposure to DU negatively impacts cellular function and development through disruption of mitochondrial metabolism. Using a novel shrapnel model with TEM/SEM+EDS, we showed uranium microparticles caused proximity-dependent mitochondrial disruption. In waterborne exposure paradigms, larval movement was reduced and hatching delayed as a result of reduced movement and not enzyme deficiencies in response to 18 ppb DU, below the MCL. Increased DNA damage accumulation was detected in exposed larva and cells. DNA-damage quantitative PCR of DU-exposed larvae showed increased damage in the ahr1 locus (nuclear gene) and decreased mitochondrial DNA (mtDNA) copy number, but mtDNA damage levels varied across experiments. Mitochondrial function was assessed using a resazurin-based assay in the presence and absence of antioxidants and showed diminished cytoplasmic reductive capacity. DU exposure alone did not enrich antioxidant gene expression, contrasting with arsenic exposure, a known ROS-inducer and Nrf2-activator. Sulforaphane (SFN), a potent Nrf2-activator, did not blunt the effects of DU exposure, despite activation of antioxidant response element (ARE) genes (gstp and gss), but did blunt the effects of arsenic exposure. The most enriched transcript in DU-exposed larvae coded for slingshot protein phosphatase (ssh), further exploration revealed ssh1b as the zebrafish-specific ortholog activated in response to DU, and inhibition using an identified SSH1 inhibitor, Sennoside A, partially rescued the metabolic and hatching defects observed. Our data points to a cytotoxic mechanism in which DU disrupts mitochondrial function through ssh1b enrichment that impairs normal mitophagy, leading to decreased cellular reductive potential independent of either ROS production or ARE-activation. Our results suggest that health impacts from DU exposure may be directly linked to impaired mitochondrial functions.

Nanoparticles (NPs) are important in a variety of sectors, including disease diagnostics, medicine, nutrition, and many other industries. The risk of human exposure demands an early evaluation of both the basic dynamics of NPs interaction with biological systems and their potential consequences. Deciphering these occurrences will provide critical information regarding the health hazards and safety advantages associated with next-generation nanoformulations in clinical practice. We examined the HepG2 cell line in a systematic manner to determine the cellular response to single-walled carbon nanotubes (SWCNTs) and zinc oxide (ZnO) NPs. With the use of high-throughput transcriptomic methods, we found that both NPs induce comparable dysregulation of the endocytic and proteasomal complex genes in liver hepatocellular carcinoma cells, at levels (> 80 percent cell viability) that do not cause over-toxicity at early incubation period (6 h). SWCNT and ZnO NPs were shown to enter cells through clathrin-mediated pathways, affecting cytoskeleton gene expression, DNA damage and repair, protein ubiquitination, and cell transcriptional machinery. Our findings indicate that early response strategies activate stress-related mechanisms. Finally, this method for studying nanomaterial-cell interactions demonstrates how changes in the transcriptome profile may predict downstream consequences even at doses that do not cause acute toxicity.

Airborne nanoplastics constitute an emerging class of environmental contaminants, but their mitoepigenetic effects on human immune cells have not been systematically investigated. Ex vivo human lymphocytes were used to investigate integrated mitochondrial, epigenetic, and inflammatory responses induced by polystyrene (PS), polypropylene (PP), and polyvinyl chloride (PVC) nanoplastics. Fluorescence microscopy at multiple exposure time points and flow cytometry confirmed efficient cellular internalization and progressive intracellular accumulation of nanoplastics. Exposure elicited coordinated transcriptional remodeling of genes regulating mitochondrial dynamics (DRP1, MFN1), mitochondrial DNA encoded oxidative phosphorylation components (MT-ATP6, MT-COX1, MT-ND6), DNA repair (OGG1, APE1), DNA methylation machinery (DNMT1, DNMT3a, DNMT3b), and mitochondrial-associated miRNAs (miR-21, miR-34a, miR-155). Functional analyses revealed polymer and time-dependent disruption of mitochondrial membrane potential and respiratory chain activities, with Complex I identified as the primary site of vulnerability. Correlation analysis showed strong positive associations among DRP1, OMA1, DELE1, and ND6 (r > 0.9, R{superscript 2} > 0.8, p < 0.001), reflecting coordinated mitochondrial stress and epigenetic signaling, while negative correlations between DRP1 and MFN1 (r = -0.54, R{superscript 2} = 0.29, p < 0.01) and between APE and ND6 (r {approx} -0.42, R{superscript 2} {approx} 0.18, p < 0.05) highlight antagonistic regulation and impaired mitochondrial network stability linked to Complex I dysfunction. In silico docking of oxidized nanoplastic oligomers identified high-affinity interactions at the Complex I Fe-S cluster and cofactor-binding sites, suggesting direct interference with electron transfer. A random forest-based model accurately predicted MT-ND6 expression from Complex I activity (R{superscript 2} > 0.85), establishing a data-driven Complex I-ND6 axis. Collectively, these findings demonstrate that airborne nanoplastics induce integrated mitoepigenetic and immunometabolic dysregulation, underpinned by coordinated and antagonistic regulatory interactions in lymphocytes.

Tellurium (Te) is a rare element in the chalcogen group, and its biogeochemical cycle has been investigated for decades. As the most soluble Te species, tellurite (Te(IV)) possess the highest toxicity to the organisms. Chemical or biological Te(IV) reduction to elemental tellurium (Te0) is generally considered as an effective detoxification route for Te(IV)-containing wastewater. Here, we reported a previously overlooked Te0 oxidation process mediated by manganese-oxidizing bacterium Bacillus sp. FF-1. This strain has both Mn(II)-oxidizing and Te(IV)-reducing activities, which could produce manganese oxides (BioMnOx) and Te0 (BioTe0) when incubating with Mn(II) and Te(IV), respectively. Te(IV) can co-precipitated with Mn(II) to form highly stable Te(IV)-Mn(II) compounds with low bioavailability. While when 5 mM Mn(II) was added after incubating 0.1 mM or 1 mM Te(IV) with strain FF-1 for 16 hours, the BioTe0 were certainly re-oxidized to Te(IV) by BioMnOx according to the results of X-ray photoelectron spectra (XPS) and Transmission electron microscope (TEM). The chemogenic and exogenous biogenic Te0 can also be oxidized by the BioMnOx, although with different rates. This study highlights a new transformation process of tellurium species mediated by manganese-oxidizing bacteria, revealing that the environmental fate and ecological risks of Te0 needed to be re-evaluated. ImportanceBiogeochemical cycle of Te mediated by bacteria mainly focus on the Tellurite reduction and methylation. In this study, the indirect tellurium (Te0) oxidation driven by manganese-oxidizing bacterium is firstly confirmed. As Te0 usually considered as a stable and safe products during Te(IV)-containing wastewater treatment, we suppose the ecological risks of Te0 needed to be re-evaluated due to the possible oxidation by manganese-oxidizing bacterium and its generated manganese oxides.

Urease is a nickel-dependent enzyme that plays an important role in urea hydrolysis and in a process named as microbial-induced calcium carbonate precipitation (MICP), which is widely used in sustainable environmental biotechnology. Despite its ecological importance, urease powers Biogrout (biocementation), a promising green technology for soil stabilization and infrastructure repair. Yet, the relationship between nickel availability, enzyme activation, and bacterial fitness remains poorly understood. In this study, we reveal a striking dual effect of nickel on Sporosarcina pasteurii: while high Ni{superscript 2} concentrations strongly inhibit growth (IC {approx} 637.7 {micro}M), they simultaneously boost specific urease activity up to six-fold. This uncoupling between biomass and enzymatic efficiency highlights a previously overlooked adaptive strategy under metal stress. Using structural bioinformatics and molecular docking, we show that Ure1--the catalytic subunit--exhibits the strongest nickel affinity (-4.3 kcal{middle dot}mol-{superscript 1}), supported by highly conserved active-site residues, whereas accessory proteins UreE and UreG display moderate and weak binding, consistent with their roles in metal delivery and GTP-dependent maturation. In addition, microscopic observations confirmed that calcium carbonate precipitation was most pronounced at intermediate nickel concentrations (approximately 400-1000 {micro}M), whereas higher concentrations ([&ge;]1000-1300 {micro}M) led to reduced mineral formation due to loss viable cells. Taken together, these results indicates that nickel availability controls both urease activation and bacterial fitness, and that an optimal balance is required to maximize biomenerilization efficiency in environmental applications, particularly in biocementation technology. ImportanceUrease-driven biomineralization is widely used in sustainable technologies such as soil stabilization and self-healing concrete. However, optimizing these systems requires a clear understanding of how environmental factors influence enzyme performance. This study shows that nickel, an essential cofactor for urease, plays a dual role by enhancing enzymatic activity while inhibiting bacterial growth at high concentrations. By integrating experimental data with computational analysis, we demonstrate that efficient biomineralization depends on maintaining nickel within an optimal range that balances enzyme activation and microbial viability. These findings provide practical guidance for improving biocementation processes and highlight nickel as a key regulator of urease-based environmental biotechnology applications.

Chemically complex pharmaceutical mixtures in wastewater and sludge can affect microbial adaptation; however, the responses to different co-occurring compounds have not been elucidated well. In this study, the adaptation of a strain derived from hospital sludge, Klebsiella pneumoniae SS02, to 17-ethinylestradiol (EE2), warfarin sodium, and their combination has been studied. The organism grows under all three conditions, and pre-exposure experiments show induction and cross-induction to substrates. UHPLC MS/MS analyses demonstrated that there is conditional depletion of the parent compound EE2 by [~]15% at 36 h post-treatment compared to initial concentrations, but not for the abiotic and non-adapted controls. The rate of warfarin sodium depletion was approximately [~]30% within 36 h and was in accordance with first order kinetics (k = 0.0102 /h; t{square}/{square}= 67.9 h). Under the combined treatment regime, there was a delay in warfarin sodium depletion, suggesting staged substrate consumption. Growth inhibition with efflux inhibitors confirmed transport-driven tolerance. A genome-based study revealed the coordinated response strategy that involved a proposed flavin-dependent monooxygenase (RutA), an oxidative entry into the pathway; redox processing linked to Hpa; aromatic metabolism through {beta}-ketoadipate pathway; and RND efflux system. The structural study additionally supported ligand-mediated decrease in DNA binding affinity of RutR, which is in agreement with de-repression of the substrate-activated regulatory mechanism. All these findings lead to the development of a dual-strategy for adaptation model in which oxidative modification and efflux-mediated protection work together under the influence of a mixture of pharmaceuticals.

Nanoplastics (NPs) are emerging environmental contaminants able to cross biological barriers, disrupt cellular and organelle homeostasis, and alter the brain microenvironment. This study investigated whether NPs affect microglia to neuron communication, a key mechanism underlying neuronal resilience, via the nuclear factor erythroid 2 like 2 (NFE2L2) pathway. Using an in vitro model, we evaluated the effects of polystyrene nanoplastics on microglial metabolic fitness and microglia-mediated neuronal stress responses. Increasing NP concentrations induced a dose dependent biphasic effect. Low to intermediate concentrations increased intracellular adenosine triphosphate (ATP) levels in microglia and enhanced microglia-mediated activation of neuronal NFE2L2. In contrast, high NP concentration impaired microglial metabolism, reduced ATP availability, and decreased microglia to neuron communication. These findings indicate that NPs alter microglial energetic status and modulate neuroprotective signalling, potentially contributing to impaired neuron to microglia interactions and increased susceptibility to neurotoxicity.

The discovery of cisplatin and its anti-tumor activities but also its side-effects led to the development of new cytotoxic metal complexes. Metal-based compounds and especially gold N-heterocyclic carbene complexes have shown their antitumoral activities and present a great interest of use in medicine. These metallodrugs have been shown to target nuclear DNA, but also other organelles such as mitochondria. The mechanisms of action have been studied and would involve the triggering of cell death, in particular by apoptosis, highlighting mitochondrial dysfunctions. The organometallic compound used in this study has been characterized by its IC50 and GI50 in two prostatic cancer cell lines (LNCaP and PC3). Its capacity to enter the cells and particularly mitochondria was also analyzed. Furthermore, its effects on several parameters (proliferation, cell death, cell cycle) have been determined in vitro. The compound displayed a cytotoxic effect (IC50 < 5{micro}M) confirmed by the MTT assays and cell death analysis by flow cytometry. It also displayed a cytostatic effect confirmed by the determination of the GI50, and induced a brief cell cycle arrest, depending on the cell line and the metallocarbene concentration. Furthermore, the incubation with the gold N-heterocyclic carbene led to mitochondrial membrane potential changes and decreased the accumulation of the mitochondrial protein Rieske. All our results show a global cytotoxic and cytostatic effects of the gold N-heterocyclic carbene that can involve mitochondria.

This study presents the first exploratory assessment of antibiotic resistance genes (ARGs) and antibiotic residues in agricultural environments on Reunion Island, a French tropical territory in the south-western Indian Ocean. Sixteen samples from diverse matrices (manure, soil, water, and vegetables) across different agroecosystems were analyzed using high-throughput qPCR targeting 332 ARGs and chemical methods targeting 58 antibiotic compounds and trace elements. ARGs were widely detected across all matrices, with highest abundance observed in amended soils and manure. Surprisingly, ARG profiles, in terms of both abundance and average number, were comparable between unamended soils and natural soils. Antibiotic residues were found in only five manure and soil samples, with no clear correlation between the presence of these residues, trace elements and ARG abundance. Organic amendments significantly increased ARG levels in soils and non-metric multidimensional scaling revealed that ARG profiles clustered primarily by matrix type rather than by location. High-risk ARGs were widely prevalent, with 86% detected and 23% ubiquitous across all samples, and their occurrence in water and raw vegetables suggests potential human exposure through the food chain. This study highlights the influence of agricultural practices on environmental antimicrobial resistance in tropical island contexts and supports the need for expanded One Health surveillance integrating the environmental, animal and human compartments. SynopsisThis study shows that agricultural practices can shape the environmental spread of antibiotic resistance in tropical island ecosystems, highlighting potential risks for ecosystems, food safety, and human health. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=73 SRC="FIGDIR/small/702181v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@1d07b87org.highwire.dtl.DTLVardef@5e1150org.highwire.dtl.DTLVardef@1c2afe4org.highwire.dtl.DTLVardef@a9be55_HPS_FORMAT_FIGEXP M_FIG C_FIG

Application of carbonaceous nanomaterials (CNMs) to the soil-plant system can affect plant physiology, with positive results ranging from enhanced seed germination and root system development to improved stress tolerance. The underlying mechanisms are not fully understood. Plant rhizosphere microbiomes at the soil-root interface are strongly influenced by the host plant and play a key role in the plant hosts development and health. Yet few studies have characterized changes in plant rhizosphere microbiomes following applications of CNMs to the soil-plant system. Here we investigated the effects of multi-walled carbon nanotube (CNT) and graphene on microbial communities in the ectorhizosphere of tomato plants versus surrounding bulk soil. Pot experiments were conducted where tomato plants were exposed to CNT or graphene at 200 mg/kg soil for four weeks. Ectorhizosphere and bulk soils were then collected and analyzed for physicochemical properties and microbiome structure and function. While graphene had a limited impact on the tomato rhizosphere microbiome, CNT significantly increased microbial alpha diversity, induced greater divergence of beta diversity, enhanced microbial interactions, and potentially impacted community functions such as aromatic compound degradation, antioxidant synthesis, and redox cofactor biosynthesis. Furthermore, CNT induced stronger and/or unique microbiome alterations in the tomato rhizosphere compared to bulk soil. Our findings reveal the differential modulating effects of two widely-used CNMs on plant rhizosphere microbiomes and highlight an imminent need to understand complex plant root-microbe interplays in the CNM-impacted rhizosphere. These results have implication for realizing the full potential of phytoapplication of CNMs toward improved and sustainable plant production.

Bacteria innately monitor their environment by dynamically regulating gene expression to respond to fluctuating conditions. Through synthetic biology, we can harness this natural capability to design cell-based sensors. Bacillus megaterium, a soil bacterium, stands out due to its remarkable heavy metal tolerance and sporulation ability, making it an ideal candidate for heavy metal detection with low transportation costs. However, challenges persist: the synthetic biology toolkit for this strain is underdeveloped and conventional whole-cell sensors necessitate specialized laboratory equipment to read the output. In our study, we genetically modified B. megaterium for arsenic detection, establishing a detection threshold below the EPA recommendation of 10 ppb for drinking water in both vegetative cell form and spore form. Additionally, we integrated both engineered B. megaterium living cells and spores with CMOS chip for field-deployable arsenic detection. We show that the limit of detection of our integrated sensor is applicable in soil and air arsenic contamination testing. As a proof of concept, this work paves the way for deploying our sensor in resource-limited settings, ensuring real-time arsenic detection in challenging environments. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=108 SRC="FIGDIR/small/604150v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@1940e83org.highwire.dtl.DTLVardef@144da0aorg.highwire.dtl.DTLVardef@146e906org.highwire.dtl.DTLVardef@6cb8c1_HPS_FORMAT_FIGEXP M_FIG C_FIG

Various environmental aged plastic wastes were collected in the environment and crushed to the nanometric scale to get a mix of nanoplastics (NPs) of different natures - mostly polyolefins (PE, PP), polyesters (PET) and polyvinylics (PS and PVC) - and undefined shapes (noted NP-L, mean hydrodynamic diameter at 285 nm). We aimed to test the toxicity of NPs of environmentally relevance on freshwater bivalves and compare results to commonly used styrenic NP-PS (206 nm). Corbicula fluminea were exposed to four different conditions with NPs (0.008 to 10 g/L), for 21 days and kept under depuration conditions for 21 additional days: 1) waterborne exposure to NP-L, 2) diet borne exposure to NP-L, 3) synergic waterborne exposure to NP-L and AlCl3 salt (1 mg/L), 4) waterborne exposure to NP-PS. Enzyme activities, gene expressions and behavioural tests were assessed. Trophic and synergic exposures with Al triggered more gene modulations than direct exposure to NP-L (namely on 12s, atg12, gal, segpx, p53 and ache). NP-PS were also more harmful than NP-L, but only at high concentrations (10 g/L). The effects of each treatment lasted until 7 days of depuration and no more gene inductions were observed after 21 days in clean water. Very few effects were shown on phenol-oxidase (PO), and glutathione S-transferase (GST). However, the inhibition of acetylcholinesterase (AchE) was concomitant with an increase of the filtration activity of bivalves exposed to NP-L (trophic route) and NP-PS, suggesting neurotoxic effects. By disturbing the ventilatory activity, NPs could have direct effects on xenobiotic accumulation and excretion capacities. The results point out how the structure, aging, exposure routes and additional xenobiotics can interact with adverse outcomes of NPs in bivalves. These findings underline the importance to consider naturally aged environmental NPs in ecotoxicological studies rather than synthetic latexes, i.e. crosslinked nanospheres prepared from virgin polymers. This manuscript presents the first data of toxicity on freshwater organisms exposed to nanoplastics coming from natural sources. Whereas the majority of papers are dealing with non-environmentally representative plastics (mainly commercially-available polystyrene latexes) to evaluate nanoplastic effects on organisms, this study develops methods to prepare model nanoplastics from plastic wastes collected in rivers, and to assess their real adverse effects on aquatic organisms. Our results show significant differences between the inflammatory effects triggered by nanoplastics coming from natural sources and polystyrene nanobeads. This work suggests that the data published so far in the literature may underestimate the toxicity of nanoplastics spread into the environment on the aquatic organisms at the bottom of the food chain, which might consequently impart halieutic resources on the long term.

Environmentally-friendly and low emission extraction methods are needed to meet worldwide rare earth element (REE) demand. Within a greenhouse setting, we assessed the REE hyperaccumulation ability of four plant species (e.g., Phalaris arundinacea, Solanum nigrum, Phytolacca americana, and Brassica juncea) and the impact of amending REE-rich soil with biochar or fertilizer and watering with citric acid solution. Harvested samples were pyrolyzed, and the resulting bio-ores were acid-digested and underwent elemental analysis to determine REE content. Amending soil with fertilizer and biochar increased bio-ore production, while plant species explained most variation in bioaccumulation factor. Phalaris arundinacea achieved the highest average REE concentration of 27,940 ppm for targeted REEs (i.e., cerium, lanthanum, neodymium, praseodymium, and yttrium) and 37,844 ppm for total REEs. We successfully extracted REE-rich bio-ore from plant biomass and determined that soil amendment and plant species will be critical parameters in design and implementation of Idaho-based REE phytomining operations. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/606409v1_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@f616a6org.highwire.dtl.DTLVardef@490d9borg.highwire.dtl.DTLVardef@1c6a72org.highwire.dtl.DTLVardef@1908340_HPS_FORMAT_FIGEXP M_FIG C_FIG