Chlorinated polyfluorinated ether sulfonate (Cl-PFESA) is a novel alternative compound for perfluorooctane sulfonate (PFOS), with its environmental risk not well known. The bioaccumulation and toxic effects of Cl-PFESA in the freshwater alga is crucial for the understanding of its potential hazards to the aquatic environment. Scenedesmus obliquus was exposed to Cl-PFESA at ng L⁻¹ to mg L⁻¹, with the exposure regime beginning at the environmentally relevant level. The total log BAF of Cl-PFESA in S. obliquus was 4.66, higher than the reported log BAF of PFOS in the freshwater plankton (2.2–3.2). Cl-PFESA adsorbed to the cell surface accounted for 33.5–68.3% of the total concentrations. The IC50 of Cl-PFESA to algal growth was estimated to be 40.3 mg L⁻¹. Significant changes in algal growth rate and chlorophyll a/b contents were observed at 11.6 mg L⁻¹ and 13.4 mg L⁻¹ of Cl-PFESA, respectively. The sample cell membrane permeability, measured by the fluorescein diacetate hydrolyzation, was increased by Cl-PFESA at 5.42 mg L⁻¹. The mitochondrial membrane potential, measured by Rh123 staining, was also increased, indicating the hyperpolarization induced by Cl-PFESA. The increasing ROS and MDA contents, along with the enhanced SOD, CAT activity, and GSH contents, suggested that Cl-PFESA caused oxidative damage in the algal cells. It is less possible that current Cl-PFESA pollution in surface water posed obvious toxic effects on the green algae. However, the bioaccumulation of Cl-PFESA in algae would contribute to its biomagnification in the aquatic food chain and its effects on membrane property could potentially increase the accessibility and toxicity of other coexisting pollutants.

The effects of the ionic liquid 1-octyl-3-methylimidazolium chloride ([OMIM]Cl) was studied in hydroponically grown rice seedlings. Observed effects included increased root length and weight at concentrations of 0.1 mg/L [OMIM]Cl, however, as concentrations increased a reversed response was observed where roots and stems grew shorter and the weight decreased. The inhibitory concentration 50 (IC50,5d) values for root length and stem length were 0.59 mg/L and 0.70 mg/L, respectively. The Hill reaction activity and root system activity in [OMIM]Cl-treated rice seedlings were observed to be lower than the controls, however, root membrane permeability increased. The antioxidant enzyme activity in roots decreased, while in leaves there was an initial stimulation followed by a decrease. Malondialdehyde (MDA) content was found to be greater in seedlings subjected to [OMIM]Cl treatment. The cellular structures, such as chloroplasts, mitochondria and rough endoplasmic reticulum in rice root and leaf cells were affected at concentrations of 0.6 mg/L [OMIM]Cl.

Per- and Poly-fluoroalkyl substances (PFAS) are one of the major persistent environmental contaminants. Epidemiological studies have linked PFAS exposures to altered immunity and increased occurrence of infections in children. However, the mechanisms leading to immune susceptibility to bacterial infections remains unclear. To elucidate the mechanism, transcriptional alteration in the Caenorhabditis elegans model caused by a PFAS contaminated environmental water and two reconstituted PFAS solutions were evaluated using RNA-sequencing. PFAS affected the expression of several genes involved in C. elegans immune surveillance to Gram-positive bacteria (cpr-2, tag-38, spp-1, spp-5, clec-7, clec-172). The combined exposure to PFAS and Staphylococcus aureus significantly reduced C. elegans survival and increased intestinal membrane permeability. Furthermore, the growth of S. aureus in the presence of PFAS increased the expression of virulence genes, specifically, the virulence gene regulator saeR and α-hemolysin, hla, which resulted in increased hemolytic activity. The present study demonstrated that PFAS exposure not only increased C. elegans susceptibility to pathogens by reducing host immunity and increasing intestinal membrane permeability, but also increased bacteria virulence. This presents a broader implication for humans and other animals, where environmental contaminants simultaneously reduce host resilience, while, increasing microbial pathogenicity.

Co-selection of antibiotic resistance genes (ARGs) by heavy metals might facilitate the spread of ARGs in the environments. Cadmium contamination is ubiquitous, while, it remains unknown the extent to which cadmium (Cd²⁺) impact plasmid-mediated transfer of ARGs in aquatic bacterial communities. In the present study, we found that Cd²⁺ amendment at sub-inhibitory concentration significantly increased conjugation frequency of RP4 plasmid from Pseudomonas putida KT2442 to a fresh water microbial community by liquid mating method. Cd²⁺ treatment (1–100 mg/L) significantly increased the cell membrane permeability and antioxidant activities of conjugation mixtures. Amendments of 10 and 100 mg/L Cd²⁺ significantly enhanced the mRNA expression levels of mating pair formation gene (trbBp) and the DNA transfer and replication gene (trfAp) due to the repression of regulatory genes (korA, korB and trbA). Phylogenetic analysis of transconjugants indicated that Proteobacteria was the dominant recipients and high concentration of Cd²⁺ treatment resulted in expanded recipient taxa. This study suggested that sub-inhibitory Cd²⁺ contamination would facilitate plasmid conjugation and contributed to the maintenance and spread of plasmid associated ARGs, and highlighted the urgent need for effective remediation of Cd²⁺ in aquatic environments.

The current study for the first time demonstrates the interference of a free-living, N₂-fixing, and nanoparticle (NP) tolerant Azotobacter salinestris strain ASM recovered from metal-polluted soil with tomato plant-metal oxide NPs (ZnO, CuO, Al₂O₃, and TiO₂) interactions in a sandy clay loam soil system with bulk materials as control. Tomato plants were grown till full maturity in soils amended with 20–2000 mg kg⁻¹ of each metal-oxide NP with and without seed biopriming and root-inoculation of A. salinestris. A. salinestris was found metabolically active, producing considerably high amounts of bioactive indole-3-acetic-acid, morphologically unaffected, and with low alteration of cell membrane permeability under 125–1500 μgml⁻¹ of NPs. However, ZnO-NPs slightly alter bacterial membrane permeability. Besides, A. salinestris secreted significantly higher amounts of extracellular polymeric substance (EPS) even under NP exposure, which could entrap the NPs and form metal-EPS complex as revealed and quantified by SEM-EDX. NPs were also found adsorbed on bacterial biomass. EPS stabilized the NPs and provided negative zeta potential to NPs. Following soil application, A. salinestris improved the plant performance and augmented the yield of tomato fruits and lycopene content even in NPs stressed soils. Interestingly, A. salinestris inoculation enhanced photosynthetic pigment formation, flower attributes, plant and fruit biomass, and reduced proline level. Bacterial inoculation also reduced the NP’s uptake and accumulation significantly in vegetative organs and fruits. The organ wise order of NP’s internalization was roots > shoots > fruits. Conclusively, A. salinestris inoculation could be an alternative to increase the production of tomato in metal-oxide NPs contaminated soils.

3-Acetyldeoxynivalenol (3-Ac-DON), the acetylated derivative of deoxynivalenol (DON), has been reported to be coexisted with DON in various cereal grains. Ingestion of grain-based food products contaminated by 3-Ac-DON might exert deleterious effects on the health of both humans and animals. However, the biological toxicity of 3-Ac-DON on macrophages and the underlying mechanisms remain largely unknown. In the present study, we showed that RAW 264.7 macrophages treated with 0.75 or 1.50 μg/mL of 3-Ac-DON resulted in DNA damage and the related cell cycle arrest at G1 phase and cell death, activation of the ribotoxic stress and the endoplasmic reticulum (ER) stress responses. The 3-Ac-DON-induced cell death was accompanied by a protective autophagy, because gene silencing of Atg5 using the small interfering RNA enhanced cell death. Results of further experiments revealed a role for lysosomal membrane permeabilization in the 3-Ac-DON triggered inhibition of autophagic flux. Additional work also showed that increased lysosomal biogenesis and leakage of cathepsin B (CTSB) from lysosomes to cytosol was critical for the 3-Ac-DON-induced cell death. Importantly, 3-Ac-DON-induced DNA damage and cell death were rescued by CA-074-me, a CTSB inhibitor. Collectively, these results indicated a critical role of lysosomal membrane permeabilization in the 3-Ac-DON-induced apoptosis of RAW 264.7 macrophages.

Though the main toxic mechanisms of graphene oxide (GO) to algae have been accepted as the shading effect, oxidative stress and mechanical damage, the effect of algal characteristics on these three mechanisms of GO toxicity have seldom been taken into consideration. In this study, we investigated GO toxicity to green algae (Chlorella vulgaris, Scenedesmus obliquus, Chlamydomonas reinhardtii), cyanobacteria (Microcystis aeruginosa) and diatoms (Cyclotella sp.). The aim was to assess how the physiological characteristics of algae affect the toxicity of GO. Results showed that 10 mg/L of GO significantly inhibited the growth of all tested algal types, while S. obliquus and C. reinhardtii were found to be the most susceptible and tolerant species, respectively. Then, scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to observe the physiological characteristics of the assessed algae. The presence of locomotive organelles, along with smaller and more spherical cells, was more likely to alleviate the shading effect. Variations in cell wall composition led to different extents of mechanical damage as shown by Cyclotella sp. silica frustules and S. obliquus autosporine division being prone to damage. Meanwhile, growth inhibition and cell division were significantly correlated with the oxidative stress and membrane permeability, suggesting the latter two indicators can effectively signal GO toxicity to algae. The findings of this study provide novel insights into the toxicity of graphene materials in aquatic environments.

Silver nanoparticles (AgNP) are commonly used in medical, cosmetics, clothing, and industrial applications for their antibacterial and catalytic properties. As AgNP become more prevalent, the doses to which humans are exposed may increase and pose health risks, particularly through incidental inhalation. This exposure was evaluated through in-vitro methods simulating lung fluids and lung epithelium, and through computational fluid dynamics (CFD) methods of AgNP transport. A high-dose scenario simulated a short-term inhalation of 10 μg AgNP/m³, based on an exposure limit recommended by the National Institute of Occupational Safety and Health for the case of a health-care worker who handles AgNP-infused wound dressings, and regularly wears AgNP-imbedded clothing. Bioaccessibility tests were followed by a Parallel Artificial Membrane Permeability Assay (PAMPA) and supported by CFD models of the lung alveoli, membrane, pores, and blood capillaries. Results indicate that such exposure produces an average and maximum AgNP flux of approximately 4.7 × 10⁻²¹ and 6.5 × 10⁻¹⁹ mol m⁻²·s⁻¹ through lung tissue, respectively, yielding a blood-silver accumulation of 0.46–64 mg per year, which may exceed the lowest adverse effect level of 25 mg for an adult male. Results from in-silico simulations were consistent with values estimated in vitro (within an order of magnitude), which suggest that CFD models may be used effectively to predict silver exposure from inhaled AgNP. Although the average short-term exposure concentrations are 3 orders of magnitude smaller than the reported threshold for mammalian cytotoxicity effects (observed at 5000 ppb), cumulative effects resulting from constant exposure to AgNP may pose risks to human health in the long-term, with predicted bioaccumulation reaching potential toxic effects after only five months of exposure, based on maximum flux.

Perfluorooctanoic acid (PFOA) has received an increasing attention in the agricultural and food industries due to its risk to human health. To facilitate the development of novel biomarkers of Escherichia coli against PFOA through multi-omics technologies, and to reveal the resistance mechanism of E. coli against PFOA at protein levels, the interactions among pollutant stress, protein expression and cell metabolism was investigated by using iTRAQ-based quantitative proteomic analysis. The results revealed that the 63 up-regulated proteins mainly involved in tricarboxylic acid cycle, glyoxylate and dicarboxylate metabolism and fatty acid biosynthesis, whereas, the 69 down-regulated proteins related to oxidative phosphorylation, pyruvate metabolism and the cell cycle-caulobacter pathway, were also associated with the increase of membrane permeability, excessive expenditure of ATP, disruption of fatty acid biosynthesis under PFOA stress. The results provide novel insights into the influence mechanisms of PFOA on fatty acid and protein networks.

Heterosigma akashiwo is a commonly found harmful microalgae, however, there are only few studies on its control using algicidal components particularly those identified from algicidal bacteria. In our previous study, ortho-tyrosine and urocanic acid identified from Bacillus sp. B1 showed a significantly high algicidal effect on H. akashiwo. The growth inhibition rates of H. akashiwo after 96 h of treatment with 300 μg/mL o-tyrosine and 500 μg/mL urocanic acid were 91.06% and 88.07%, respectively. Through non-destructive testing by Pulse Amplitude Modulation fluorometry and flow cytometer, the effects of o-tyrosine and urocanic acid on H. akashiwo PS II and physiological parameters (cell volume, mitochondrial membrane potential, and membrane permeability) were estimated. This study shows that o-tyrosine affected the photosynthesis system of H. akashiwo, decreased the mitochondrial membrane potential, and increased the membrane permeability of the algal cells. Treatment with urocanic acid decreased the mitochondrial membrane potential, resulting in the inhibition of algal cell growth and reproduction, but had little effect on membrane permeability and photosynthetic system. Our results may imply that when uridine degrades, surviving H. akashiwo cells may be reactivated. Therefore, o-tyrosine and urocanic acid have the potential to become new biological algicides, which can effectively control the growth of H. akashiwo.