Size-dependent influences of nano- and micro-plastics exposure on feeding, antioxidant systems, and organic sulfur compounds in ciliate Uronema marinum.

Protozoa play a pivotal role in the microbial cycle, and ciliated protozoan grazing habits are associated with dimethyl sulfide (DMS) cycle. Many studies have explored the impacts of nanoplastics (NPs) and microplastics (MPs) on ecotoxicological effects of ciliates. However, limited research exists on NPs and MPs influences on the production of organic sulfur compounds. The impact of NPs and MPs on the production of dimethyl sulfoxide (DMSO) and carbonyl sulfide (COS) remains unclear. Therefore, we examined the impacts of three concentrations (1 × 105, 5 × 105, and 1 × 106 items/mL) of polystyrene (PS) NPs (50 nm) and MPs (1 and 5 µm) on the ecotoxicology and DMS/dimethylsulfoniopropionate (DMSP)/DMSO/COS production in the ciliate Uronema marinum. NPs and MPs exposure were found to reduce the abundance, growth rate, volume, and biomass of U. marinum. Additionally, NPs and MPs increased the superoxide anion radical (O2˙─) production rates and malondialdehyde (MDA) contents (24 h), leading to a decline in glutathione (GSH) content and an ascend in superoxide dismutase (SOD) activity to mitigate the effects of reactive oxygen species (ROS). Exposure to PS NPs and MPs decreased the ingestion rates of algae by 7.5-14.4%, resulting in decreases in DMS production by 56.8-85.4%, with no significant impact on DMSO production. The results suggest a distinct pathway for the production of DMSO or COS compared to DMS. These findings help us to understand the NPs and MPs impacts on the marine ecosystem and organic sulfur compound yield, potentially influencing the global climate.

Impacts of nano- and micro-plastics exposure on zooplankton grazing, bacterial communities, and dimethylated sulfur compounds production in the microcosms.

Dimethyl sulfide (DMS) is a prevalent volatile organic sulfur compound relevant to the global climate. Ecotoxicological effects of nano- and microplastics (NPs and MPs) on phytoplankton, zooplankton, and bacteria have been investigated by numerous studies. Yet, the influences of NPs/MPs on dimethylated sulfur compounds remains understudied. Herein, we investigated the impacts of polystyrene (PS) NPs/MPs (80 nm, 1 µm, and 10 µm) on zooplankton grazing, chlorophyll a (Chl a) concentration, bacterial community, dimethylsulfoniopropionate (DMSP), and DMS production in the microcosms. Our findings revealed that rotifer grazing increased the production of DMS in the absence of NPs/MPs but did not promote DMS production when exposed to NPs/MPs. The ingestion rates of the rotifer and copepod exposed to NPs/MPs at high concentrations were significantly reduced. NPs/MPs exposure significantly decreased DMS levels in the treatments with rotifers compared to the animal controls. In the bacterial microcosms, smaller NPs/MPs sizes were more detrimental to Chl a concentrations compared to larger sizes. The study revealed a stimulatory effect on Chl a concentrations, DMSPd concentrations, and bacterial abundances when exposed to 10 µm MP with low concentrations. The effects of NPs/MPs on DMS concentrations were both dose- and size-dependent, with NPs showing greater toxicity compared to larger MPs. NPs/MPs led to changes in bacterial community compositions, dependent on both dosage and size. NPs caused a notable decrease in the alpha diversities and richness of bacteria compared to MPs. These results provide insights into the influences of NPs/MPs on food webs, and subsequently organic sulfur compounds cycles.

Low-toxicity natural pyrite on electro-Fenton catalytic reaction in a wide pH range.

The resource utilization of natural pyrite not only reduces secondary pollution but also brings certain environmental benefits. However, the green and efficient use of pyrite presents certain challenges. In this study, a novel electro-Fenton (EF) system was constructed utilizing copper modified graphite felt (GF/Cu) as cathode and natural pyrite (com-FeS2) as catalyst. The results demonstrated that the system exhibited a remarkable stability over an extensive pH range (3.0-10.0) and remained effective even under adverse environmental conditions, such as high salinity or elevated antibiotic concentration. After optimizing the reaction conditions, 0.2 mM sulfamerazine (SMZ) was almost completely degraded within 1.5 h. The results highlighted the catalytic role of Fe(II) on the com-FeS2 surface. Combined with quenching experiments and quantitative analysis of reactive oxygen species (ROS), the removal of SMZ was primarily attributed to the generation of •OH, ordered by 1O2 > â€¢O2- > â€¢OHads, a possible degradation pathway was proposed by HR-LC-MS. The biological toxicity after the reaction was detected, and the introduction of polyvinylpyrrolidone (PVP) was beneficial to reduce the biological toxicity of iron dissolution. This work provides new insights into the green and efficient resource utilization of natural pyrite and significantly expands the pH applicability range of the Fenton process, demonstrating the large-scale industrial application potential of pyrite.

The alleviation effect and its mechanism of Niuhuang Jiedu prescription on realgar-induced genotoxicity in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Realgar (As2S2 or As4S4) is a traditional Chinese medicine (TCM) containing arsenic. Existing studies have shown that it has genotoxicity under long-term use with large doses. Niuhuang Jiedu (NHJD) is a Chinese medicine prescription containing realgar and seven other TCMs. Whether the multiple TCMs combination in NHJD can reduce the genotoxicity induced by realgar in equivalent doses is still unknown. AIM OF THE STUDY: To research the effect of NHJD on realgar's genotoxicity and the possible mechanism involved based on the arsenic methylation metabolic pathway. MATERIAL AND METHODS: Six groups (control, realgar (0.8 g/kg), NHJD (12.48 g/kg), as well as Glycyrrhiza uralensis Fisch (GU), Scutellaria baicalensis Georg (SB), Rheum palmatum L (RP) plus equivalent doses of realgar, respectively) were set up. ICR mice were intragastric administered for 12 weeks. First, genotoxicology tests were conducted to evaluate the effect of NHJD, GU, SB, and RP on reducing realgar's genotoxicity. The inorganic arsenic (iAs), dimethyl arsenic acid (DMA), and monomethyl arsenic acid (MMA) were determined by HPLC-AFS, and the iAs%, MMA%, DMA%, primary methylation index (PMI), etc. Were calculated. Meanwhile, the S-adenosyl methionine (SAM) and arsenate reductase (ARR) levels, the arsenic (+3)methyltransferase (As3MT), purine-nucleoside phosphorylase (PNP), glutathione S-transfer omega1 (GSTO1) gene expression were detected, aimed to explore the possible alleviation mechanisms of NHJD. RESULTS: The combination of multiple TCMs in NHJD decreased the levels of MN‰, SPA%, and DNA damage caused by realgar, with similar effects observed when SB, RP, and GU were used separately with realgar. Notably, the iAs% significantly decreased, while DMA% and PMI notably increased in the NHJD and realgar + SB (or RP) groups compared to the realgar-only group (P < 0.05). Increases in SAM and ARR levels were observed across various groups, but only the ARR increase in the NHJD group was statistically significant. Moreover, significant increases in As3MT mRNA and GSTO1 mRNA were noted in the NHJD group, and PNP mRNA levels significantly rose in the realgar + SB group. CONCLUSIONS: This study revealed that NHJD could attenuate the genotoxic effects of realgar. The botanicals SB, RP, and GU within NHJD may be key contributors to this effect. Enhancements in arsenic methylation capabilities through increased levels of SAM and ARR and elevated gene expressions of As3MT, PNP, and GSTO1 suggest potential mechanisms behind these findings.

Neurotoxicity and Developmental Neurotoxicity of Copper Sulfide Nanoparticles on a Human Neuronal In-Vitro Test System.

Nanoparticles (NPs) are becoming increasingly important novel materials for many purposes, including basic research, medicine, agriculture, and engineering. Increasing human and environmental exposure to these promising compounds requires assessment of their potential health risks. While the general direct cytotoxicity of NPs is often routinely measured, more indirect possible long-term effects, such as reproductive or developmental neurotoxicity (DNT), have been studied only occasionally and, if so, mostly on non-human animal models, such as zebrafish embryos. In this present study, we employed a well-characterized human neuronal precursor cell line to test the concentration-dependent DNT of green-manufactured copper sulfide (CuS) nanoparticles on crucial early events in human brain development. CuS NPs turned out to be generally cytotoxic in the low ppm range. Using an established prediction model, we found a clear DNT potential of CuS NPs on neuronal precursor cell migration and neurite outgrowth, with IC50 values 10 times and 5 times, respectively, lower for the specific DNT endpoint than for general cytotoxicity. We conclude that, in addition to the opportunities of NPs, their risks to human health should be carefully considered.

Cytotoxicity of Quantum Dots in Receptor-Mediated Endocytic and Pinocytic Pathways in Yeast.

Despite the promising applications of the use of quantum dots (QDs) in the biomedical field, the long-lasting effects of QDs on the cell remain poorly understood. To comprehend the mechanisms underlying the toxic effects of QDs in yeast, we characterized defects associated with receptor-mediated endocytosis (RME) as well as pinocytosis using Saccharomyces cerevisiae as a model in the presence of cadmium selenide/zinc sulfide (CdSe/ZnS) QDs. Our findings revealed that QDs led to an inefficient RME at the early, intermediate, and late stages of endocytic patch maturation at the endocytic site, with the prolonged lifespan of GFP fused yeast fimbrin (Sac6-GFP), a late marker of endocytosis. The transit of FM1-43, a lipophilic dye from the plasma membrane to the vacuole, was severely retarded in the presence of QDs. Finally, QDs caused an accumulation of monomeric red fluorescent protein fused carbamoyl phosphate synthetase 1 (mRFP-Cps1), a vacuolar lumen marker in the vacuole. In summary, the present study provides novel insights into the possible impact of CdSe/ZnS QDs on the endocytic machinery, enabling a deeper comprehension of QD toxicity.

Genome-wide profiling of DNA methylome and transcriptome reveals epigenetic regulation of Urechis unicinctus response to sulfide stress.

Sulfide is a well-known environmental pollutant that can have detrimental effects on most organisms. However, few metazoans living in sulfide-rich environments have developed mechanisms to tolerate and adapt to sulfide stress. Epigenetic mechanisms, including DNA methylation, have been shown to play a vital role in environmental stress adaptation. Nevertheless, the precise function of DNA methylation in biological sulfide adaptation remains unclear. Urechis unicinctus, a benthic organism inhabiting sulfide-rich intertidal environments, is an ideal model organism for studying adaptation to sulfide environments. In this study, we conducted a comprehensive analysis of the DNA methylome and transcriptome of U. unicinctus after exposure to 50 µM sulfide. The results revealed dynamic changes in the DNA methylation (5-methylcytosine) landscape in response to sulfide stress, with U. unicinctus exhibiting elevated DNA methylation levels following stress exposure. Integrating differentially expressed genes (DEGs) and differentially methylated regions (DMRs), we identified a crucial role of gene body methylation in predicting gene expression. Furthermore, using a DNA methyltransferase inhibitor, we validated the involvement of DNA methylation in the sulfide stress response and the gene regulatory network influenced by DNA methylation. The results indicated that by modulating DNA methylation levels during sulfide stress, the expression of glutathione S-transferase, glutamyl aminopeptidase, and cytochrome c oxidase could be up-regulated, thereby facilitating the metabolism and detoxification of exogenous sulfides. Moreover, DNA methylation was found to regulate and enhance the oxidative phosphorylation pathway, including NADH dehydrogenase, isocitrate dehydrogenase, and ATP synthase. Additionally, DNA methylation influenced the regulation of Cytochrome P450 and macrophage migration inhibitory factor, both of which are closely associated with oxidative stress and stress resistance. Our findings not only emphasize the role of DNA methylation in sulfide adaptation but also provide novel insights into the potential mechanisms through which marine organisms adapt to environmental changes.

Biological effects of molybdenum(IV) sulfide nanoparticles and microparticles in the rat after repeated intratracheal administration.

In this study, molybdenum(IV) sulfide (MoS2 ) nanoparticles (97 ± 32 nm) and microparticles (1.92 ± 0.64 µm) stabilized with poly (vinylpolypyrrolidone) (PVP) were administered intratracheally to male and female rats (dose of 1.5 or 5 mg/kg bw), every 14 days for 90 days (seven administrations in total). Blood parameters were assessed during and at the end of the study (hematology, biochemistry including glucose, albumins, uric acid, urea, high density lipoprotein HDL, total cholesterol, triglycerides, aspartate transaminase, and alanine transaminase ALT). Bronchoalveolar lavage fluid (BALF) analyses included cell viability, biochemistry (total protein concentration, lactate dehydrogenase, and glutathione peroxidase activity), and cytokine levels (tumor necrosis factor α, TNF-α, macrophage inflammatory protein 2-alpha, MIP-2, and cytokine-induced neutrophil chemoattractant-2, CINC-2). Tissues were subjected to routine histopathological and electron microscopy (STEM) examinations. No overt signs of chronic toxicity were observed. Differential cell counts in BALF revealed no significant differences between the animal groups. An increase in MIP-2 and a decrease in TNF-α were observed in BALF in the exposed males. The histopathological changes in the lung evaluated according to a developed classification system (based on severity of inflammation, range 0-4, with 4 indicating the most severe changes) showed average histopathological score of 1.33 for animals exposed to nanoparticles and microparticles at the lower dose, 1.72 after exposure to nanoparticles at the higher dose, and 2.83 for animals exposed to microparticles at the higher dose. In summary, it was shown that nanosized and microsized MoS2 can trigger dose-dependent inflammatory reactions in the lungs of rats after multiple intratracheal instillation irrespective of the animal sex. Some evidence indicates a higher lung pro-inflammatory potential of the microform.

Detrimental impact of sulfide on the seagrass Zostera marina in dark hypoxia.

Sulfide poisoning, hypoxia events, and reduced light availability pose threats to marine ecosystems such as seagrass meadows. These threats are projected to intensify globally, largely due to accelerating eutrophication of estuaries and coastal environments. Despite the urgency, our current comprehension of the metabolic pathways that underlie the deleterious effects of sulfide toxicity and hypoxia on seagrasses remains inadequate. To address this knowledge gap, I conducted metabolomic analyses to investigate the impact of sulfide poisoning under dark-hypoxia in vitro conditions on Zostera marina, a vital habitat-forming marine plant. During the initial 45 minutes of dark-hypoxia exposure, I detected an acclimation phase characterized by the activation of anaerobic metabolic pathways and specific biochemical routes that mitigated hypoxia and sulfide toxicity. These pathways served to offset energy imbalances, cytosolic acidosis, and sulfide toxicity. Notably, one such route facilitated the transformation of toxic sulfide into non-toxic organic sulfur compounds, including cysteine and glutathione. However, this sulfide tolerance mechanism exhibited exhaustion post the initial 45-minute acclimation phase. Consequently, after 60 minutes of continuous sulfide exposure, the sulfide toxicity began to inhibit the hypoxia-mitigating pathways, culminating in leaf senescence and tissue degradation. Utilizing metabolomic approaches, I elucidated the intricate metabolic responses of seagrasses to sulfide toxicity under in vitro dark-hypoxic conditions. My findings suggest that future increases in coastal eutrophication will compromise the resilience of seagrass ecosystems to hypoxia, primarily due to the exacerbating influence of sulfide.

A study on the mechanism of Indium phosphide/zinc sulfide core/shell quantum dots influencing embryo incubation of rare minnow (Gobiocypris rarus).

Quantum dots (QDs) inhibit fish hatching, but the mechanism is still unclear. In this study, the effect of Indium phosphide/zinc sulfide quantum dots (InP/ZnS QDs) on the embryo incubation of rare minnow was investigated. Five experimental concentration groups were set up according to the preliminary experimental results, which were 0, 50, 100, 200 and 400 nM. A direct exposure method was adopted to expose embryos to InP/ZnS QDs solution. The results showed that InP/ZnS QDs significantly inhibited the embryo hatching rate, delayed embryo emergence, affected the expression of genes associated with hatching gland cells and hatching enzymes. InP/ZnS QDs also destroy the structure of the embryo chorion. In addition, QDs can cause oxidative stress in embryos. Transcriptional sequencing analysis showed that InP/ZnS QDs InP/ZnS QDs may have induced the production of a hypoxic environment and triggered induce abnormal cardiac muscle contraction, inflammatory response and apoptosis process in embryos. In conclusion, QDs influences embryo hatchability largely through egg chorion mediation.

Fast and slow releasing sulphide donors engender distinct transcriptomic alterations in Atlantic salmon hepatocytes.

Hydrogen sulphide (H2S) is a naturally occurring compound generated either endogenously or exogenously and serves both as a gaseous signalling molecule and an environmental toxicant. Though it has been extensively investigated in mammalian systems, the biological function of H2S in teleost fish is poorly identified. Here we demonstrate how exogenous H2S regulates cellular and molecular processes in Atlantic salmon (Salmo salar) using a primary hepatocyte culture as a model. We employed two forms of sulphide donors: the fast-releasing salt form, sodium hydrosulphide (NaHS) and the slow-releasing organic analogue, morpholin-4-ium 4-methoxyphenyl(morpholino) phosphinodithioate (GYY4137). Hepatocytes were exposed to either a low (LD, 20 µg/L) or high (HD, 100 µg/L) dose of the sulphide donors for 24 hrs, and the expression of key sulphide detoxification and antioxidant defence genes were quantified by qPCR. The key sulphide detoxification genes sulfite oxidase 1 (soux) and the sulfide: quinone oxidoreductase 1 and 2 (sqor) paralogs in salmon showed pronounced expression in the liver and likewise responsive to the sulphide donors in the hepatocyte culture. These genes were ubiquitously expressed in different organs of salmon as well. HD-GYY4137 upregulated the expression of antioxidant defence genes, particularly glutathione peroxidase, glutathione reductase and catalase, in the hepatocyte culture. To explore the influence of exposure duration, hepatocytes were exposed to the sulphide donors (i.e., LD versus HD) either transient (1h) or prolonged (24h). Prolonged but not transient exposure significantly reduced hepatocyte viability, and the effects were not dependent on concentration or form. The proliferative potential of the hepatocytes was only affected by prolonged NaHS exposure, and the impact was not concentration dependent. Microarray analysis revealed that GYY4137 caused more substantial transcriptomic changes than NaHS. Moreover, transcriptomic alterations were more marked following prolonged exposure. Genes involved in mitochondrial metabolism were downregulated by the sulphide donors, primarily in NaHS-exposed cells. Both sulphide donors influenced the immune functions of hepatocytes: genes involved in lymphocyte-mediated response were affected by NaHS, whereas inflammatory response was targeted by GYY4137. In summary, the two sulphide donors impacted the cellular and molecular processes of teleost hepatocytes, offering new insights into the mechanisms underlying H2S interactions in fish.

Cellular mechanisms underlying extraordinary sulfide tolerance in a crustacean holobiont from hydrothermal vents.

The shallow-water hydrothermal vent system of Kueishan Island has been described as one of the world's most acidic and sulfide-rich marine habitats. The only recorded metazoan species living in the direct vicinity of the vents is Xenograpsus testudinatus, a brachyuran crab endemic to marine sulfide-rich vent systems. Despite the toxicity of hydrogen sulfide, X. testudinatus occupies an ecological niche in a sulfide-rich habitat, with the underlying detoxification mechanism remaining unknown. Using laboratory and field-based experiments, we characterized the gills of X. testudinatus that are the major site of sulfide detoxification. Here sulfide is oxidized to thiosulfate or bound to hypotaurine to generate the less toxic thiotaurine. Biochemical and molecular analyses demonstrated that the accumulation of thiosulfate and hypotaurine is mediated by the sodium-independent sulfate anion transporter (SLC26A11) and taurine transporter (Taut), which are expressed in gill epithelia. Histological and metagenomic analyses of gill tissues demonstrated a distinct bacterial signature dominated by Epsilonproteobacteria. Our results suggest that thiotaurine synthesized in gills is used by sulfide-oxidizing endo-symbiotic bacteria, creating an effective sulfide-buffering system. This work identified physiological mechanisms involving host-microbe interactions that support life of a metazoan in one of the most extreme environments on our planet.

Acute sulfide exposure induces hemocyte toxicity and microbiota dysbiosis in blood clam Tegillarca granosa.

Sulfide are widely accumulated in aquatic environments under anaerobic conditions, which cause health problems of aquatic animals, yet their toxic effects to benthic bivalves are not well understood. We investigated the effects of sulfide on innate immunity of the blood clam Tegillarca granosa. Immunity-related indicators and hemolymph microbiota were investigated in the clams exposed to sulfide (via 10, 100 and 1000 µmol/L of Na2S) over a 7-day period. The results showed that cellular immune responses in T. granosa were affected by exposure to high sulfide concentration (1000 µmol/L Na2S), as indicated by total counts of hemocytes (THC), cell viability, ROS levels and phagocytic activities, suggesting that sulfide stress induces T. granosa more vulnerable to pathogen challenges. In addition, the Na2S-induced stress also reshaped the hemolymph microbial community structure of T. granosa that some original genera decreased, such as Lactobacillus, Desulfovibrio and Akkermansia; some genera increased, such as Vibrio and Pseudoalteromonas in sulfide stress group. Sulfide exposure promoted the proliferation of opportunistic pathogen and reduced the diversity of microbial community in the hemolymph of T. granosa. In summary, sulfide stress had marked hemocytotoxicity, reduced immune-cell activity and increased bacterial infections in the blood clam.

The inhibitory effects and underlying mechanism of high ammonia stress on sulfide-driven denitrification process.

Sulfide-driven denitrification (SD) process has been widely studied for treating wastewater containing sulfate and ammonia in recent years. But influence of high ammonia stress on the SD process and microbial community remained unclear. In this work, a series of tests were conducted to investigate effects of different ammonia stress (200-3000 mg-total ammonia nitrogen (TAN)/L) on denitrification efficiency, byproduct accumulation and microbial community of the SD process. According to our results, the SD process was severely inhibited, and 32.67 ± 5.15 mg/L NO2--N was accumulated when ammonia stress reached 3000 mg TAN/L. But the inhibited SD process could recover in about 40 days when ammonia stress was decreased to 200 mg TAN/L. After analyzing the microbial community, Thiobacillus sp. (Thiobacillus sp. 65-29, Thiobacillus sp. SCN 64-317, Thiobacillus sp. 63-78 and Thiobacillus denitrificans) was confirmed as dominant bacteria responsible for the SD process. Further, expression of narG, napA, nirK and nirS were inhibited under high ammonia stress, thus making the SD process stuck in NO3- and NO2- reduction step. This study reveals the inhibitory effects of high ammonia stress on the SD process and its possible underlying mechanism with discussion in gene level.

Response of simultaneous sulfide and nitrate removal process on acute toxicity of substrate concentration and salinity: Single toxicity and combined toxicity.

Simultaneous sulfide and nitrate removal process has performed excellent to treat nitrogen and sulfur pollutants in wastewater treatment. A high salinity stress poses a great challenge to the treatment of highly saline wastewater containing nitrate and sulfide. In addition, sulfide and nitrates are also toxic for the process, and their high concentration would inhibit the process. Therefore, the current work explores the single acute toxic effect and combined toxic effect of salinity and substrate concentration on the performance of the process from the perspective of toxicology. Considering sulfide and nitrate removal performance as an indicator, the IC50 values of sulfide were 293.20 mg S/L and 572.30 mg S/L, respectively; while those of salinity were 6.14% wt (91.78 mS/cm) and 6.63% wt (98.73 mS/cm), respectively. High substrate concentration or salinity resulted in elemental sulfur generation. The molar ratio of generated elemental sulfur to consumed sulfide(R-Sulfate) was close to 1. The response of nitrate reduction product to the elevating substrate concentration was not obvious, while its response to increasing salinity was on the contrary. With the increasing salinity (1.2% wt to 9.6% wt), molar ratio of generated nitrogen gas to consumed nitrate (R-Nitrogen gas) increased from 0.58 to 1, while molar ratio of generated nitrite to consumed nitrate (R-Nitrite) decreased from 0.43 to 0. Factorial analysis test revealed that the combined acute toxicity of substrate and salinity on sulfide oxidization and nitrate reduction were both antagonistic effects.

Comparison of acid volatile sulphide, metal speciation, and diffusive gradients in thin-film measurement for metal toxicity assessment of sediments in Lake Chaohu, China.

The toxicity of heavy metals in sediments is inseparable from their forms in the environment. Traditional sediment toxicity assessment systems, such as total metals, dissolved metals in pore water, metals extracted by the Community Bureau of Reference procedure, and acid volatile sulphide (AVS)-simultaneously extracted metal (SEM), have their own limitations. This study revealed the horizontal and vertical distribution characteristics of AVS and SEM in Lake Chaohu and three typical groups of two-dimensional profiles of diffusive gradients in thin-film (DGT)-labile S(-II) were obtained at representative sampling sites. There was a positive correlation between DGT-labile S(-II) and AVS due to sulphate-reducing bacteria and a negative correlation due to the high sulphate reduction rate induced by high total organic carbon. Moreover, there was no correlation between DGT-labile S(-II) and AVS when bioturbation was dominant in the sediments. To realise the application of DGT measurement in toxicity assessment of heavy metals in sediment through the sandwich relationship of DGT-labile metals vs. metals speciation vs. sediment toxicity assessment, the key relationship of DGT-labile metals vs. metals speciation was explored. DGT-labile Ni showed potential to reveal this relationship.

Sulfide removal characteristics, pathways and potential application of a novel chemolithotrophic sulfide-oxidizing strain, Marinobacter sp. SDSWS8.

Sulfide generally exists in wastewater, black and odor river, as well as aquaculture water, and give rise to adverse effect on ecological stability and biological safety, due to the toxicity, corrosivity and malodor of sulfide. In the present study, a chemolithotrophic sulfide-oxidizing bacteria (SOB) was isolated and identified as Marinobacter maroccanus strain SDSWS8. And it produced no hemolysin and was susceptible to most antibiotics. There were no accumulation of sulfide, sulfate and thiosulfate during the sulfide removal process. The optimum conditions of sulfide removal were temperature 15-40 °C, initial pH value 4.5-9.5, salinity 10-40‰, C/N ratio 0-20 and sulfide concentration 25-150 mg/L. The key genes of sulfide oxidation, Sox system (soxB, soxX, soxA, soxZ, soxY, soxD, soxC), dissimilatory sulfur oxidation (dsrA, aprA and sat) and sqr, were successfully amplified and expressed, indicating the three pathways coordinated to complete the sulfide oxidation. Besides, strain SDSWS8 had inhibitory effect on four pathogen Vibrio (V. harveyi, V. parahaemolyticus, V. anguillarum and V. splendidus). Furthermore, efficient removal of sulfide from real aquaculture water and sludge mixture could be accomplished by strain SDSWS8. This study may provide a promising candidate strain for sulfide-rich water treatment.

Preclinical safety and hepatotoxicity evaluation of biomineralized copper sulfide nanoagents.

Albumin-biomineralized copper sulfide nanoparticles (Cu2-xS NPs) have attracted much attention as an emerging phototheranostic agent due to their advantages of facile preparation method and high biocompatibility. However, comprehensive preclinical safety evaluation is the only way to meet its further clinical translation. We herein evaluate detailedly the safety and hepatotoxicity of bovine serum albumin-biomineralized Cu2-xS (BSA@Cu2-xS) NPs with two different sizes in rats. Large-sized (LNPs, 17.8 nm) and small-sized (SNPs, 2.8 nm) BSA@Cu2-xS NPs with great near-infrared absorption and photothermal conversion efficiency are firstly obtained. Seven days after a single-dose intravenous administration, SNPs distributed throughout the body are cleared primarily through the feces, while a large amount of LNPs remained in the liver. A 14-day subacute toxicity study with a 28-day recovery period are conducted, showing long-term hepatotoxicity without recovery for LNPs but reversible toxicity for SNPs. Cellular uptake studies indicate that LNPs prefer to reside in Kupffer cells, leading to prolonged and delayed hepatotoxicity even after the cessation of NPs administration, while SNPs have much less Kupffer cell uptake. RNA-sequencing analysis for gene expression indicates that the inflammatory pathway, lipid metabolism pathway, drug metabolism-cytochrome P450 pathway, cholesterol/bile acid metabolism pathway, and copper ion transport/metabolism pathway are compromised in the liver by two sizes of BSA@Cu2-xS NPs, while only SNPs show a complete recovery of altered gene expression after NPs discontinuation. This study demonstrates that the translational feasibility of small-sized BSA@Cu2-xS NPs as excellent nanoagents with manageable hepatotoxicity.

Parental exposure to CdSe/ZnS QDs affects cartilage development in rare minnow (Gobiocypris rarus) offspring.

Cartilage development is a sensitive process that is easily disturbed by environmental toxins. In this study, the toxicity of CdSe/ZnS quantum dots on the skeleton of the next generation (F1) was evaluated using rare minnows (Gobiocypris rarus) as model animals. Four-month-old sexually mature parental rare minnows (F0) were selected and treated with 0, 100, 200, 400 and 800 nmol/L CdSe/ZnS quantum dots for 4 days. Embryos of F1 generation rare minnows were obtained by artificial insemination. The results showed that with increasing maternal quantum dots exposure, the body length of F1 embryos decreased, the overall calcium content decreased, and the deformity and mortality rates increased. Alcian blue staining results showed that the lengths of the craniofacial mandible, mandibular arch length, mandibular width, and CH-CH and CH-PQ angles of larvae of rare minnows increased; histological hematoxylin-eosin staining further indicated that quantum dots affected the development of chondrocytes. Furthermore, high concentrations of CdSe/ZnS quantum dots inhibited the transcript expression of the bmp2b, bmp4, bmp6, runx2b, sox9a, lox1 and col2α1 genes. In conclusion, CdSe/ZnS quantum dots can affect the skeletal development of F1 generation embryos of rare minnows at both the individual and molecular levels, the damage to the craniofacial bone is more obvious, and the toxic effect of high concentrations of quantum dots (400 nmol/L and 800 nmol/L) is more significant.