Industrial fluoride emissions and their spatial characteristics in the Nansi Lake Basin, Eastern China.

Excessive fluoride emissions threaten ecological stability and human health. Previous studies have noted that industrial sources could be significant. However, quantifying industrial fluoride emissions has not been yet reported. In this study, both bottom-up and top-down approaches were used to estimate the fluoride emissions in the Nansi Lake Basin. Global and local spatial autocorrelation were adopted to reveal the spatial agglomeration effects. The fluoride emissions calculated by the bottom-up approach were larger than those calculated by the top-down method. The highest fluoride input mainly occurred in Zoucheng and Mudan. The highest fluoride emissions mainly occurred in Zoucheng and Rencheng using the bottom-up approach. The highest fluoride emissions mainly occurred in Zoucheng and Yanzhou using the top-down approach. Mining and washing of bituminous coal and anthracite (BAW) was the most significant source of fluoride input and emissions. A significant spatial agglomeration effect of fluoride emissions was found. These findings could provide a method for accurate industrial fluoride emission estimation, complement the critical data on the fluoride emissions of main industrial sectors, and provide a scientific basis for tracing fluoride sources.

Regulation mechanisms of ferric ions release from iron-loaded transferrin protein caused by nano-sized polystyrene plastics-induced conformational and structural changes.

Currently, the binding of iron-binding protein transferrin (TF) with NPs and their interaction mechanisms have not been completely elucidated yet. Here, we probed the conformation-dependent release of Fe ions from TF induced by nano-sized polystyrene plastics (PS-NPs) using dialysis, ICP-MS, multi-spectroscopic techniques, and computational simulation. The results showed that the release of free Fe ions from TF was activated after PS-NPs binding, which displayed a clear dose-effect correlation. PS-NPs binding can induce the unfolding and loosening of polypeptide chain and backbone of TF. Alongside this we found that the TF secondary structure was destroyed, thereby causing TF protein misfolding and denaturation. In parallel, PS-NPs interacted with the chromophores, resulting in the occurrence of fluorescence sensitization effects and the disruption of the surrounding micro-environment of aromatic amino acids. Also, the binding of PS-NPs induced the formation of new aggregates in the PS-NPs-TF system. Further simulations indicated that PS-NPs exhibited a preference for binding to the hinge region that connects the C-lobe and N-lobe, which is responsible for the Fe ions release and structural alterations of TF. This finding provides a new understanding about the regulation of the release of Fe ions of iron-loaded TF through NPs-induced conformational and structural changes.

Molecular mechanisms of polystyrene nanoplastics and alpha-amylase interactions and their binding model: A multidimensional analysis.

Plastic fragments are widely distributed in different environmental media and has recently drawn special attention due to its difficulty in degradation and serious health and environmental problems. Among, nanoplastics (NPs) are smaller in size, larger in surface/volume ratio, and more likely to easily adsorb ambient pollutants than macro plastic particles. Moreover, NPs can be easily absorbed by wide variety of organisms and accumulate in multiple tissues/organs and cells, thus posing a more serious threat to living organisms. Alpha-amylase (α-amylase) is a hydrolase, which can be derived from various sources such as animals, plants, and microorganisms. Currently, no studies have concentrated on the binding of NPs with α-amylase and their interaction mechanisms by employing a multidimensional strategy. Hence, we explored the interaction mechanisms of polystyrene nanoplastics (PS-NPs) with α-amylase by means of multispectral analysis, in vitro enzymatic activity analysis, and molecular simulation techniques under in vitro conditions. The findings showed that PS-NPs had the capability to bind with the intrinsic fluorescence chromophores, leading to fluorescence changes of these specific amino acids. This interaction also caused the alterations in the micro-environment of the fluorophore residues mainly tryptophan (TRP) and tyrosine (TYR) residues of α-amylase. PS-NPs interaction promoted the unfolding and partial expansion of polypeptide chains and the loosening of protein skeletons, and destroyed the secondary structure (increased random coil contents and decreased α-helical contents) of this protein, forming a larger particle size of the PS-NPs-α-amylase complex. Moreover, the enzymatic activity of α-amylase in vitro was found to be inhibited in a concentration dependent manner, thereby impairing its physiological functions. Further molecular simulation found that PS-NPs had a higher tendency to bind to the active site of α-amylase, which is the cause for its structural and functional changes. Additionally, the hydrophobic force played a major role in mediating the binding interactions between PS-NPs and α-amylase. Taken together, our study indicated that PS-NPs interaction can initiate the abnormal physiological functions of α-amylase through PS-NPs-induced structural and conformational alternations.

Molecular mechanisms of nano-sized polystyrene plastics induced cytotoxicity and immunotoxicity in Eisenia fetida.

Nanoplastics (NPs) are currently everywhere and environmental pollution by NPs is a pressing global problem. Nevertheless, until now, few studies have concentrated on the mechanisms and pathways of cytotoxic effects and immune dysfunction of NPs on soil organisms employing a multidimensional strategy. Hence, earthworm immune cells and immunity protein lysozyme (LZM) were selected as specific receptors to uncover the underlying mechanisms of cytotoxicity, genotoxicity, and immunotoxicity resulting from exposure to polystyrene nanoplastics (PS-NPs), and the binding mechanisms of PS-NPs-LZM interaction. Results on cells indicated that when earthworm immune cells were exposed to high-dose PS-NPs, it caused a notable rise in the release of reactive oxygen species (ROS), resulting in oxidative stress. PS-NPs exposure significantly decreased the cell viability of earthworm immune cells, inducing cytotoxicity through ROS-mediated oxidative stress pathway, and oxidative injury effects, including reduced antioxidant defenses, lipid peroxidation, DNA damage, and protein oxidation. Moreover, PS-NPs stress inhibited the intracellular LZM activity in immune cells, resulting in impaired immune function and immunotoxicity by activating the oxidative stress pathway mediated by ROS. The results from molecular studies revealed that PS-NPs binding destroyed the LZM structure and conformation, including secondary structure changes, protein skeleton unfolding/loosening, fluorescence sensitization, microenvironment changes, and particle size changes. Molecular docking suggested that PS-NPs combined with active center of LZM easier and inhibited the protein function more, and formed a hydrophobic interaction with TRP 62, a crucial amino acid residue closely associated with the function and conformation of LZM. This is also responsible for LZM conformational changes and functional inhibition /inactivation. These results of this research offer a fresh outlook on evaluating the detriment of NPs to the immune function of soil organisms using cellular and molecular strategies.

Compound effect and mechanism of oxidative damage induced by nanoplastics and benzo [a] pyrene.

Nanoplastics and polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in soil environments. In order to objectively evaluate the toxic interaction between polystyrene nanoplastics (PS NPs) and benzo [a] pyrene (BaP), oxidative damage at the level of earthworm cells and biomacromolecules was investigated by experiments combined with molecular dynamics simulation. Studies on cells reveal that PS NPs and BaP had synergistic toxicity when it came to causing oxidative stress. Cellular reactive oxygen species (ROS) levels under combined pollutant exposure were 24% and 19% higher, respectively than when PS NPs and BaP were exposed alone (compared to the blank group). In addition, BaP and PS NPs inhibited the ability of CAT to decompose H2O2 by affecting the structure of the proximal amino acid Tyr 357 in the active center of CAT, which exacerbated oxidative stress to a certain extent. Therefore, the synergistic toxic effect of BaP and PS NPs is due to the mutual complement of the two to the induction of protein structural looseness, and the strengthening of the stability of the conjugate (CAT-BaP-PS) under the weak interaction. This work provides a new perspective and approach on how to talk about the toxicity of combined pollutants.

Environmental relevant concentrations of polystyrene nanoplastics and lead co-exposure triggered cellular cytotoxicity responses and underlying mechanisms in Eisenia fetida.

Heavy metal pollution of soils and the widespread use of plastics have caused environmental problems worldwide. Nanoplastics (NPs) contaminants in water and soil environments can adsorb heavy metals, thereby affecting the bioavailability and toxicity of heavy metals. In this paper, the effect of co-exposure of polystyrene microspheres with 100 nm particle size and lead acetate (Pb) on the Eisenia fetida coelomocytes was investigated. The environmental concentration of NPs used was 0.01 mg/L and the concentration of Pb ranged from 0.01 to 1 mg/L, and the exposed cells were incubated at 298 k for 24 h. Our study demonstrated that exposure of cells to environmental relevant concentrations of NPs did not significantly affect the cytotoxicity of Pb exposure. It was shown that co-exposure induced cellular production of reactive oxygen species (ROS, increased to 134.4 %) disrupted the antioxidant system of earthworm body cavity cells, activated superoxide dismutase and catalase (CAT), produced reduced glutathione, and inhibited glutathione-dependent enzyme (GST) activity (Reduced to 64 %). Total antioxidant capacity (T-AOC) is first enhanced against ROS due to the stress of NPs and Pb. When the antioxidant reserves of cells are exhausted, the antioxidant capacity will decrease. The level of malondialdehyde, a biomarker of eventual lipid peroxidation, increased to 231.7 %. At the molecular level, due to co-exposure to NPs and Pb, CAT was loosely structured and the secondary structure is misfolded, which was responsible for exacerbating oxidative damage in E. fetida coelomocytes. The findings of this study have significant implications for the toxicological interaction and future risk assessment of co-contamination of NPs and Pb in the environment.

Randomly-shaped nanoplastics induced stronger biotoxicity targeted to earthworm Eisenia fetida species: Differential effects and the underlying mechanisms of realistic and commercial polystyrene nanoplastics.

Nanoplastics (NPs) are widely distributed in various environments, including soil, and have been known to adversely affect soil organisms. Currently, most of the obtained studies were principally focused on the ecological risks of commercial sphere-type microbeads (SNPs), while ignoring that they might be different from randomly-shaped nanoplastics (RNPs) in a real environment. Thus, this study was undertaken to probe the shape-dependent effects of NPs on the earthworm Eisenia fetida and the corresponding poisoning mechanisms, and discriminate the toxicity differences between SNPs and RNPs at the molecule, cell, tissue, and animal levels. The results showed SNPs and RNPs exhibited lethal effects to earthworms with the LC50 determined to be 27.42 g/kg and 21.69 g/kg, respectively after a 28-day exposure. SNPs and RNPs exposure can cause ROS-induced ROS release in worm, inducing oxidative stress through mitochondria-mediated pathway, leading to lipid peroxidation, DNA damage, and histopathological changes, thereby contributing to decreased stress resistance against exogenous stressors. To reduce ROS-mediated oxidative damage, the antioxidant defense system in E. fetida can be activated, which scavenges unwanted ROS. High doses of SNPs and RNPs inhibited the AChE activity in worms, causing excess acetylcholine accumulation in the synaptic space, which finally lead to neurotoxicity. Also, two kinds of NPs can induce the abnormal expression of genes relevant to oxidative stress, reproduction, growth, and tight junction protein in E. fetida, which ultimately contribute to various detrimental effects, tissue damage and dysfunction, reproductive and developmental toxicity. The results obtained from the Integrated Biological Response (IBR) suggested that long-term exposure to high-dose SNPs and RNPs can induce the stronger toxicity effects to E. fetida worms, and RNPs-induced toxicity can be different and stronger than that of SNPs. Our results provide insights for revealing the environmental effects posed by randomly-shaped NPs-contaminated soil, and are of importance for assessing the contribution of NPs with different physical characteristics to soil eco-safety.

Combined toxicity of micro/nanoplastics loaded with environmental pollutants to organisms and cells: Role, effects, and mechanism.

Micro/nanoplastics (MPs/NPs) are ubiquitous in the environment and living organisms have been exposed to these substances for a long time. When MPs/NPs enter different organisms, they transport various pollutants, including heavy metals, persistent organic pollutants, drugs, bacteria, and viruses, from the environment. On this basis, this paper summarizes the combined toxicity induced by MPs/NPs accumulating contaminants from the environment and entering organisms through a systematic review of 162 articles. Moreover, the factors influencing toxic interactions are critically discussed, thus highlighting the dominant role of the relative concentrations of contaminants in the combined toxic effects. Furthermore, for the first time, we describe the threats posed by MPs/NPs combined with other pollutants to human health, as well as their cytotoxic behavior and mechanism. We found that the "Trojan horse" effect of nanoplastics can increase the bioaccessibility of environmental pollutants, thus increasing the carcinogenic risk to humans. Simultaneously, the complex pollutants entering the cells are observed to be constantly dissociated due to the transport of lysosomes. However, current research on the intracellular release of MP/NP-loaded pollutants is relatively poor, which hinders the accurate in vivo toxicity assessment of combined pollutants. Based on the findings of our critical review, we recommend analyzing the toxic effects by clarifying the dose relationship of each component pollutant in cells, which is challenging yet crucial to exploring the toxic mechanism of combined pollution. In the future, our findings can contribute to establishing a system modeling the complete load-translocation toxicological mechanism of MP/NP-based composite pollutants.

Hippocampal gene expression patterns in Sevoflurane anesthesia associated neurocognitive disorders: A bioinformatic analysis.

Background: Several studies indicate general anesthetics can produce lasting effects on cognitive function. The commonly utilized anesthetic agent Sevoflurane has been implicated in neurodegenerative processes. The present study aimed to identify molecular underpinnings of Sevoflurane anesthesia linked neurocognitive changes by leveraging publically available datasets for bioinformatics analysis. Methods: A Sevoflurane anesthesia related gene expression dataset was obtained. Sevoflurane related genes were obtained from the CTD database. Neurocognitive disorders (NCD) related genes were downloaded from DisGeNET and CTD. Intersecting differentially expressed genes between Sevoflurane and NCD were identified as cross-talk genes. A protein-protein interaction (PPI) network was constructed. Hub genes were selected using LASSO regression. Single sample gene set enrichment analysis; functional network analysis, pathway correlations, composite network analysis and drug sensitivity analysis were performed. Results: Fourteen intersecting cross-talk genes potentially were identified. These were mainly involved in biological processes including peptidyl-serine phosphorylation, cellular response to starvation, and response to gamma radiation, regulation of p53 signaling pathway, AGE-RAGE signaling pathway and FoxO signaling. Egr1 showed a central role in the PPI network. Cdkn1a, Egr1, Gadd45a, Slc2a1, and Slc3a2 were identified as important or hub cross-talk genes. Among the interacting pathways, Interleukin-10 signaling and NF-kappa B signaling enriched among Sevoflurane-related DEGs were highly correlated with HIF-1 signaling enriched in NCD-related genes. Composite network analysis showed Egr1 interacted with AGE-RAGE signaling and Apelin signaling pathways, Cdkn1a, and Gadd45a. Cdkn1a was implicated in in FoxO signaling, PI3K-Akt signaling, ErbB signaling, and Oxytocin signaling pathways, and Gadd45a. Gadd45a was involved in NF-kappa B signaling and FoxO signaling pathways. Drug sensitivity analysis showed Egr1 was highly sensitive to GENIPIN. Conclusion: A suite of bioinformatics analysis revealed several key candidate hippocampal genes and associated functional signaling pathways that could underlie Sevoflurane associated neurodegenerative processes.

Size-dependent effects of nanoplastics on structure and function of superoxide dismutase.

The ubiquitous existence of nano-plastics (NPs) has attracted widespread concern. Currently, the uptake of NPs by organisms and cells has been reported. However, knowledge about the interaction between NPs and protein is still limited, and there is a gap in research on the size-dependent toxicity of NPs toward protein. In this study, multi-spectroscopic techniques and enzyme activity determination were used to explore the structure and function changes of the main antioxidant enzyme superoxide dismutase (SOD), caused by the binding of NPs with different particle sizes. Results indicated NPs with different sizes can directly interact with SOD. NPs with smaller sizes result in looser skeletons of SOD, while the larger lead to tighter peptide chains. In addition, NPs can bind with SOD to form complexes, and the smaller the NPs are easier to be induced to coalesce by SOD. The surface curvature of 100 nm NPs was more conducive to varying the secondary structure of SOD. NPs of 100 nm and 500 nm can cause greater sensitization of SOD endogenous fluorescence, and increase the polarity around tyrosine residue. The enzyme activity assay further revealed the functional differences caused by the size-dependent effects of NPs. NPs of 100 nm and 20 nm induced a more significant change in SOD activity (increased by 20% and 8%, respectively), while NPs of 500 nm and 1000 nm had a little impact on it. Together, smaller NPs have a greater impact on the structure and function of SOD. This study revealed the size-dependent toxicity of NPs to protein, which provided a rationale for the necessary avoidance and substitution of NPs in engineering applications.

Behavioral, histopathological, genetic, and organism-wide responses to phenanthrene-induced oxidative stress in Eisenia fetida earthworms in natural soil microcosms.

Phenanthrene (PHE) contamination not only changes the quality of soil environment but also threatens to the soil organisms. There is lack of focus on the eco-toxicity potential of this contaminant in real soil in the current investigation. Here, we assessed the toxic effects of PHE on earthworms (Eisenia fetida) in natural soil matrix. PHE exhibited a relatively high toxicity to E. fetida in natural soil, with the LC50 determined to be 56.68 mg kg-1 after a 14-day exposure. Excessive ROS induced by PHE, leading to oxidative damage to biomacromolecules in E. fetida, including lipid peroxidation, protein carbonylation, and DNA damage. The antioxidant defense system (total antioxidant capacity, glutathione S-transferase, peroxidase, catalase, carboxylesterase, and superoxide dismutase) in E. fetida responded quickly to scavenge excess ROS and free radicals. Exposure to PHE resulted in earthworm avoidance responses (2.5 mg kg-1) and habitat function loss (10 mg kg-1). Histological observations indicated that the intestine, body wall, and seminal vesicle in E. fetida were severely damaged after exposure to high-dose PHE. Moreover, earthworm growth (weight change) and reproduction (cocoon production and the number of juvenile) were also inhibited after exposure to this pollutant. Furthermore, the integrated toxicity of PHE toward E. fetida at different doses and exposure times was assessed by the integrated biomarker response (IBR), which confirmed that PHE is more toxic to earthworms in the high-dose and long-term exposure groups. Our results showed that PHE exposure induced oxidative stress, disturbed antioxidant defense system, and caused oxidative damage in E. fetida. These effects can trigger behavior changes and damage histological structure, finally cause growth inhibition, genotoxicity, and reproductive toxicity in earthworms. The strength of this study is the comprehensive toxicity evaluation of PHE to earthworms and highlights the need to investigate the eco-toxicity potential of exogenous environmental pollutants in a real soil environment.

Landscape Characteristics Affecting Spatial Patterns of Water Quality Variation in a Highly Disturbed Region.

Spatial patterns of water quality trends for 45 stations in control units of the Shandong Province, China during 2009-2017 were examined by a non-parametric seasonal Mann-Kendall's test (SMK) for dissolved oxygen (DO), biochemical oxygen demand (BOD), chemical oxygen demand (COD), permanganate index (CODMn), total phosphorus (TP) and ammonia nitrogen (NH3-N). The DO concentration showed significant upward trends at approximately half of the stations, while other parameters showed significant downward trends at more than 40% of stations. The stations with downward trends presented significant spatial autocorrelation, and were mainly concentrated in the northwest and southwest regions. The relationship between the landscape characteristics and water quality was explored using stepwise multiple regression models, which indicated the water quality was better explained using landscape pattern metrics compared to the percentage of land use types. Decreased mean patch area and connectedness of farmland will promote the control of BOD, COD and CODMn, whereas the increased landscape percentage of urban areas were not conducive to the water quality improvement, which suggested the sprawling of farmland and urban land was not beneficial to pollution control. Increasing the grassland area was conducive to the reduction of pollutants, while the effect of grassland fragmentation was reversed.

Osthole Upregulates BDNF to Enhance Adult Hippocampal Neurogenesis in APP/PS1 Transgenic Mice.

Adult hippocampal neurogenesis occurs in the dentate gyrus (DG) of the mouse hippocampus, and plays roles in learning and memory progresses. In amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mice, a rodent model of Alzheimer's disease (AD), severe impairment of neurogenesis in the dentate subgranular zone (SGZ) of the DG has been reported. Osthole, an active constituent of Cnidium monnieri (L.) CUSSON, has been reported to exert neuroprotective effects and may promote neural stem cell proliferation. However, whether osthole ameliorates spatial memory deficits and improves hippocampal neurogenesis in APP/PS1 mice remains unknown. In this study we found that osthole (30 mg/kg intraperitoneally (i.p.) once daily) treatment dramatically ameliorated the cognitive impairments by Morris Water Maze test and passive avoidance test, and augmented neurogenesis in the DG of hippocampus in APP/PS1 mice. Furthermore, osthole treatment upregulated expression of brain-derived neurotrophic factor (BDNF) and enhanced activation of the BDNF receptor tyrosine receptor kinase B (TrkB) following increased phosphorylation of cyclic AMP response element-binding protein (CREB), indicating that osthole improves neurogenesis via stimulating BDNF/TrkB/CREB signaling in APP/PS1 transgenic mice.

Effects of different anesthesia methods on cognitive dysfunction after hip replacement operation in elder patients.

There are many risk factors for the cause of postoperative cognitive dysfunction (POCD), however, the anesthesia selection always trigger controversy for the POCD occurrence. This study aims to explore the relationship between the anesthesia and the occurrence of POCD in elder patients, and also investigate the mechanism of the POCD. One hundred elder patients with hip replacement were included in this study, which were divided into general anesthesia (GA) and epidural analgesia (EA) group. Minimum mental state examination (MMSE) method was employed to assess the nervous and mental function (POCD) in both analgesia group patients. Aß and tau protein levels in blood were detected by using the ELISA assay. The correlation between MMSE in POCD patients and Aß or tau was analyzed by employing the Spearman rank correlation method. The results indicated that epidural analgesia decreases the MMSE scoring compared to general analgesia (P < 0.05). General analgesia enhanced the Aß and tau level compared to epidural analgesia (P < 0.05). Aß and tau level were increased in the patients with POCD. The POCD occurrence rate in GA group was significantly higher compared to EA group (P < 0.05). MMSE scores of POCD patients positively correlated with Aß or tau level (P < 0.05). In conclusion, the epidural analgesia method was better than general analgesia method for the hip replacement in elder patients. The mechanism of the POCD may be caused by the enhancement of Aß and Tau protein.