Soil Cd and Zn contamination has become a serious environmental problem. This work explored the performance of wood vinegar (WV) in enhancing the phytoextraction of Cd/Zn by hyperaccumulator Sedum alfredii Hance. Rhizosphere chemical properties, enzyme activities and bacterial community were analyzed to determine the mechanisms of metal accumulation in this process. Results demonstrated that, after 120 days growth, different times dilution of WV increased the shoot biomass of S. alfredii by 85.2%–148%. In addition, WV application significantly increased soil available Cd and Zn by lowing soil pH, which facilitated plant uptake. The optimal Cd and Zn phytoextraction occurred from the 100 times diluted WV (D100), which increased the Cd and Zn extraction by 188% and 164%, compared to CK. The 100 and 50 times diluted WV significantly increased soil total and available carbon, nitrogen and phosphorus, and enhancing enzyme activities of urease, acid phosphatase, invertase and protease by 10.1–21.4%, 29.1–42.7%,12.2–38.3% and 26.8–85.7%, respectively, compared to CK. High-throughput sequencing revealed that the D 100 significantly increased the bacterial diversity compared to CK. Soil bacterial compositions at phylum, family and genera level were changed by WV addition. Compared to CK, WV application increased the relative abundances of genus with plant growth promotion and metal mobilization function such as, Bacillus, Gemmatimonas, Streptomyces, Sphingomonas and Polycyclovorans, which was positively correlated to biomass, Cd/Zn concentrations and extractions by S. alfredii. Structural equation modeling analysis showed that, soil chemical properties, enzyme activities and bacterial abundance directly or indirectly contributed to the biomass promotion, Cd, and Zn extraction by S. alfredii. To sum up, WV improved phytoextraction efficiency by enhancing plant growth, Cd and Zn extraction and increasing soil nutrients, enzyme activities, and modifying bacterial community.

Lead (Pb) exposure can induce DNA damage and alter DNA methylation but their inter-relationships have not been adequately determined. Our overall aims were to explore such relationships and to evaluate underlying epigenetic mechanisms of Pb-induced genotoxicity in Chinese workers. Blood Pb levels (BLLs) were determined and used as individual's Pb-exposure dose and the Comet assay (i.e., % tail DNA) was conducted to evaluate DNA damage. In the screening assay, 850 K BeadChip sequencing was performed on peripheral blood from 10 controls (BLLs ≤100 μg/L) and 20 exposed workers (i.e., 10 DNA-damaged and 10 DNA-undamaged workers). Using the technique, differentially methylated positions (DMPs) between the controls and the exposed workers were identified. In addition, DMPs were identified between the DNA-undamaged and DNA-damaged workers (% tail DNA >2.14%). In our validation assay, methylation levels of four candidate genes were measured by pyrosequencing in an independent sample set (n = 305), including RRAGC (Ras related GTP binding C), USP1 (Ubiquitin specific protease 1), COPS7B (COP9 signalosome subunit 7 B) and CHEK1 (Checkpoint kinase 1). The result of comparisons between the controls and the Pb-exposed workers show that DMPs were significantly enriched in genes related to nerve conduction and cell cycle. Between DNA-damaged group and DNA-undamaged group, differentially methylated genes were enriched in the pathways related to cell cycle and DNA integrity checkpoints. Additionally, methylation levels of RRAGC and USP1 were negatively associated with BLLs (P < 0.05), and the former mediated 19.40% of the effect of Pb on the % tail DNA. These findings collectively indicated that Pb-induced DNA damage was closely related to methylation of genes in cell cycle regulation, and methylation levels of RRAGC were involved in Pb-induced genotoxicity.

Slaughter wastewater is an important and wide range of environmental issues, and even threaten human health through meat production. A high efficiency and stability microsphere-immobilized Bacillus velezensis strain was designed to remove organic matter and inhibit the growth of harmful bacteria in process of slaughter wastewater. Bacillus velezensis was immobilized on the surface of sodium alginate (SA)/Polyvinyl alcohol (PVA)/Nano Zinc Oxide (Nano-ZnO) microsphere with the adhesion to bio-carrier through direct physical adsorption. Results indicated that SA/PVA/ZnO and SA/ZnO microspheres could inhibit E.coli growth with adding 0.15 g/L nano-ZnO and not affect Bacillus velezensis strain, and the removal the chemical oxygen demand (COD) rates of SA/PVA/ZnO microsphere immobilized cells are 16.99%, followed by SA/ZnO (13.69%) and free bacteria (7.61%) from 50% concentration slaughter wastewater within 24 h at 37 °C, pH 7.0, and 120 rpm, a significant difference was found between the microsphere and control group. Moreover, when the processing time reaches 36 h, COD degradation of SA/PVA/ZnO microsphere is obviously higher than other groups (SA/PVA/ZnO:SA/ZnO:control vs 18.535 : 15.446: 10.812). Similar results were obtained from 30% concentration slaughter wastewater. Moreover, protein degradation assay was detected, and there are no significant difference (SA/PVA/ZnO:SA/ZnO:control vs 35.4 : 34.4: 36.0). The design of this strategy could greatly enhance the degradation efficiency, inhibit the growth of other bacteria and no effect on the activity of protease in slaughter wastewater. These findings suggested that the nano-ZnO hydrogel immobilization Bacillus velezensis system wastewater treatment is a valuable alternative method for the remediation of pollutants from slaughter wastewater with a novel and eco-friendly with low-cost investment as an advantage.

The use of reclaimed water in agriculture represents a promising alternative to relieve pressure on freshwater supplies, especially in arid or semiarid regions facing water scarcity. However, this implies introducing micropollutants such as pharmaceutical residues into the environment. The fate and the ecotoxicological impact of valsartan, an antihypertensive drug frequently detected in wastewater effluents, were evaluated in soil-earthworm microcosms. Valsartan dissipation in the soil was concomitant with valsartan acid formation. Although both valsartan and valsartan acid accumulated in earthworms, no effect was observed on biomarkers of exposure (acetylcholinesterase, glutathione S-transferase and carboxylesterase activities). The geometric mean index of soil enzyme activity increased in the soils containing earthworms, regardless of the presence of valsartan. Therefore, earthworms increased soil carboxylesterase, dehydrogenase, alkaline phosphatase, β-glucosidase, urease and protease activities. Although bacterial richness significantly decreased following valsartan exposure, this trend was enhanced in the presence of earthworms with a significant impact on both alpha and beta microbial diversity. The operational taxonomic units involved in these changes were related to four (Proteobacteria, Bacteroidetes, Actinobacteria and Firmicutes) of the eight most abundant phyla. Their relative abundances significantly increased in the valsartan-treated soils containing earthworms, suggesting the presence of potential valsartan degraders. The ecotoxicological effect of valsartan on microbes was strongly altered in the earthworm-added soils, hence the importance of considering synergistic effects of different soil organisms in the environmental risk assessment of pharmaceutical active compounds.

Extracellular Polymeric Substances (EPS) influenced Poly Cyclic Aromatic Hydrocarbons (PAHs) degrading Klebsiella pneumoniae was isolated from the marine environment. To increase the EPS production by Klebsiella pneumoniae, several physicochemical parameters were tweaked such as different carbon sources (arabinose, glucose, glycerol, lactose, lactic acid, mannitol, sodium acetate, starch, and sucrose at 20 g/L), nitrogen sources (ammonium chloride, ammonium sulphate, glycine, potassium nitrate, protease peptone and urea at 2 g/L), different pH, carbon/nitrogen ratio, temperature, and salt concentration were examined. Maximum EPS growth and biodegradation of Anthracene (74.31%), Acenaphthene (67.28%), Fluorene (62.48%), Naphthalene (57.84%), and mixed PAHs (55.85%) were obtained using optimized conditions such as glucose (10 g/L) as carbon source, potassium nitrate (2 g/L) as the nitrogen source at pH 8, growth temperature of 37 °C, 3% NaCl concentration and 72 h incubation period. The Klebsiella pneumoniae biofilm architecture was studied by confocal laser scanning microscopy (CLSM) and scanning electron microscope (SEM). The present study demonstrates the EPS influenced PAHs degradation of Klebsiella pneumoniae.

Riverine ecosystems can have tipping points at which the system shifts abruptly to alternate states, although quantitative characterization is extremely difficult. Here we show, through critical analysis of two different reach scale (25 m and 50 m) studies conducted downstream of two point sources, two tributaries (main stem and confluences) and a 630 km segment of the Ganga River, that human-driven benthic hypoxia/anoxia generates positive feedbacks that propels the system towards a contrasting state. Considering three positive feedbacks-denitrification, sediment-P- and metal-release as level determinants and extracellular enzymes (β-D-glucosidase, protease, alkaline phosphatase and FDAase) as response determinants, we constructed a ‘river ecosystem resilience risk index (RERRI)’ to quantitatively characterize tipping points in large rivers. The dynamic fit intersect models indicated that the RERRI<4 represents a normal state, 4–18 a transition where recovery is possible, and >18 an overstepped condition where recovery is not possible. The resilience risk index, developed for the first time for a lotic ecosystem, can be a useful tool for understanding the tipping points and for adaptive and transformative management of large rivers.

Atrazine (ATR), a selective herbicide, is consistently used worldwide and has been confirmed to be harmful to the health of aquatic organisms. The release of neutrophil extracellular traps (NETs) is one of the newly discovered antimicrobial mechanisms. Although several immune functions have been analyzed under ATR exposure, the effect of ATR on NETs remains mainly unexplored. In the present study, we treated carp neutrophils using 5 μg/ml ATR and 5 μg/ml ATR combined with 100 nM rapamycin to elucidate the underlying mechanisms and to clarify the effect of ATR on phorbol myristate acetate (PMA)-induced NETs. The results of the morphological observation and quantitative analysis of extracellular DNA and myeloperoxidase (MPO) showed that NETs formation were significantly inhibited by ATR exposure. Moreover, we found that in the NETs process, ATR downregulated the expression of the anti-apoptosis gene B-cell lymphoma-2 (Bcl-2), increased the expression of the pro-apoptosis factors Bcl-2-Associated X (BAX), cysteinyl aspartate specific proteinases (Caspase3, 9), and anti-autophagy factor mammalian target of rapamycin (mTOR), decreased the expression of autophagy-related protein light chain 3B (LC3B) and glucose transport proteins (GLUT1, 4), disturbed the activities of phosphofructokinase (PFK), pyruvate kinase (PKM), and hexokinase (HK) and limited reactive oxygen species (ROS) levels, indicating that the reduced NETs release was a consequence of increased apoptosis and diminished ROS burst, autophagy and down-regulated glycolysis under ATR treatment. Meanwhile, rapamycin restored the inhibited autophagy and glycolysis and thus resisted the ATR-suppressed NETs. The present study perfects the mechanism theory of ATR immunotoxicity to fish and has a certain value for human health risk assessment.

Microplastic beads are an emerging contaminant that can cause serious environmental and public health problems. Potential bypass of microplastic beads from wastewater to sludge treatment systems is a key challenge in the conventional wastewater treatment process. Moreover, there are no systematic studies on microplastic bead degradation by hydrolytic enzymes that are rich in concentration within wastewater and sludge treatment processes (e.g., anaerobic digestion (AD)). In this study, lab-scale experiments were conducted to investigate the degradation of high-density polyethylene beads by hydrolytic enzymes (e.g., lipase) under various experimental conditions (e.g., temperature). In a 3-day batch experiment, protease was most effective in polyethylene bead degradation as 4.0% of the initial bead mass was removed at an enzyme concentration of 88 mg/L under thermophilic temperature (55 °C). It was also found that the increasing enzyme concentration and high temperature enhanced the polyethylene bead degradation. In a separate 7-day experiment with repeated doses of protease, 23.3% of the initial mass of beads was removed at thermophilic temperature, indicating that AD with a long retention time (e.g., 20 days) and heated temperature has a significant potential for polyethylene bead degradation. A mathematical model was developed and calibrated using the experimental results to estimate the kinetic constant of the high-density polyethylene bead reduction by an enzyme (k1,i) and enzyme self-decay constant (k2,ii). The calibrated k1,i ranged from 5.0 to 8.1× 10⁻⁴ L/mg/hr while k2,ii was 0.44–1.10 L/mg/hr. Using the calibrated model, degradation of polyethylene beads using a mixture of cellulase and protease was simulated, considering an interactive-decay reaction between the two enzymes. The calibrated model was used to simulate the polyethylene bead degradation in AD where 70–95% of the initial bead mass was removed at typical retention time under mesophilic digestion (37.5 °C). Based on the experimental and simulation results, it can be concluded that hydrolytic enzymes can be an efficient technology for large-scale high-density polyethylene bead removal applications.

Epidemiological studies have demonstrated a strong association of ambient fine particulate matter (PM₂.₅) exposure with the increasing mortality by ischemic heart disease (IHD), but the involved mechanisms remain poorly understood. Herein, we found that the chronic exposure of real ambient PM₂.₅ led to the upregulation of hypoxia-inducible factor-1 alpha (HIF-1α) protein in the myocardium of mice, accompanied by obvious myocardial injury and hypertrophy. Further data from the hypoxia-ischemia cellular model indicated that PM₂.₅-induced HIF-1α accumulation was responsible for the promotion of myocardial hypoxia injury. Moreover, the declined ATP level due to the HIF-1α-mediated energy metabolism remodeling from β-oxidation to glycolysis had a critical role in the PM₂.₅-increased myocardial hypoxia injury. The in-depth analysis delineated that PM₂.₅ exposure decreased the binding of prolyl hydroxylase domain 2 (PHD2) and HIF-1α and subsequent ubiquitin protease levels, thereby leading to the accumulation of HIF-1α. Meanwhile, factor-inhibiting HIF1 (FIH1) expression was down-regulated by PM₂.₅, resulting in the enhanced translocation of HIF-1α to the nucleus. Overall, our study provides valuable insight into the regulatory role of oxygen sensor-mediated HIF-1α stabilization and translocation in PM-exacerbated myocardial hypoxia injury, we suggest this adds significantly to understanding the mechanisms of haze particles-caused burden of cardiovascular disease.

Imidacloprid (IMI) is widely used in agriculture, and is toxic to non-target aquatic species. Quercetin (Que) is a flavonoid abundant in fruits and vegetables that exhibits anti-oxidant activity. In the present study, we treated grass carp hepatocytes (L8824) with 0.1 μM Que and/or 1 mM IMI for 24 h to explore the effect of Que on IMI-induced mitochondrial apoptosis. We found that IMI exposure enhanced reactive oxygen species (ROS) generation, inhibiting the activities of SOD, CAT and T-AOC, exacerbating the accumulation of MDA, aggravating the expression of mitochondrial apoptosis pathway (Cyt-C, BAX, Caspase9 and Caspase3) related genes and decreased the expression of anti-apoptosis gene B-cell lymphoma-2 (Bcl-2). In addition, Que and IMI co-treatment significantly restored the activity of anti-oxidant enzymes, downregulated ROS level and apoptosis rate, thereby alleviating the depletion of mitochondrial membrane potential (ΔΨm) and the expression of cytochrome c (Cyt-C), Bcl-2-associated X (BAX), and cysteinyl aspartate specific proteinases (Caspase9 and 3), increasing the Bcl-2 level. Furthermore, we elucidated that Que could inhibit the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), thus activating phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway to attenuate IMI-induced apoptosis. Molecular docking provides assertive evidence for the interaction between Que ligand and PTEN receptor. Consequently, these results indicate that Que effectively antagonizes IMI-induced mitochondrial apoptosis in grass carp hepatocytes via regulating the PTEN/PI3K/AKT pathway.