Opposite effects of the earthworm Eisenia fetida on the bioavailability of Zn in soils amended with ZnO and ZnS nanoparticles.

The increasing release of metallic nanoparticles (NPs) or their sulfidized forms into soils have raised concerns about their potential risks to soil ecosystems. Hence, there is a need for novel strategies to remediate metallic NPs pollution in soils. In this study, to explore the feasibility of using earthworm Eisenia fetida to manage soils contaminated with metallic NPs, we simultaneously investigated the chronic soil toxicities of ZnO NPs and ZnS NPs to E. fetida, and the effects of E. fetida on Zn extractability in soils amended with ZnO NPs and ZnS NPs. After a 28 d exposure, survival rate and weight loss of earthworms were not impacted by either ZnO NPs or ZnS NPs at a concentration of 400 mg Zn per kg soil. Further, while ZnO NPs activated earthworm antioxidative system, ZnS NPs resulted in significant alleviation of oxidative damage in earthworm. The presence of earthworms significantly decreased the bioavailability of Zn in ZnO NPs contaminated soil, whereas significantly increased the bioavailability of Zn in ZnS NPs contaminated soil. These findings implied that the earthworm E. fetida could play an important role in altering the mobilization of metals originating from metallic NPs in soils, which may further aid in the development of a method for the treatment of metallic NPs pollution in soils.

Nitrate removal from low carbon-to-nitrogen ratio wastewater by combining iron-based chemical reduction and autotrophic denitrification.

Nitrate removal from low carbon-to-nitrogen ratio (C/N) wastewater has always been a knotty problem due to the deficiency of organics. Here, a novel iron-based chemical reduction and autotrophic denitrification (ICAD) system was developed. ICAD system could maintain average nitrate removal efficiency of 97.2% for 131 days with feeding 20.3 mg NO3--N/L at hydraulic retention time (HRT) of 24 h. The optimal operational conditions was further explored, and results demonstrated that average nitrate removal efficiency of 85.5% and 98.4% could be achieved at HRT of 12 h and 24 h (influent 20.3 mg NO3--N/L), while average nitrate removal efficiency could reach 96.3% at optimal HRT of 12 h (influent 10.3 mg NO3--N/L). Hydrogenophaga, which can carry out hydrogenotrophic denitrification, showed a positive correlation with nitrate removal efficiency of the ICAD system. Low cost and simple operation make the ICAD system suitable for large-scale application.

1,2-Dichloroethane induces cerebellum granular cell apoptosis via mitochondrial pathway in vitro and in vivo.

1,2-Dichloroethane (1,2-DCE) is a widely used chlorinated organic toxicant, but little is known about the cerebellar dysfunction induced by excessive exposure to it. To uncover 1,2-DCE-induced neurotoxicity in cerebellar granular cells (CGCs), and to investigate the underlying mechanisms, we explored this, both in vitro and in vivo. Our findings showed significant cell viability inhibition in human CGCs (HCGCs) treated with 1,2-DCE. Flow cytometry and mitochondrial membrane potential analyses discovered an increase in apoptotic-mediated cell death in HCGCs after 1,2-DCE treatment. This HCGC apoptosis was involved in the increases of protein expression in Cytochrome c, Caspase-3, Bad, Bim, transformation related protein 53, Caspase-8, tumor necrosis factor-α, and Survivin. Quantitative real-time PCR (qPCR) and western blot confirmed the increases in Cytochrome c, Caspase-3, cleaved Caspase-3, and Bad in HCGCs after 1,2-DCE treatment. Bax inhibitor peptide V5 rescued 1,2-DCE-induced HCGC apoptosis. Furthermore, 80 CD-1 male mice were exposed to 1,2-DCE by inhalation at 0, 100, 350, and 700 mg/m3 for 6 h/day for 4 weeks. An open field test found abnormal neurobehavioral changes in the mice exposed to 1,2-DCE. Histopathological examination showed significantly shrunken and hypereosinophilic cytoplasm with nuclear pyknosis in mouse CGCs from the 700 mg/m3 1,2-DCE group. TdT-mediated dUTP nick-end labeling assay verified significant increases in apoptotic positive cells in the mouse CGCs after 1,2-DCE exposure. We confirmed the increases in the expressions of Cytochrome c, Caspase-3, cleaved Caspase-3 and Bad in the mice exposed to 1,2-DCE. These findings suggest that 1,2-DCE exposure can induce CGC apoptosis and cerebellar dysfunction, at least in part, through mitochondrial pathway.

The contributions and mechanisms of iron-microbes-biochar in constructed wetlands for nitrate removal from low carbon/nitrogen ratio wastewater.

The removal efficiency of nitrate from low carbon/nitrogen ratio wastewater has been restricted by the lack of organics for several decades. Here, a system coupling chemical reduction, microbial denitrification and constructed wetlands (RDCWs) was developed to investigate the effect and possible mechanisms for nitrate degradation. The results showed that this coupling system could achieve a nitrate removal efficiency of 97.07 ± 1.76%, 85.91 ± 3.02% and 56.63 ± 2.88% at a hydraulic retention time of 24 h, 12 h and 6 h with feeding nitrate of 15 mg L-1, respectively. These removal efficiencies of nitrate were partly caused by microbes and biochar with a contribution rate of 31.08 ± 4.43% and 9.50 ± 3.30%. Besides, microbes were closely related to iron and biochar for the removal of nitrate. Simplicispira was able to utilize hydrogen produced by iron corrosion as an electron donor while nitrate accepted electrons to be reduced. Porous biochar could release dissolved organic matter, which provided a good living circumstance and carbon source for microbes. Therefore, the RDCW system is potential for large-scale application due to its low cost and simple operation.

Bacteria-supported iron scraps for the removal of nitrate from low carbon-to-nitrogen ratio wastewater.

A novel bacteria-supported iron scraps (BSIS) system was developed for nitrate removal from low carbon-to-nitrogen ratio (C/N) wastewater. The system consisted of low-cost iron scraps and the accumulated denitrifying-related bacteria enriched from an Fe-wastewater environment when the system was operating. After operating for 39 d, the nitrate removal rate of the system increased to 73.55% within 24 h. The extraction of bacteria from the system revealed that iron scraps and bacteria had a synergistic effect on nitrate removal and bacteria only took effect when cooperating with iron. Microbial analysis using high-throughput sequencing showed that Hydrogenophaga, which is closely related to hydrogenotrophic denitrification, became the dominant genus in the system. The system provides a promising approach to the treatment of nitrate in low C/N wastewater and it has the potential for large-scale application due to the low cost, simple operation and relatively high removal rate.

Facile one-step hydrothermal synthesis of α-Fe2O3/g-C3N4 composites for the synergistic adsorption and photodegradation of dyes.

With the expansion of industrialization, dye pollution has become a significant hazard to humans and aquatic ecosystems. In this study, α-Fe2O3/g-C3N4-R (where R is the relative percentage of α-Fe2O3) composites were fabricated by a one-step method. The as-prepared α-Fe2O3/g-C3N4-0.5 composites showed excellent adsorption capacities for methyl orange (MO, 69.91 mg g-1) and methylene blue (MB, 29.46 mg g-1), surpassing those of g-C3N4 and many other materials. Moreover, the ionic strength and initial pH influenced the adsorption process. Relatively, the adsorption isotherms best fitted the Freundlich model, and the pseudo-second-order kinetic model could accurately describe the kinetics for the adsorption of MO and MB by α-Fe2O3/g-C3N4-0.5. Electrostatic interaction and π-π electron donor-acceptor interaction were the major mechanisms for MO/MB adsorption. In addition, the photocatalytic experiment results showed that more than 79% of the added MO/MB was removed within 150 min. The experimental results of free-radical capture revealed that holes (h+) were the major reaction species for the photodegradation of MO, whereas MB was reduced by the synergistic effect of hydroxyl radicals (·OH) and holes (h+). This study suggests that the α-Fe2O3/g-C3N4 composites have an application potential for the removal of dyes from wastewater.

Aberrant expression of miR-451a contributes to 1,2-dichloroethane-induced hepatic glycerol gluconeogenesis disorder by inhibiting glycerol kinase expression in NIH Swiss mice.

The identification of aberrant microRNA (miRNA) expression during chemical-induced hepatic dysfunction will lead to a better understanding of the substantial role of miRNAs in liver diseases. 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to hepatic abnormalities in occupationally exposed populations. To explore whether aberrant miRNA expression is involved in liver abnormalities mediated by 1,2-DCE exposure, we examined alterations in miRNA expression patterns in the livers of NIH Swiss mice after dynamic inhalation exposure to 350 or 700 mg m-3 1,2-DCE for 28 days. Using a microarray chip, we discovered that only mmumiR-451a was significantly upregulated in the liver tissue of mice exposed to 700 mg m-3 1,2-DCE; this finding was validated by quantitative real-time polymerase chain reaction. In vitro study revealed that it was metabolite 2-chloroacetic acid, not 1,2-DCE that resulted in the upregulation of mmu-miR-451a in the mouse AML12 cell line. Furthermore, our data showed that the upregulation of mmu-miR-451a induced by 2-chloroacetic acid could suppress the expression of glycerol kinase and lead to the inhibition of glycerol gluconeogenesis in mouse liver tissue and AML12 cells. These observations provide evidence that hepatic mmu-miR-451a responds to 1,2-DCE exposure and might induce glucose metabolism disorders by suppressing the glycerol gluconeogenesis process.

1,2-Dichloroethane Induces Reproductive Toxicity Mediated by the CREM/CREB Signaling Pathway in Male NIH Swiss Mice.

1,2-Dichloroethane (1,2-DCE) is a widely used chlorinated organic toxicant but little is known about the reproductive disorders induced by its excessive exposure. To reveal 1,2-DCE-induced male reproductive toxicity and to elucidate the underlying mechanisms, we exposed male National Institutes of Health Swiss mice to 1,2-DCE by inhalation at 0, 100, 350, and 700 mg/m3 for 6 h/day, for 1 and 4 weeks. Our findings showed a significant decrease in body weight with increased testis/body weight ratio, reduced sperm concentration and induced malformation of spermatozoa, and vacuolar degeneration of germ cells in the seminiferous tubules of testes in mice exposed to 1,2-DCE. Cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB) and cAMP-response element modulator (CREM) were significantly inhibited by 1,2-DCE. This is consistent with the declines in the transducer of regulated CREB activity 1 and activator of CREM in testis, which results in the decrease in lactate dehydrogenase C and testis-specific kinase 1 in the testes. Moreover, the activation of p53 and Bax with the inhibition of Bcl-2 might be the reason for the upregulation of caspase-3 in the apoptosis, as detected by TdT-mediated dUTP nick-end labeling assay in the testes induced by 1,2-DCE. Finally, elevated testosterone levels were found along with increased levels of gonadotropin-releasing hormone, cAMP, luteinizing hormone (LH), and LH receptors in the testes. These findings suggest that 1,2-DCE inhibits CREM/CREB signaling cascade and subsequently induces apoptosis associated with p53 activation and mitochondrial dysfunction. This also results in induced malformation of spermatozoa, reduced sperm concentration, and pathological impairment of the testes.

1,2-Dichloroethane impairs glucose and lipid homeostasis in the livers of NIH Swiss mice.

Excessive exposure to 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to liver dysfunction. To fully explore the mechanism of 1,2-DCE-induced hepatic abnormalities, 30 male National Institutes of Health (NIH) Swiss mice were exposed to 0, 350, or 700mg/m3 of 1,2-DCE, via inhalation, 6h/day for 28days. Increased liver/body weight ratios, as well as serum AST and serum ALT activity were observed in the 350 and 700mg/m3 1,2-DCE exposure group mice, compared with the control group mice. In addition, decreased body weights were observed in mice exposed to 700mg/m3 1,2-DCE, compared with control mice. Exposure to 350 and 700mg/m3 1,2-DCE also led to significant accumulation of hepatic glycogen, free fatty acids (FFA) and triglycerides, elevation of blood triglyceride and FFA levels, and decreases in blood glucose levels. Results from microarray analysis indicated that the decreases in glucose-6-phosphatase catalytic subunit (G6PC) and liver glycogen phosphorylase (PYGL) expression, mediated by the activation of AKT serine/threonine kinase 1 (Akt1), might be responsible for the hepatic glycogen accumulation and steatosis. Further in vitro study demonstrated that 2-chloroacetic acid (1,2-DCE metabolite), rather than 1,2-DCE, up-regulated Akt1 phosphorylation and suppressed G6PC and PYGL expression, resulting in hepatocellular glycogen accumulation. These results suggest that hepatic glucose and lipid homeostasis are impaired by 1,2-DCE exposure via down-regulation of PYGL and G6PC expression, which may be primarily mediated by the 2-chloroacetic acid-activated Akt1 pathway.