Pyrite-activated persulfate to degrade 3,5,6-trichloro-2-pyridyl in water: Degradation and Fe release mechanism.

TCP (3,5,6-trichloro-2-pyridinol), the main recalcitrant degradation product of chlorpyrifos, poses a high risk to human health and ecological systems. This study provided a comprehensive exploration of the pyrite-activated persulfate (PS) system for the removal of TCP in water and placed particular emphasis on the pyrite oxidation process that releases Fe. The results showed that the pyrite-activated PS system can completely degrade TCP within 300 min at 5.0 mmol/L PS and 1000 mg/L pyrite at 25 °C, wherein small amounts of PS (1 mmol/L) can effectively facilitate TCP removal and the oxidation of pyrite elements, while excessive PS (>20 mmol/L) can lead to competitive inhibitory effects, especially in the Fe release process. Aimed at the dual effects, the evident positive correlation (R2 > 0.90) between TCP degradation (kTCP) and Fe element release (kFe), but the value of k (0.00237) in the pyrite addition variable experiment was less than that in the PS experiment (k = 0.00729), further indicating that the inhibition effect of excessive addition consists of PS but not notably pyrite. Moreover, the predominant free radicals and non-free radicals produced in the pyrite/PS system were tested, with the order of significance being •OH < Fe (Ⅳ) < SO4•- < â€¢O2- < 1O2, wherein 1O2 emerged as the principal player in both TCP degradation and Fe release from the pyrite oxidation process. Additionally, CO32- can finitely activate PS but generally slows TCP degradation and inhibit pyrite oxidation releasing Fe process. This study provides a theoretical basis for the degradation of TCP using pyrite-activated PS.

Antibiotics in fish caught from ice-sealed waters: Spatial and species variations, tissue distribution, bioaccumulation, and human health risk.

Antibiotics are increasingly detected in fish caught in ice-free waters, but information on fish caught in ice-sealed waters is insufficient. The concentrations of 23 antibiotics in the gills, muscles, kidneys, livers, biles, and brains of Cyprinus carpio and Hypophthalmichthys nobilis caught during winter fish-hunting activities in Chagan Lake, Haernao Reservoir, and Shitoukoumen Reservoir were systematically studied to ascertain the variations among fish species and fishing regions, tissue distribution, and bioaccumulation, as well as the potential risk to humans via the consumption of contaminated fish. The results indicated that the individual antibiotic concentration in tissues ranged from undetectable to 35.0 ng/g ww. The total antibiotic concentration in fish muscles from Shitoukoumen Reservoir was lower than that from Chagan Lake and Haernao Reservoir, but showed no significant difference between Cyprinus carpio and Hypophthalmichthys nobilis. Chloramphenicols had a high proportion in most fish tissues ranging from 28.3% to 44.0%, and the antibiotics were mainly distributed in the livers with a total concentration of 54.8 ± 9.9 ng/g ww. The mean values of bioaccumulation factors (BAF) of antibiotics in tissues ranged from 79.4 to 1000 L/kg, with the higher values found in the fish livers. The hazard quotient and hazard index value of antibiotics in the muscles of fish from ice-sealed were less than 1, indicating a negligible risk to human health via the consumption of fish muscles. This study revealed that the total antibiotic concentration in muscles showed spatial variations but not fish species-dependence. The antibiotics mainly accumulated in the livers. In addition, the target antibiotic concentrations in the muscles of fish from ice-sealed waters met the safe for consumption criteria.

UMSCs Attenuate LPS/D-GalN-induced Acute Liver Failure in Mice by Down-regulating the MyD88/NF-κB Pathway.

BACKGROUND AND AIMS: Acute liver failure (ALF) is an inflammatory process of acute liver cell injury. Mesenchymal stem cells (MSCs) are undifferentiated, primitive cells with anti-inflammatory, anti-apoptotic, and multi-directional differentiation abilities. This study aimed to explore the therapeutic mechanism of umbilical cord (U)MSCs in ALF. METHODS: D-galactosamine (D-GalN) combined with lipopolysaccharide (LPS) was used to establish an ALF model. After model establishment, UMSCs were injected via the tail vein. After UMSC transplantation, the number of mouse deaths was monitored every 12 h. A fully automatic biochemical analyzer was used to detect changes in biochemical analysis. Pathological changes was observed by stained with hematoxylin and eosin.The expression of My D88 was detected by immunohistochemical analysis, quantitative reverse transcription, and western blotting. The expression of NF-κB was detected by quantitative reverse transcription, western blotting.The expression of Bcl-2,Bax were detected by quantitative reverse transcription, western blotting.The expression of TNF-α, IL-1ß, IL-6 were detected by enzyme-linked immunosorbent assay. RESULTS: The 48-h survival rate of the UMSC-treated group was significantly higher than that of the LPS/D-GalN-exposed group. After 24 h of LPS/D-GalN exposure, UMSCs reduced serum alanine aminotransferase and aspartate aminotransferase levels and improved the liver structure. Western blot and real-time fluorescence quantitative nucleic acid amplification analyses showed that UMSCs decreased MyD88 expression, thereby inhibiting LPS/GalN-induced phosphorylation and degradation of inhibitor of nuclear factor (NF)-κB (IκB). Additionally, NF-κB p65 underwent nuclear translocation, inhibiting the production of the inflammatory factors interleukin (IL)-1ß, IL-6 and tumor necrosis factor (TNF)-α and played a protective role in ALF by down-regulating the pro-apoptotic gene Bax and up-regulating the anti-apoptotic gene Bcl-2. In summary, these findings indicate that UMSCs play a protective role in LPS/GalN-induced acute liver injury via inhibition of the MyD88 pathway and subsequent inhibition of NF-κB-mediated cytokine production. CONCLUSIONS: Through the above mechanisms, UMSCs can effectively reduce LPS/D-GalN-induced ALF, reduce mouse mortality, and restore damaged liver function and damaged liver tissue.

Occurrence, distribution, and ecological risk of pharmaceuticals in a seasonally ice-sealed river: From ice formation to melting.

Occurrence, distribution, and ecological risk of 21 pharmaceuticals in the Jilin Songhua River were investigated during its freeze-thaw periods, including ice formation, sealed, and breakup. Florfenicol was the most abundant pharmaceutical, with mean concentrations of 123.4 ± 61.1 ng L-1 in water and 73.8 ± 66.3 ng kg-1 in ice. Sulfadiazine occurred at a higher mean concentration in downstream areas (45.6 ± 7.4 ng L-1) than in upstream areas (0.7 ± 0.7 ng L-1). Most pharmaceuticals appeared in relatively high concentrations in water during the ice-breakup period. Complex factors including pharmaceutical usage patterns, ice-regulated photodegradation, biodegradation, water flow, and freeze-concentration effects, as well as the release of pharmaceuticals from ice, were responsible for the temporal variation of pharmaceuticals. Pseudo-ice/water distribution coefficients showed the distribution of pharmaceuticals in ice and demonstrated the effects of their release from the ice on their temporal variations. Most pharmaceuticals posed a risk to algae; of these, amoxicillin exhibited the highest risk. In addition, thawing increased the concentration of thiamphenicol in water, which elevated its ecological risk level. The findings suggest that the pharmaceuticals retained in ice should be considered with regard to regulating pharmaceuticals' temporal variations in seasonal ice-covered rivers during the freeze-thaw process.