Pyrite-assisted degradation of methoxychlor by laccase immobilized on Fe3S4/earthworm-like mesoporous SiO2.

Laccase immobilized and cross-linked on Fe3S4/earthworm-like mesoporous SiO2 (Fe3S4/EW-mSiO2) was used to degrade methoxychlor (MXC) in aqueous environments. The effects of various parameters on the degradation of MXC were determined using free and immobilized laccase. Immobilization improved the thermal stability and reuse of laccase significantly. Under the conditions of pH 4.5, temperature 40 °C, and reaction time 8 h, the degradation rate of MXC by immobilized laccase reached a maximum value of 40.99% and remained at 1/3 of the original after six cycles. The excellent degradation performance of Fe3S4/EW-mSiO2 was attributable to the pyrite (FeS2) impurity in Fe3S4, which could act as an electron donor in reductive dehalogenation. Sulfide groups and Fe2+ reduced the activation energy of the system resulting in pyrite-assisted degradation of MXC. The degradation mechanism of MXC in aqueous environments by laccase immobilized on Fe3S4/EW-mSiO2 was determined via mass spectroscopy of the degradation products. This study is a new attempt to use pyrite to support immobilized laccase degradation.

Degradation of trichloroacetic acid by Fe/Ni bimetallic reactive PMS with hierarchical layered structure.

Overuse of chlorinated disinfectants leads to a significant accumulation of disinfection by-products. Trichloroacetic acid (TCA) is a typical carcinogenic disinfection by-product. The efficacy of the conventional degradation process is reduced by the complex nature of its structure, causing a yearly increase in its prevalence within the ecological environment and consequent infliction of significant harm. In this paper, TCA was chosen as the research subject, Fe/Ni bimetallic nanoparticles were employed as the reducing catalyst, ZIF-8@HMON as the catalytic carrier combined with Fe/Ni nanoparticles, and peroxymonosulfate (PMS) was introduced to construct the reducing-advanced oxidation synergistic system and investigated the effect of this system on the degradation performance and degradation pathway of TCA. Various characterization techniques, including TEM, SEM, XRD, FT-IR, XPS, BET, were employed to investigate the morphology, element composition and structure of composite materials analysis. Moreover, the conditions for TCA degradation can be optimized by changing the experimental environment. The results showed that 25 mg of composite catalyst (mole ratio Fe: Ni = 1:1) and 10 mg of PMS effectively degraded TCA within 20-80 mg/L range at pH = 3 and 55 °C, achieving maximum degradation within 20 min. Finally, the potential pathways of TCA degradation were analyzed using EPR and LC-MS, and the corresponding reaction mechanisms were proposed.

A bi-metallic MOF catalyst via sensitive detection & adsorption of Fe3+ ions for size-selective reaction prompting.

A cadmium(ii)-based MOF, Cd-MDIP, was successfully prepared by hydrothermal reaction between the tetra-carboxylic ligand 5,5'-methylenebisophthalic acid (H4MDIP) and cadmium perchlorate. The X-ray crystal structure analysis showed that there are two uncoordinated carboxyl groups in each ligand and a 1D elliptical channel along the [001] direction. Because of the existence of uncoordinated carboxyl groups within open frameworks, Cd-MDIP exhibited a high sensitivity (Stern-Volmer constant KSV = 4.13 × 104 L mol-1) and a low detection limit (80 nM) for Fe3+ ions in pure water, which is much lower than the national standard for Fe3+ in daily drinking water (5.4 µM) set by the Ministry of Environmental Protection of P. R. China. Most importantly, Cd-MDIP also featured the ultrahigh adsorption of Fe3+ in aqueous solution that cannot be destroyed even by EDTA/base. Importantly, the MOF material (Cd-MDIP⊃Fe3+) after adsorbing Fe3+ could act as the first example of an excellent bi-metallic Lewis-acid catalyst for the cyanosilylation reaction of aromatic aldehydes in a size-selective fashion, and its efficiency was almost 10-times higher than that of the original Cd-MDIP.

IL-6 promotes ICAM-1 expression and cell motility in human osteosarcoma.

Osteosarcoma is characterized by a high malignant and metastatic potential. Interleukin-6 (IL-6) is a multifunctional cytokine that is associated with the disease status and outcomes of cancers. However, the effect of IL-6 on migration activity in human osteosarcoma cells is mostly unknown. Here we found that IL-6 increased the migration and expression of intercellular adhesion molecule-1 (ICAM-1) in human osteosarcoma cells. Transfection of cells with ICAM-1 siRNA reduced IL-6-mediated cell migration. We also found that expression of IL-6 was significantly greater in human osteosarcoma tissues than in normal bone. The integrin-linked kinase (ILK)/Akt/AP-1 pathway was activated after IL-6 treatment, and IL-6-induced expression of ICAM-1 and migration activity was inhibited by the specific inhibitor and siRNA of ILK, Akt, and AP-1 cascades. In addition, over-expression of IL-6 shRNA inhibited the migratory ability and ICAM-1 expression in osteosarcoma cells. Taken together, these results indicate that IL-6 and IL-6 receptor interaction occurs through ILK and Akt, which in turn activates AP-1, resulting in the activations of ICAM-1 and contributing the migration of human osteosarcoma cells.

Interleukin-6 induces vascular endothelial growth factor expression and promotes angiogenesis through apoptosis signal-regulating kinase 1 in human osteosarcoma.

Osteosarcoma is characterized by a high malignant and metastatic potential. Angiogenesis is essential for the caner metastasis. Interleukin-6 (IL-6) is a multifunctional cytokine that is associated with the disease status and outcomes of cancers. However, the relationship between IL-6 and vascular endothelial growth factor (VEGF) expression in human osteosarcoma is mostly unknown. Here we found that the IL-6 and VEGF expression was correlated with tumor stage and significantly higher than that in normal bone. Incubation of osteosarcoma cells with IL-6 increased VEGF mRNA and protein expression. Pretreatment of cells with IL-6R antibody reduced IL-6-mediated VEGF production. The apoptosis signal-regulating kinase 1 (ASK1)/p38/AP-1 pathway was activated after IL-6 treatment, and IL-6-induced VEGF expression was abolished by the specific inhibitor and siRNA of ASK1, p38, and AP-1 cascades. Importantly, knockdown IL-6 reduced VEGF expression and abolished osteosarcoma conditional medium-mediated angiogenesis. Taken together, these results indicate that IL-6 occurs through ASK1 and p38, which in turn activates AP-1, resulting in the activations of VEGF expression and contributing the angiogenesis of human osteosarcoma cells.