RESUMEN
Rapid decomposition of wastewater contaminants using sulfurized limonite (S-limonite) was investigated. Limonite is used for desulfurization of biogases, and S-limonite is obtained from desulfurization plants as solid waste. In this work, the profitable use of S-limonite in water treatment was examined. The divalent Fe in S-limonite was expected to produce OH radicals, as Fe(2+) ions and limonite thermally treated with H2 do. Methylene blue was used for batch-wise monitoring of the decomposition performance. The decomposition rate was fast and the methylene blue solution color disappeared in only 10s when a small amount of H2O2 was added (1mM in the sample solution) in the presence of S-limonite. The OH radicals were formed by a heterogeneous reaction on the S-limonite surface and Fenton reaction with dissolved Fe(2+). The decomposition of pentachlorophenol was also examined; it was successfully decomposed in batch-wise tests. The surfaces of limonite before sulfurization, S-limonite, and S-limonite after use for water treatment were performed using scanning electron microscopy and X-ray photoelectron spectroscopy. The results show that S-limonite reverted to limonite after being used for water treatment.
Asunto(s)
Compuestos Férricos/química , Peróxido de Hidrógeno/química , Azul de Metileno/química , Azufre/química , Contaminantes Químicos del Agua/química , Colorantes/química , Sulfuro de Hidrógeno/química , Concentración de Iones de Hidrógeno , Pentaclorofenol/química , Eliminación de Residuos Líquidos/métodosRESUMEN
Vascular endothelial cells play important roles in atherogenesis, and bradykinin is associated with atherosclerosis. The effect of bradykinin on apoptosis in human umbilical vein endothelial cells (HUVECs) was investigated, with a focus on Ca2+ kinetics and nitric oxide production. In serum-free conditions, the number of apoptotic cells increased in a time-dependent manner, but this increase was inhibited by bradykinin in a dose-dependent manner. The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine. Bradykinin increased influx of extracellular Ca2+, generation of inositol 1,4,5-trisphosphate, and release of Ca2+ from intracellular storage sites, thus increasing the total intracellular Ca2+ concentration ([Ca2+]i). Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine. Sodium nitroprusside (SNP) dose-dependently increased nitric oxide production and inhibited apoptosis; however, 10(-5) M SNP did not inhibit apoptosis. Caspase-3 inhibitor, acetyl-Asp-Met-Gln-Asp-aldehyde, enhanced bradykinin-induced inhibition of apoptosis but did not effect bradykinin-induced nitric oxide production. These findings suggest that bradykinin inhibits serum-depletion-induced apoptosis in HUVECs by enhancing nitric oxide production via an increase in [Ca2+]i.