Nano-oxides washcoat for enhanced catalytic oxidation activity toward the perovskite-based monolithic catalyst.

In order to explore a superior washcoat material to give full play to the catalytic activity of perovskite active components on the monolithic catalysts, three novel types of LaCoO3/washcoat/cordierite monolith catalysts were prepared by a facile two-step procedure which employed the cordierite honeycomb ceramic as the monolith substrate, the nano-oxides (ZrO2, ɤ-Al2O3, TiO2) as the washcoat, and the perovskite of LaCoO3 as the active components. The blank cordierite, powdered LaCoO3, semi-manufactured monolithic catalysts (washcoat/cordierite), and manufactured monolithic catalysts (LaCoO3/washcoat/cordierite) were characterized by XRD, SEM, XPS, N2 adsorption-desorption, H2-TPR, and ultrasonic test, and their catalytic activities and catalytic stability were evaluated by the toluene oxidation test. The research results indicate that the nanoparticles coated on the cordierite substrate as the washcoat can give full play to the catalytic ability of the LaCoO3 active components and also showed high catalytic stability. However, the catalytic properties of the monolithic catalysts vary notably with the species of nano-washcoat. Among all the catalysts, the porous honeycomb surface structure, uniform distribution, high ratio of surface adsorbed oxygen, and strong reducing ability together give the LaCoO3/ZrO2/cordierite monolithic catalyst the highest catalytic activity on the oxidation of toluene at low temperature, which could be attributed to the excellent interactions of perovskite and nano-ZrO2 washcoat. Therefore, the nano-oxides, especially the nano-ZrO2, have a broad practical application potential for toluene oxidation at low temperature as the washcoat of perovskite-based monolithic catalysts.

Effects of Chahuangjing on Decorporation and Radiation Protection Against Tritiated Water.

The purpose of this study was to investigate the effects of Chahuangjing, a novel traditional Chinese medicinal compound, on decorporation and radiation protection against tritiated water (HTO). Sixty male specific-pathogen-free-grade C57BL/6J mice were randomly divided into 12 groups: mice in 4 control groups were intraperitoneally injected with sterile water; mice in 4 HTO groups were intraperitoneally injected with 11.1 × 105 Bq/g of HTO; and mice in the other 4 groups were administered with HTO and a Chahuangjing compound (0.2 mL, once daily). After 1, 7, 14, and 21 days, the mice were killed and samples were collected. A liquid scintillation counting method was used for tritium measurement. A fully automated hematology analyzer was used to assess blood samples. The superoxide dismutase (SOD) and malondialdehyde (MDA) content was analyzed using commercial kits. Chahuangjing significantly increased decorporation and shortened the effective half-life of tritium. To a certain extent, Chahuangjing alleviated the HTO-induced reduction in white blood cells and elevated red blood cells after HTO exposure. Moreover, Chahuangjing alleviated the HTO-induced reduction in SOD activity and reduced MDA. Our study demonstrated that Chahuangjing can enhance the elimination of tritium and reduce free radicals to alleviate HTO-induced radiation injury.

Protective effect of polydatin on radiation-induced injury of intestinal epithelial and endothelial cells.

This study aimed to examine the radioprotective effect of polydatin (PD) on crypt and endothelial cells of the small intestines of C57BL/6 mice that received abdominal irradiation (IR). Mice were treated with 6 MV X-ray (20 Gy) abdominal IR at a dose rate of 200 cGy/min. Thirty minutes before or after IR, mice were intraperitoneally injected with PD. The rate of survival of the mice at 30 days after IR was determined. The duodenum (upper small intestine), jejunum (middle small intestine), and ileum (lower small intestine) were collected and subjected to hematoxylin and eosin staining. Tissue sample sections were analyzed through light microscopy, and the lengths of at least 20 intestinal villi were measured in each group; the average number of crypts was obtained from 10 intestinal samples in each group. Microvessel density was assessed using CD31-positive (brown) vascular endothelial cells/cell clusters. FHs74Int cell proliferation was measured using the CCK-8 assay. PD administration (25 mg/kg) before IR was the most effective in prolonging the survival of C57BL/6 mice. PD reduced radiation-induced injury of intestinal villi, prevented loss of crypts, increased intestinal crypt growth, protected against IR-induced intestinal injury, and enhanced the proliferative potential and reduced the apoptosis of FHs74Int cells after IR. Moreover, PD increased small intestinal MVD and reduced the apoptosis of intestinal microvascular endothelial cells in mice after IR. Therefore, PD was found to be able to protect the two types of cells from radiation damage and to thus alleviate radiation-induced injury of small intestine.

Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress.

The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction. In addition, there is increasing evidence suggesting that NP is detrimental to various organs, including the pancreas. This study investigated the adverse effects of NP exposure on the pancreas. Sprague-Dawley rats were treated with different doses of NP for 90 consecutive days. The data suggested that the body weights of the rats treated with NP decreased, and the highest dose of NP treatment (180 mg kg-1) dramatically increased water consumption by rats. Meanwhile, H&E staining and immunohistochemistry indicated that islets in the pancreases shrunk when the rats were treated with the indicated doses of NP. TUNEL staining demonstrated that NP exposure up-regulated the level of apoptosis in the pancreases in a dose-dependent manner. Besides this, NP exposure inhibited the secretion of insulin and disrupted glucose tolerance. The levels of reactive oxygen species (ROS) and intracellular calcium ([Ca2+]i) in the islets were up-regulated in the groups of rats treated with NP, but the levels of Mitochondrial Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which causes disruption of glucose tolerance and decrease in insulin secretion.