RESUMEN
The ZnO-CdS core-shell composite nanorods with CdS shell layer thicknesses of 5 and 20 nm were synthesized by combining the hydrothermal growth of ZnO nanorods with the sputtering thin-film deposition of CdS crystallites. The microstructures and optical properties of the ZnO-CdS nanorods were associated with the CdS shell layer thickness. A thicker CdS shell layer resulted in a rougher surface morphology, more crystal defects, and a broader optical absorbance edge in the ZnO-CdS rods. The ZnO-CdS (20 nm) nanorods thus engaged in more photoactivity in this study. When they were further subjected to a postannealing procedure in ambient Ar/H2, this resulted in the layer-like CdS shell layers being converted into the serrated CdS shell layers. By contrast, the ZnO-CdS nanorods conducted with the postannealing procedure exhibited superior photoactivity and photoelectrochemical performance; the substantial changes in the microstructures and optical properties of the composite nanorods following postannealing in this study might account for the observed results.
RESUMEN
This study aimed to investigate the effect of sesame oil on oxidative stress-associated renal injury induced by lipopolysaccharide in rats. The effects of sesame oil on renal injury, oxidative stress, hydroxyl radical, superoxide anion, nitric oxide, and proinflammatory cytokines were assessed after a lipopolysaccharide challenge. Sesame oil attenuated lipopolysaccharide-induced renal injury, decreased lipid peroxidation, increased the activities of superoxide dismutase, catalase, and glutathione peroxidase, reduced hydroxyl radical generation and nitric oxide production, and had no effect on superoxide anion generation in lipopolysaccharide-challenged rats. In addition, sesame oil significantly decreased tumor necrosis factor-alpha and interleukin 1beta production 1 and 6 h, respectively, after lipopolysaccharide administration in mice. Thus, sesame oil attenuates oxidative stress-associated renal injury via reduction of the production of nitric oxide and the generation of proinflammatory cytokines in endotoxemic rats.