RESUMO
V-doped TiO2 materials (0.01, 0.05, 0.10, and 1.00 nominal atomic %) were synthesized by the sol-gel method and characterized by X-ray diffraction, Raman spectroscopy, UV-visible diffuse reflectance spectroscopy, N2 adsorption-desorption isotherms, X-ray photoelectron spectroscopy, and H2-temperature programmed reduction. Two vanadium precursors (vanadyl acetylacetonate and ammonium metavanadate) and three calcination temperatures (400, 500, and 600 °C, with and without air circulation) were assayed. The efficiency of the materials as photocatalysts was studied by the degradation of phenol with UV and visible lamps. The photocatalyst prepared from vanadium acetylacetonate, with a vanadium content of 0.01 nominal atomic %, calcination at 400 °C without air circulation (0.01VTi-400), showed the best performance, reaching 100% and 30% degradation of phenol (50 µM) by irradiation with UV lamps (3 h) and visible lamps (5 h), respectively. To evaluate the efficiency of this catalyst in the degradation of other structurally related compounds, two substituted phenols were selected: 4-chlorophenol and 4-nitrophenol. The 0.01VTi-400 photocatalyst showed to be applicable to the degradation of phenolic compounds when the substituent was an activating group or a weakly deactivating group (for electrophilic reactions). Additionally, the selectivity of 0.01VTi-400 for phenol degradation in the presence of Aldrich humic acid was tested: phenol degradation reached 68% (3 h, UV lamps). The performance of 0.01VTi-400 indicated that it is a promising material for further applications.
Assuntos
Poluentes Ambientais , Catálise , Fenol , Titânio , Difração de Raios XRESUMO
Vanadyl sulfate (VS) is an ingredient in some food supplements and experimental drugs. This study was designed to assay the effects of VS on biomarkers of oxidative stress and inflammation in renal tissue of rats with diabetes type 2. 30 male Wistar rats were divided into three equal groups as follow: non-diabetics, non-treated diabetics and VS-treated diabetics. Diabetes type 2 has been induced through high fat diet and fructose in the animals. Diabetic rats were treated with 25 mg/kgBW of VS in water for 12 weeks. At the end of study, glucose and insulin were measured using commercially available kits in serum and biomarkers of oxidative stress and inflammation in renal homogenates of animals were measured by related methods. Compared to controls, glucose and insulin were increased significantly in non-treated diabetic rats (p-value <0.05) that showed the induction of diabetes type 2 in rats. The results showed that in VS-treated diabetic rats compared to the non-treated diabetic group, vanadyl sulfate significantly reduced the glucose and insulin secretion and changed renal inflammatory and oxidative markers, except protein carbonyl so that we couldn't find any significant changes. Our study showed that vanadyl supplementation had positive effects on oxidative stress and inflammation biomarkers in kidney of diabetic rats
Assuntos
Animais , Masculino , Ratos , Sulfatos/análise , Vanadatos/análise , Biomarcadores/análise , Preparações Farmacêuticas/administração & dosagem , Interleucina-1/antagonistas & inibidores , Interleucina-10/antagonistas & inibidores , Estresse Oxidativo/imunologia , Suplementos Nutricionais/efeitos adversos , Diabetes Mellitus Tipo 2/patologia , Secreção de Insulina , Insulina/farmacologiaRESUMO
Non-small lung cell carcinoma has a high morbidity and mortality rates. The elective treatment for stage III and IV is cisplatinum that conveys serious toxic side effects. Vanadium compounds are metal molecules with proven antitumor activity that depends on its valence. Therefore, a better understanding of the mechanism of action of vanadium compounds is required. The aim of our study was to investigate the mechanisms of cell death induced by sodium metavanadate (NaVO3 [V(+5)]) and vanadyl sulfate (VOSO4 [(+4)]), both of which have reported apoptotic-inducing activity. We exposed the A549 cell line to various concentrations (0-100 µM) and to different exposure times to each compound and determined the cell viability and expression of caspases, reactive oxygen species (ROS) production, Bcl2, Bax, FasL and NO. Our results showed that neither compounds modified the basal expression of caspases or pro- and anti-apoptotic proteins. The only change observed was the 12- and 14-fold significant increase in ROS production induced by NaVO3 and VOSO4 , respectively, at 100 µm concentrations after 48 hours. Our results suggest that classical apoptotic mechanisms are not related to the cell death induced by the vanadium compounds evaluated here, and showed that the higher ROS production was induced by the [(+4)] valence compound. It is possible that the difference will be secondary to its higher oxidative status and thus higher ROS production, which leads to higher cell damage. In conclusion, our results suggest that the efficacy of the cell death mechanisms induced by vanadium compounds differ depending on the valence of the compound.
Assuntos
Compostos de Vanádio/toxicidade , Células A549 , Caspases/genética , Morte Celular/efeitos dos fármacos , Humanos , Fosfatidilserinas/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Vanadatos/toxicidadeRESUMO
The loss of the modulator role of the endothelium could be involved in the pathogenesis of diabetic vascular complications. Transition metal compounds, such as tungsten and vanadium, have been proposed as possible agents in the treatment of diabetes by simulating the effects of insulin. The mesenteric vascular bed intervenes in vascular resistance and is a source of vasoactive compounds, such as prostanoids. The aim of this work was to study the effects of sodium tungstate and vanadyl sulphate treatments on the metabolic parameters and the release of prostanoids of the mesenteric vascular bed in an experimental model of Streptozotocin-induced diabetes. In diabetic rats, a significant increase was observed in plasma levels of glucose, triglycerides and total cholesterol. On the other hand, there was a significant reduction in the release of vasodilator prostanoids, such as prostacyclin and prostaglandin E2 and vasoconstrictor thromboxane A2 through the mesenteric vascular bed. Both sodium tungstate and vanadyl sulphate normalised glycaemia, triglyceridaemia and cholesterolaemia in rats diabetics. On the other hand, only treatment with sodium tungstate reversed the reduction in the release of vasodilator prostanoids, improving in diabetic animals the prostacyclin/thromboxane ratio, an indicator of vascular dysfunction. In conclusion, unlike vanadyl sulphate, sodium tungstate is shown to be more effective in controlling metabolic changes and the production of vasodilator prostanoids observed in experimental diabetes induced by streptozotocin.