Characterization of a mineral coating of the plant Dyerophytum indicum.

The mineral coating of Dyerophytum indicum Kuntze (Plumbaginaceae) was analyzed by isotope ratio mass spectrometry, X-ray diffraction, thermogravimetric and differential thermal analysis, and scanning electron microscopy/energy-dispersive X-ray spectroscopy methods. Its composition was found to be similar to those of the carbonate mixtures isolated from rotting cacti and speleothems. The coating consisted of three major phases (monohydrocalcite, nesquehonite, and calcite), a minor phase of hydromagnesite, and traces of silica and sylvite. This is the first time that the occurrence of monohydrocalcite, nesquehonite, and hydromagnesite in a living higher plant has been reported. A possible mechanism of the formation of the coating is also discussed.

Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO(2) nanorods.

Nanomaterials are extensively used in medicines, industry and daily life, but little is known about their possible health effects. Titanium dioxide (TiO2) nonmaterial-based photocatalysis is useful in the complete mineralization of organic pollutants in waste water and air. While the Fe-doping of TiO2 enhances their photocatalytic activity, their potential pathophysiologic effects are unknown. Here, rutile Fe-doped (9%) pure titanium dioxide (TiO2) nanorods were prepared and characterized. Subsequently, we assessed the acute (24 h) pulmonary and extrapulmonary effects of intratracheal (i.t.) instillation of these nanorods (1 and 5 mg/kg) in Wistar rats. In the bronchoalveolar lavage, the treatment induced a significant and dose-dependent increase of neutrophils, an increase of interleukin-6 (IL-6, at 5 mg/kg), and caused a dose-dependent-decrease of superoxide dismutase (SOD) activity. The lung sections of rats exposed to rutile Fe-TiO2 nanorods showed infiltration of inflammatory cells in dose-dependent manner. Similarly, the heart rate, systolic blood pressure, plasma IL-6, and leukocyte and platelet numbers were increased at 5 mg/kg. The plasma SOD and reduced glutathaione activities were dose-dependently decreased after exposure to the nanorods. Histopathologically, the liver showed mild inflammatory cells infiltration of few portal tracts, but the kidneys and heart were unaffected. In plasma, the levels of lactate dehydrogenase and hepatic enzymes, i.e., alanine aminotranferease and aspartate aminotransferase were increased significantly. The in vitro exposure of human lung cancer cells NCI-H460-Luc2 and human hepatoma cells HepG2 to FeTiO2 (6.25-100 µg/ml) dose-dependently reduced cellular viability. Also, the In vitro direct addition of these nanorods (0.1-1 µg/ml) to untreated rat blood, significantly and dose-dependently induced platelet aggregation. In conclusion, exposure to rutile Fe-TiO2 promotes pulmonary and systemic inflammation and oxidative stress. It affects the liver, enhances thrombotic potential, heart rate and systolic blood pressure. Moreover, the rutile Fe-TiO2 elicited direct toxicity on NCI-H460-Luc2 and HepG2 cells.

Use of alumina spent catalyst and RFCC wastes from petroleum refinery to substitute bauxite in the preparation of Portland clinker.

Bauxite was substituted with spent catalysts for clinker preparation. Three different clinkers were prepared: one with bauxite as a reference, one with spent alumina catalyst and another with reduced fluid cracking catalyst. Powder X-ray diffraction technique, thermal analysis and scanning electron microscope were used to characterize each clinker sample. Rietveld refinement shows that, in all clinkers prepared, alite was formed with hexagonal lattice and monoclinic belite has higher unit cell volume compared to the known beta-Ca(2)SiO(4). The physical and mechanical properties (specific area, setting time, heat of hydration, soundness and compressive strength) of the cement samples were studied. The results show that substitution of bauxite by spent catalysts gave close results in terms of chemical composition, physical and mechanical properties of the Portland clinker. Also it shows the spent catalysts do not affect the quality of the prepared cement.

The acute proinflammatory and prothrombotic effects of pulmonary exposure to rutile TiO2 nanorods in rats.

Nanotechnology is extensively used in industry and is widely explored for possible applications in medicine. However, its potential respiratory and systemic adverse effects remain unknown. Here pure titanium dioxide (TiO2) nanorods with rutile structure were prepared at room temperature by using a soft chemistry technique. The structure of the TiO2 rutile nanorods was confirmed by powder X-ray diffraction, and the size was revealed by transmission electron microscopy. Thereafter, we investigated, in Wistar rats, the acute (24-hr) effects of intratracheal instillation of these rutile TiO2 nanorods (1 and 5 mg/kg) on lung inflammation (assessed by bronchoalveolar lavage), systemic inflammation, and platelet aggregation in whole blood. Compared with vehicle-exposed rats, rats that underwent intratracheal instillation of TiO2 nanorods experienced a dose-dependent increase in macrophage numbers at 1 (+50%) and 5 mg/kg (+81%; P < 0.05) and an influx of neutrophils at 1 (+294%) and 5 mg/kg (+4117%; P < 0.01) in their bronchoalveolar lavage fluid. Both doses of rutile TiO2 nanorods caused pulmonary and cardiac edema, assessed by analysis of the wet weight-to-dry weight ratios. Similarly, the numbers of monocytes and granulocytes in the blood were increased in a dose-dependent manner after exposure to rutile TiO2 nanorods. In contrast, the number of platelets was significantly reduced after pulmonary exposure to 5 mg/kg TiO2 nanorods; this result indicated the occurrence of platelet aggregation in vivo. The direct addition of TiO2 nanorods (0.4-10 microg/ml) to untreated rat blood significantly induced platelet aggregation in a dose-dependent fashion in vitro. It is concluded that the intratracheal instillation of rutile TiO2 nanorods caused upregulation of lung inflammation, pulmonary and cardiac edema, and systemic inflammation. Rutile TiO2 nanorods also triggered platelet aggregation in vivo and in vitro.