Ultrasound-assistant preparation of Cu-SAPO-34 nanocatalyst for selective catalytic reduction of NO by NH3

The influence of the various preparation methods of Cu-SAPO-34 nanocatalysts on the selective catalytic reduction of NO with NH₃ under excess oxygen was studied. Cu-SAPO-34 nanocatalysts were prepared by using four techniques: conventional impregnation (IM), ultrasound-enhanced impregnation (UIM), conventional deposition precipitation (DP) using NaOH and homogeneous deposition precipitation (HDP) using urea. These catalysts were characterized in detail by various techniques such as N₂-sorption, XRD, TEM, H₂-TPR, NH₃-TPD and XPS to understand the catalyst structure, the nature and the dispersed state of the copper species, and the acid sites for NH₃ adsorption. All of the nanocatalysts showed high activities for NO removal. However, the activities were different and followed the sequence of Cu-SAPO-34 (UIM) > Cu-SAPO-34 (HDP) > Cu-SAPO-34 (IM) > Cu-SAPO-34 (DP). Based on the obtained results, it was concluded that the NO conversion on Cu-SAPO-34 nanocatalysts was mainly related to the high reducibility of the isolated Cu^2 + ions and CuO species, the number of the acid sites and the dispersion of CuO species on SAPO-34.     

Release behavior of metals from tin-lined copper cookware into food simulants during cooking and cold storage

Environmental Science and Pollution Research - The copper pots with an inner coating layer of tin have been remarkably used in many countries for a long time. In this study, leaching of some metals...     

Toxicity of cigarette smoke on isolated lung,heart, and brain mitochondria: induction of oxidative stress and cytochrome c release

Cigarette smoking is one of the main risk factors for premature human death which is associated with a variety of respiratory and vascular diseases, and cancer due to exposure to hundreds of toxicants. Rat mitochondria were obtained by differential ultracentrifugation and incubated with different concentrations (1%, 10%, or 100%) of standardized cigarette smoke extract (CSE). Our results showed that CSE induced a rise in mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation, and mitochondrial membrane potential (MMP) collapse before mitochondrial swelling ensued in isolated pulmonary mitochondria. Disturbance in oxidative phosphorylation was also confirmed by decrease in ATP concentration in the CSE-treated mitochondria. In addition, collapse of MMP and mitochondrial swelling produced release of cytochrome c via outer membrane rupture or mitochondrial permeability transition (MPT) pore opening. Our results suggested that CSE-induced toxicity in lung tissue is the result of disruptive effect on mitochondrial respiratory chain that leads to ROS formation, lipid peroxidation, MMP decline, and cytochrome c expulsion which results in apoptosis signaling and cell loss.