Comparison of Titanium Dioxide and Zinc Oxide Photocatalysts for the Inactivation of Escherichia coli in Water Using Slurry and Rotating-Disk Photocatalytic Reactors.

The application of photocatalysis for the disinfection of water has been extensively reported over the past 30 years. Titanium dioxide (TiO2) has been the most widely and successfully used photocatalyst to date; however, it is not without its limitations. Frequently observed long lag times, sometimes up to 60 min, before bacterial inactivation begins and the presence of residual microorganisms, for example, up to 104 colony forming units, remaining after treatment are ongoing challenges with this particular photocatalyst. It is therefore important to find alternative photocatalysts that can address these issues. In this study, we compared the disinfection capacity of TiO2 with that of zinc oxide (ZnO) using Escherichia coli as a model organism in both a suspended and immobilized catalyst system. Our results showed that ZnO was superior to TiO2 in a number of areas. Not only were bacterial rates of destruction much quicker with ZnO, but no lag time was observed prior to inactivation in suspended systems. Furthermore, complete bacterial destruction was observed within the treatment times under investigation. The greater efficiency of ZnO is believed to be due to the decomposition of the bacterial cell wall being driven by hydrogen peroxide as opposed to hydroxyl radicals. The results reported in this paper show that ZnO is a more efficient and cost-effective photocatalyst than TiO2 and that it represents a viable alternative photocatalyst for water disinfection processes.

Removal of phthalates from aqueous solution by semiconductor photocatalysis: A review.

While phthalate esters are commonly used as plasticizers to improve the flexibility and workability of polymeric materials, their presence and detection in various environments has become a significant concern. Phthalate esters are known to have endocrine-disrupting effects, which affects reproductive health and physical development. As a result, there is now increased focus and urgency to develop effective and energy efficient technologies capable of removing these harmful compounds from the environment. This review explores the use of semiconductor photocatalysis as an efficient and promising solution towards achieving removal and degradation of phthalate esters. A comprehensive review of photocatalysts reported in the literature demonstrates the range of materials including commercial TiO2, solar activated catalysts and composite materials capable of enhancing adsorption and degradation. The degradation pathways and kinetics are also considered to provide the reader with an insight into the photocatalytic mechanism of removal. In addition, through the use of two key platforms (the technology readiness level scale and electrical energy per order), the crucial parameters associated with advancing photocatalysis for phthalate ester removal are discussed. These include enhanced surface interaction, catalyst platform development, improved light delivery systems and overall system energy requirements with a view towards pilot scale and industrial deployment.

Synergism of photocycloaddition and photoinduced electron transfer for multi-state responsive materials with high-stability and reversibility.

A dual-photoresponsive coordination polymer displaying color-distinguishable olefin/cyclobutane-linked pyridinium radical states through photoinduced electron transfer and photocycloaddition has been successfully assembled based on the monoquaternized trans-1,2-bis(4-pyridyl)ethylene and electron-rich benzenetetra-carboxylate anion. The synergy of charge-transfer and cation-π interactions within the framework endows the compound with excellent stability toward high temperature (350 °C), acidic/basic environments (pH = 2-12) and organic solvents. Reversible recovery from the radical states to their initial states, and reverse-cyclization can be achieved upon heat-treatment.

Stress-induced interleukin-6 release in mice is mast cell-dependent and more pronounced in Apolipoprotein E knockout mice.

OBJECTIVE: Interleukin-6 (IL-6) is elevated in the serum of patients with coronary artery disease (CAD) and acute coronary syndromes (ACS). Intracoronary release of IL-6 was reported in ACS that can also be triggered by acute stress. In rats, acute restraint stress increases serum IL-6 and histamine, both of which may derive from mast cells. The current study was carried out in order to determine any possible difference in stress-induced IL-6 release in atherosclerotic mice and the contribution of mast cells, corticotropin-releasing hormone (CRH) and urocortin (Ucn). METHODS: C57BL/6J, W/W(v) mast cell-deficient, Apolipoprotein E (ApoE) and CRH knockout (k/o) mice were stressed in plexiglass restraint chambers for 15 to 120 min. Serum corticosterone and IL-6 levels were measured. Some C57BL and ApoE k/o mice were pretreated with either the mast cell stabilizer disodium cromoglycate (cromolyn) or the peptide CRH receptor (CRH-R) antagonist Astressin. Cardiac mast cell activation was studied in both C57BL and ApoE k/o mice using light microscopy. RESULTS: Acute stress increased serum IL-6 in mice, an effect much greater in ApoE k/o atherosclerotic mice. Stress-induced IL-6 release was absent in W/W(v) mast cell-deficient mice and it was partially inhibited by cromolyn in C57BL and ApoE mice. Mast cells were found adjacent to atherosclerotic vessels in ApoE k/o mice and were activated after stress. CRH k/o mice released more IL-6 in response to stress than their wild types, but Astressin significantly inhibited IL-6 release. Stress-induced IL-6 release may, therefore, be at least partly due to peripheral Ucn and/or CRH, with Ucn possibly overcompensation for CRH deficiency. CONCLUSION: The present findings indicate that acute stress leads to mast cell-dependent serum IL-6 increase that may help explain stress-related coronary inflammation.

Acute stress induces cardiac mast cell activation and histamine release, effects that are increased in Apolipoprotein E knockout mice.

OBJECTIVES: Cardiac mast cells have recently been found to be activated in atherosclerotic coronary arteries, but no mediator has so far been documented to be released from them, nor have they been investigated in Apolipoprotein (Apo) E knockout (k/o) mice that develop atherosclerosis. Psychological stress triggers acute coronary syndrome, while acute restraint stress stimulates rat cardiac mast cells, the main mediator of which histamine is a coronary constrictor. Here, we investigated the effect of acute stress on the activation of cardiac mast cells morphologically, as well as the levels of cardiac and serum histamine in normal and genetically deficient mice. METHODS: Male, 8-14 week-old ApoE k/o mice and their corresponding control C57BL/6J mice were used. Significant reduction of cardiac histamine from 396.7+/-45.6 to 214.6+/-41.5 ng/g was observed over 120 min restraint stress with a corresponding increase in serum histamine from 126.9+/-4.0 to 188.4+/-17.3 ng/ml in C57BL mice. Cardiac mast cell activation was observed by light and electron microscopy. Both basal cardiac and serum histamine in ApoE k/o mice was significantly higher than that in C57BL mice. Although the extent of mast cell activation in ApoE k/o mice was similar to that of C57BL mice, the number of cardiac mast cells in ApoE k/o mice was 37% higher. Histamine levels were hardly detectable with or without stress in W/W(v) mast cell deficient mice. CONCLUSIONS: Acute restraint stress triggered cardiac histamine release in mice that was clearly derived from mast cells, as it was absent in W/W(v) mice. The high basal cardiac and serum histamine in ApoE k/o mice, along with the high number of cardiac mast cells, suggest possible ongoing cardiac mast cell activation that may participate in atherosclerosis. These results may possibly help better understand stress-related cardiovascular pathology.