Interference of inorganic ions on phenol degradation by the Fenton reaction

The addition of Cu2+ ions to the classical Fenton reaction (Fe2+ plus H2O2 at pH 3) is found to accelerate the degradation of organic compounds. This synergic effect causes an approximately 15 % additional reduction of the total organic carbon (TOC), representing an overall improvement of the efficiency of the mineralization of phenol. Although Fe2+ exhibits a high initial rate of degradation, the degradation is not complete due to the formation of compounds refractory to the hydroxyl radical. The interference of copper ions on the degradation of phenol by the Fenton reaction was investigated. In the presence of Cu2+, the degradation is slower, but results in a greater reduction of TOC at the end of the reaction (t = 120 min). In the final stages of the reaction, when the Fe3+ in the solution is complexed in the form of ferrioxalate, the copper ions assume the role of the main catalyst of the degradation.Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), BrasiliaConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), BrasiliaFUNDECTFUNDECTCNPqCNPqINCT CatalysisINCT- CatalysisFAPEALFAPEA

Mechanistic implications of zinc(II) ions on the degradation of phenol by the fenton reaction

A study of the interference of Zn2+ ions on phenol degradation by Fenton reaction (Fe2+/Fe3+ + H2O2) is reported. One of the first intermediates formed in the reaction, catechol, can reduce Fe3+ to Fe2+ and, in the presence of H2O2 initiates an efficient catalytic redox cycle. In the initial stages of the reaction, this catechol-mediated cycle becomes the principal route of thermal degradation of phenol and its oxidation products. The Zn2+ ion addition enhances the persistence time of catechol, probably by stabilization of the corresponding semiquinone radical via complexation

Expression of SPIG1 Reveals Development of a Retinal Ganglion Cell Subtype Projecting to the Medial Terminal Nucleus in the Mouse

Visual information is transmitted to the brain by roughly a dozen distinct types of retinal ganglion cells (RGCs) defined by a characteristic morphology, physiology, and central projections. However, our understanding about how these parallel pathways develop is still in its infancy, because few molecular markers corresponding to individual RGC types are available. Previously, we reported a secretory protein, SPIG1 (clone name; D/Bsp120I #1), preferentially expressed in the dorsal region in the developing chick retina. Here, we generated knock-in mice to visualize SPIG1-expressing cells with green fluorescent protein. We found that the mouse retina is subdivided into two distinct domains for SPIG1 expression and SPIG1 effectively marks a unique subtype of the retinal ganglion cells during the neonatal period. SPIG1-positive RGCs in the dorsotemporal domain project to the dorsal lateral geniculate nucleus (dLGN), superior colliculus, and accessory optic system (AOS). In contrast, in the remaining region, here named the pan-ventronasal domain, SPIG1-positive cells form a regular mosaic and project exclusively to the medial terminal nucleus (MTN) of the AOS that mediates the optokinetic nystagmus as early as P1. Their dendrites costratify with ON cholinergic amacrine strata in the inner plexiform layer as early as P3. These findings suggest that these SPIG1-positive cells are the ON direction selective ganglion cells (DSGCs). Moreover, the MTN-projecting cells in the pan-ventronasal domain are apparently composed of two distinct but interdependent regular mosaics depending on the presence or absence of SPIG1, indicating that they comprise two functionally distinct subtypes of the ON DSGCs. The formation of the regular mosaic appears to be commenced at the end of the prenatal stage and completed through the peak period of the cell death at P6. SPIG1 will thus serve as a useful molecular marker for future studies on the development and function of ON DSGCs

Environmental chemical stressors as epigenome modifiers:a new horizon in assessment of toxicological effects

In eukaryotic cells, chromatin transformation from euchromatin into heterochromatin as a means of controlling gene expression and replication has been known as the ?accessibility hypothesis?. The interplay of epigenetic changes including histone modifications, DNA methylation, RNA interference (RNAi) and other functional epigenetic components are intricate. It is believed that these changes are well-programmed, inherited and can be modified by environmental contaminant stressors. Environmentally-driven epigenetic alterations during development, e.g. embryonic, foetal or neonatal stage, may influence disease susceptibility in adulthood. Therefore, understanding how epigenome modifications develop in response to environmental chemicals and, how epigenetic-xenobiotic interactions influence human health will shed new insights into gene-environment interactions in the epidemiology of several diseases including cancer. In this review, we consider studies of chemical modifiers including nutritional and xenobiotic effects on epigenetic components in vitro or in vivo. By examining the most-studied epigenome modifications and how their respective roles are interlinked, we highlight the central role of xenbiotic-modified epigenetic mechanisms. A major requirement will be to study and understand effects following environmentally-relevant exposures. We suggest that the study of epigenetic toxicology will open up new opportunities to devise strategies for the prevention or treatment of at-risk populations

ESTUDO MECANÍSTICO DAS REAÇÕES FENTON E CUPRO-FENTON POR ANÁLISE VOLTAMÉTRICA IN SITU

Although the classical Fenton process exhibits a high initial rate of the organic compounds degradation, this process is not complete due to the formation of refractory compounds which resist the attack of the hydroxyl radicals. In the presence of Cu(II), the degradation is slower, but results in a greater reduction of TOC (total organic carbon) measurements of net mineralization at the end of the reaction (t=120min). The addition of Cu(II) ions to classical Fenton reaction conditions (Fe(II) plus H2O2 at pH 3) is shown to accelerate the degradation of organic compounds. This synergic effect causes an approximately 15% additional reduction of the TOC. Voltammetric studies confirm the catalytic role of catechol in the presence of Fe(III)/Fe(II) and Cu(II)/Cu(I). Addition of aliphatic acids to the reaction medium, did not interfere with the cupro-Fenton reaction, but had an inhibitory effect on the classical Fenton reaction, consistent with the following order of interaction with the ion Fe(III): Oxalic Acid (OA) >> Formic Acid (FA) ~ Acetic acid (AA)

Time-resolved fluorescence quenching studies of sodium lauryl ether sulfate micelles

Aggregation numbers (N Ag) of micelles of the commercial anionic detergent sodium lauryl ether sulfate (SLES), with an average of two ethylene oxide subunits, were determined at 30 and 40º C by the time-resolved fluorescence quenching method with pyrene as the fluorescent probe and the N-hexadecylpyridinium ion as the quencher. The added-salt dependent growth of SLES micelles (γ = 0.11-0.15, where γ is the slope of a plot of log aggregation number vs. log [Yaq] and [Yaq] is the sodium counterion concentration free in the intermicellar aqueous phase) is found to be significantly lower than that of sodium alkyl sulfate micelles (γ ca. 0.25), a difference attributed to the larger headgroup size of SLES. The I1/I3 vibronic intensity ratio and the rate constant for intramicellar quenching of pyrene show that the pyrene solubilization microenvironment and the intramicellar microviscosity are insensitive to micelle size or the presence of added salt