Prediction and optimization of electrochemical oxidation efficiency using machine learning: Insights from carbon-based anodes for water treatment.

The electrochemical oxidation (EO) process has the unique advantage of in situ generation of reactive oxygen species for organic synthesis and wastewater purification. However, the strong binding of H 2 O and anode inhibits the desorption of reactive oxygen species, exacerbating their peroxidation into oxygen and thus weakening EO performance. In this work, an electron delocalization strategy is proposed by introducing Cu 2+ into the tetrahedral sites (A Td 2+ ) of Co 3 O 4 (Cu x Co 3‐x O 4 ) to trigger the super‐exchange effect of Cu Td 2+ ─O─Co Oh 3+ , constructing the electron‐rich Co Oh 3+ sites and accelerating the desorption *OH for the promotion of EO performance. Experimental results confirm the electron‐delocalized Cu Td 2+ ─O─Co Oh 3+ disrupts the kinetic equilibrium of oxygen evolution reaction and balances the energy barriers of H 2 O adsorption, H 2 O dehydrogenation, and *OH desorption over Co Oh 3+ sites, thus realizing the •OH‐mediated EO process. The required free energy for •OH generation decreases from 1.14 to 0.70 eV. The Cu x Co 3‐x O 4 anode has extraordinary EO activity for the elimination of multiple aromatic contaminants and demonstrates feasibility in practical landfill leachate treatment. This study offers an in‐depth understanding of active species formation in EO systems and guides the design and synthesis of superior and stable electrodes for efficient conversion of organic matter.

Thermal treatment is the most widely used method of food preservation. However, it also results in losses in some quality due to undesirable chemical reactions. Sugars such as fructose in aqueous solution have been shown to accelerate the degradation of some food components such as ascorbic acid and anthocyanin (Cao et al., 2009; Rojas & Gerschenson, 2001), possibly due to oxidation. However, the mechanism of underlying this deleterious effect of sugars during thermal treatment is unclear. Previous studies have shown that monosaccharaides such as fructose and glucose can be autoxidized and generate reactive oxidative species (ROS) under physiological condition in the presence of oxygen and metal ions (P. Thornalley, Wolff, Crabbe, & Stern, 1984). However, information on ROS generation at elevated temperature is limited. The overall hypothesis for this project is to determine that sugars generate similar oxidative compounds at elevated temperatures. The objective of this study is to identify the generation of oxidative species during thermal treatment of sugars, and to understand the mechanism of the oxidative reactivity. To achieve this purpose, I measured the levels of oxidative species such as hydrogen peroxide and singlet oxygen generated from sugar solutions during thermal treatment. The effects of various factors such as types of sugars, fructose, glucose and sucrose; temperature, pH and the presence of phosphate buffer were investigated. To study the role of oxygen in oxidative species generation during thermal treatment of sugars, the consumption of dissolved oxygen by sugar solution during thermal treatment was also investigated. Further, acids generation during thermal treatment of sugar solution were measured and confirmed by pH measurement and acid-base titration. This study demonstrated that ROS are generated from sugar solutions during thermal treatment. The results suggested that dissolved oxygen in solution is crucial for ROS generation. Elevated temperature, lower pH and the presence of phosphate buffer showed a significant promotion effect on ROS generation from sugars during thermal treatment. The results from this study indicated that ROS generation from thermal treatment of sugars shared a similar mechanism as sugar autoxidation. We believe that the results of this study will provide methods to understand better the oxidation mechanism of sugar solutions and will be useful to improve the thermal treatment of food products containing sugars.

Persulfate enhanced electrochemical oxidation of phenol with CuFe2O4/ACF (activated carbon fibers) cathode

Ethylenediaminetetraacetic acid (EDTA) is widely employed as a chelating agent in the electroless nickel plating industry to form stable metal–organic complexes (e.g., Ni-EDTA). These metal–organic complexes cannot be removed from plating wastewaters by traditional treatments in a cost-effective way. While electrochemical advanced oxidation processes (EAOPs) have been utilized for the efficient degradation of Ni-EDTA at the anode, challenges remain in the simultaneous and effective recovery of nickel at the cathode. In this study, we investigate the efficacy of five cathode materials [i.e., carbon felt (CF), titanium plate, graphite plate (GP), copper plate, and stainless-steel plate] with respect to Ni recovery. The highest Ni removal efficiency of 81.6 ± 0.1% was achieved with the carbon felt cathode which was 30% higher than that of the titanium cathode (52.1 ± 1.4%) with the improvement in performance attributed to the higher rate of mass transport of Ni ions (CF: 4.3 ± 0.4 × 10–4 s–1 vs Ti: 1.8 ± 0.2 × 10–4 s–1) toward the nanowire structure of carbon felt and to the large surface area of the carbon felt cathode compared with the other cathodes. While the chemical composition of the deposits was independent of the cathodic material or structure, the morphology of deposition varied with the cathode material. The accumulated Ni on the carbon felt surface was successfully recovered either as a nickel salt solution by acid leaching or as high purity NiO by calcinating the Ni-loaded carbon felt cathode at over 800 °C. The performance of the regenerated carbon felt after acid leaching was comparable to that of the fresh cathode even after 10 cycles of use and regeneration via acid leaching with this result confirming the stability and reusability of the carbon felt material.

Application of electrochemical flow-through oxidation technology in the treatment of concentrated water from nanofiltration and reverse osmosis in the coal chemical industry

The application of combined chemical coagulation and electrochemical oxidation processes to treat a leachate from an intermunicipal sanitary landfill was evaluated.Chemical coagulation (CC) experiments were performed with lime (Ca(OH)2), and the influence of the lime concentration, stirring speed and assay duration were studied.In the electrochemical oxidation (EO) assays, a boron-doped diamond anode was used, and two applied current intensities were tested.It was also evaluated the influence of the lime concentration used in the CC pre-treatment on the EO performance.In the CC assays, the highest COD removals were obtained for lime concentrations of 20 and 25 g L -1 , at 100 rpm stirring speed, during 2 h.In the CC+EO combined treatment the highest removals were obtained at the applied current intensity of 0.6 A, being the influence of the lime concentration used in the pre-treatment almost insignificant.The highest current efficiency was obtained for the combined treatment with EO assays performed at 0.4 A.

Mitochondria play a critical role in regulating cellular processes including ATP production, intracellular calcium signaling and generation of reactive oxidative species (ROS). Neurons rely on mitochondrial function to perform a range of complex processes, and mitochondrial dysfunctions have been shown to have an impact in pathologies of the nervous system. Yet, neurons contain a finite number of mitochondria, and their location is known to change in response to a number of factors including age and cellular activity, thereby impacting neuronal response. In this paper, we introduce a novel computational model of mitochondria motility that focuses on their movements along the axon. We describe the biological processes involved and the main parameters of the model. We use the model to investigate how some of these parameters affect the ability of mitochondria to position themselves in regions of high energy demand. Finally, we discuss the significance of our work and its downstream applications in further understanding pathologies of the nervous system such as Alzheimer's disease, and help identify potential novel therapeutic targets.

Self-disinfecting carbon filter: In situ spontaneous generation of reactive oxidative species via oxygen reduction reaction for efficient water treatment

Chronic exposure to inorganic arsenic severely damages the central nervous system (CNS). Glutamate (GLU) is the major excitatory amino acid and is highly neurotoxic when levels in the synaptic cleft are not properly regulated by a family of Na⁺-dependent excitatory amino acid transporters. Within the cerebellum, the activity of the Bergmann glia Na⁺-dependent GLU/aspartate transporter (GLAST) excitatory amino acid transporter 1 (EAAT1/GLAST) accounts for more than 90% of GLU uptake. Because exposure to the metalloid arsenite results in CNS toxicity, we examined whether EAAT1/GLAST constitutes a molecular target. To this end, primary cultures of chick cerebellar Bergmann glial cells were exposed to sodium arsenite for 24 h, and EAAT1/GLAST activity was evaluated via ³H-D-aspartate uptake. A sharp decrease in GLU transport was observed, and kinetic studies revealed protein kinase A, protein kinase C, and p38 mitogen-activated protein kinase-dependent decreases in K(M) and V(max) concomitant with diminished chglast transcription. To gain insight into the molecular mechanisms involved in these phenomena, we investigated the generation of reactive oxidative species and the lipid peroxidative damage caused by arsenite exposure. None of these responses were found, although we did observe an increase in nuclear factor (erythroid-derived 2)-like 2 DNA-binding activity correlated with a rise in total glutathione levels. Our results clearly suggest that EAAT1/GLAST is a molecular target of arsenite and support the critical involvement of glial cells in brain function and dysfunction.

Intracellular labile iron pools as direct targets of iron chelators: a fluorescence study of chelator action in living cells

Defects in Klotho gene expression in mice result in a vulnerability to oxidative injuries. We aimed to identify the expression of Klotho in a mouse tubular epithelial (TCMK-1) cell line, and also to investigate changes in Klotho expression induced by oxidative stress and the potential role of intra- and extracellular Klotho protein. During exposure to hydrogen peroxide (H2O2), an overexpression of the Klotho gene was induced and exogenous Klotho protein was added in TCMK-1 cells. The generation of reactive oxidative species (ROS) was examined by flow cytometry, and cell viability was assessed by Cell Counting Kit-8. Cellular apoptosis was determined by flow cytometry and Hoechst 33258 staining followed by Western blotting to evaluate the expression of Klotho, antioxidant enzymes, and apoptosis-associated proteins. While H2O2 significantly suppressed Klotho expression, cell viability, and the expression of antioxidant enzymes in a concentration-dependent manner, cellular apoptosis was increased and p38/MAPK and JNK/MAPK were activated. Intra- and extracellular Klotho remarkably ameliorated viability inhibition, ROS generation, and cellular apoptosis induced by H2O2. Intra- and extracellular Klotho also reversed the loss of antioxidant enzymes, the elevation of cleaved Caspase-3 and Bax/Bcl-2, and the phosphorylation of JNK/MAPK and p38/MAPK. Klotho has posed antioxidant and anti-apoptotic effects on oxidative injuries in TCMK-1 cells, which might be partially related to its inhibition of JNK/MAPK and p38/MAPK phosphorylation and subsequent elevation of antioxidant enzymes. Increasing Klotho expression has played a protective role against oxidative stress in tubular epithelial cells.

Interleukin 1ß Modulates the Ventricular L-Type Calcium Current Through ROS Signalling

Most damaging plant diseases have been caused by viruses in the entire world. In tropical and subtropical areas, the damage caused by plant virus leads to great economic and agricultural losses. Single stranded DNA viruses (geminiviruses) are the most perilous pathogens which are responsible for major diseases in agronomic and horticultural crops. Significantly begomoviruses and mastreviruses are the biggest genus of plant infecting viruses, transmitted though Bemisia tabaci and members of Cicadellidae respectively. Plants possesses some naturally existing chemicals term as phyto-chemicals which perform important functions in the plant. Some antioxidant enzymes are used by plants for self-defense upon foreign invasion of infection. This review explains the present perceptive of influence of viral infections on phyto-chemicals, oxidative enzymes and biochemical changes occurring in the plant. Viral infection mediated phyto-chemical changes in plants mainly includes: up and down regulation of photosynthetic pigment, increase in the concentration of phenolic compounds, elevation of starch content in the leaf and up & down regulation of anti-oxidative enzymes including (GPX) guaiacol peroxidase, (PPO) polyphenol oxidase, (APX) ascorbate peroxidase, (SOD) superoxide dismutase and (CTA) catalase. These changes lead to initiation of hypersensitive response, by thicken of the leaf lamina, lignification under the leaf surface, blocking to stomatal openings, systematic cell death, generation of reactive oxidative species (ROS), activation of pathogen mediated resistance pathways i.e., production of salicylic acid and jasmonic acid. Collectively all the physiological changes in the plant due to viral infection supports the activation of defense mechanism of the plant to combat against viral infection by limiting virus in specific area, followed with the production of barriers for pathogen, accumulation of starch in the leaf and excess production of (ROS). These strategies used by the plant to prevent the spread of virus in whole plant and to minimize the risk of severe yield loss.

Pancreatic ductal adenocarcinoma (PDAC) is the most prevalent form, accounting for more than 90% of all pancreatic malignancies. In a previous study, we found that hypoxia and chemotherapy induced expression of Heme Oxygenase-1 (HO-1) in PDAC cells and tissues. Arsenic trioxide (ATO) is the first-line chemotherapeutic drug for acute promyelocytic leukemia (APL). ATO increases the generation of reactive oxidative species (ROS) and induces apoptosis in treated cells. The clinical use of ATO for solid tumors is limited due to severe systemic toxicity. In order to reduce cytotoxic side effects and resistance and improve efficacy, it has become increasingly common to use combination therapies to treat cancers. In this study, we used ATO-sensitive and less sensitive PDAC cell lines to test the effect of combining HO-1 inhibitors (SnPP and ZnPP) with ATO on HO-1 expression, cell survival, and other parameters. Our results show that ATO significantly induced the expression of HO-1 in different PDAC cells through the p38 MAPK signaling pathway. ROS production was confirmed using the oxygen-sensitive probes DCFH and DHE, N-acetyl cysteine (NAC), an ROS scavenger, and oxidized glutathione levels (GSSG). Both ATO and HO-1 inhibitors reduced PDAC cell survival. In combined treatment, inhibiting HO-1 significantly increased ATO cytotoxicity, disrupted the GSH cycle, and induced apoptosis as measured using flow cytometry. ATO and HO-1 inhibition modulated autophagy as shown by increased expression of autophagy markers ATG5, p62, and LC3B in PDAC cells. This increase was attenuated by NAC treatment, indicating that autophagy modulation was through an ROS-dependent mechanism. In conclusion, our work explored new strategies that could lead to the development of less toxic and more effective therapies against PDAC by combining increased cellular stress and targeting autophagy.

Flow cytometric intracellular myeloperoxidase (MPO) staining of leukemic blasts is a useful tool in diagnosis of leukemia subtype. Interpretation of high MPO-positivity can be a diagnostic challenge in B-lineage acute lymphoblastic leukemia (B-ALL). While very few such cases have been reported, high MPO positive B-ALL cases without additional myeloid antigen positivity are suspect and require further investigation. Three pediatric cases of B-ALL with strong MPO staining (clone 8E6; Invitrogen) at diagnosis and three others with negative MPO staining were studied by flow cytometry and immunohistochemistry. In-vitro drug cytotoxicity, oxidative stress generation, and immunophenotyping using other MPO clones were performed to further investigate MPO presence. Expectedly, normal myeloid cells in all six samples were positive and mature lymphocytes negative for MPO staining. However, MPO monoclonal antibody (mAb) obtained from clones other than Invitrogen and other myeloid-specific mAbs gave negative results suggesting false positivity of the initial MPO staining. Immunohistochemistry for MPO was also negative on all six cases tested. Furthermore, in-vitro vincristine cytotoxicity was greater in leukemic cells from MPO false-positive cases compared with MPO-negative B-ALL samples, demonstrating indirect lack of MPO activity. Moreover, drug treatment did not lead to generation of reactive oxidative species, also reflective of lack of significant MPO presence. The cause of false-positive MPO staining remains unknown in these three cases; a cross reactivity could be the culprit. Caution should be given to similar phenomena and detailed investigation may contribute to the understanding of altered protein expression in such outlier cases. © 2017 International Clinical Cytometry Society.