High-efficiency treatment of electroless nickel plating effluent using core-shell MnFe2O4-C@Al2O3 combined with ozonation: Performance and mechanism

The normal microbial occupants of the mammalian intestine are crucial for maintaining gut homeostasis, yet the mechanisms by which intestinal cells perceive and respond to the microbiota are largely unknown. Intestinal epithelial contact with commensal bacteria and/or their products has been shown to activate noninflammatory signaling pathways, such as extracellular signal-related kinase (ERK), thus influencing homeostatic processes. We previously demonstrated that commensal bacteria stimulate ERK pathway activity via interaction with formyl peptide receptors (FPRs). In the current study, we expand on these findings and show that commensal bacteria initiate ERK signaling through rapid FPR-dependent reactive oxygen species (ROS) generation and subsequent modulation of MAP kinase phosphatase redox status. ROS generation induced by the commensal bacteria Lactobacillus rhamnosus GG and the FPR peptide ligand, N-formyl-Met-Leu-Phe, was abolished in the presence of selective inhibitors for G protein-coupled signaling and FPR ligand interaction. In addition, pretreatment of cells with inhibitors of ROS generation attenuated commensal bacteria-induced ERK signaling, indicating that ROS generation is required for ERK pathway activation. Bacterial colonization also led to oxidative inactivation of the redox-sensitive and ERK-specific phosphatase, DUSP3/VHR, and consequent stimulation of ERK pathway signaling. Together, these data demonstrate that commensal bacteria and their products activate ROS signaling in an FPR-dependent manner and define a mechanism by which cellular ROS influences the ERK pathway through a redox-sensitive regulatory circuit.

Efficient degradation of 2,3,5-trimethylpyrazine by catalytic ozonation over MnOx supported on biochar derived from waste tea leaves

Hypoxia is known to stimulate reactive oxygen species (ROS) generation. Because reduced glutathione (GSH) is compartmentalized in cytosol and mitochondria, we examined the specific role of mitochondrial GSH (mGSH) in the survival of hepatocytes during hypoxia (5% O2). 5% O2 stimulated ROS in HepG2 cells and cultured rat hepatocytes. Mitochondrial complex I and II inhibitors prevented this effect, whereas inhibition of nitric oxide synthesis with Nomega-nitro-L-arginine methyl ester hydrochloride or the peroxynitrite scavenger uric acid did not. Depletion of GSH stores in both cytosol and mitochondria enhanced the susceptibility of HepG2 cells or primary rat hepatocytes to 5% O2 exposure. However, this sensitization was abrogated by preventing mitochondrial ROS generation by complex I and II inhibition. Moreover, selective mGSH depletion by (R,S)-3-hydroxy-4-pentenoate that spared cytosol GSH levels sensitized rat hepatocytes to hypoxia because of enhanced ROS generation. GSH restoration by GSH ethyl ester or by blocking mitochondrial electron flow at complex I and II rescued (R,S)-3-hydroxy-4-pentenoate-treated hepatocytes to hypoxia-induced cell death. Thus, mGSH controls the survival of hepatocytes during hypoxia through the regulation of mitochondrial generation of oxidative stress.

Catalase overexpression attenuates angiotensinogen expression and apoptosis in diabetic mice

Progress in MnO2/MnO2-based materials catalytic ozonation process for water and wastewater treatment.

Reactive oxygen species and nuclear factor-kappa B pathway mediate high glucose-induced Pax-2 gene expression in mouse embryonic mesenchymal epithelial cells and kidney explants

Heterogeneous catalytic ozonation of bisphenol a with oxygen vacancy-rich montmorillonite supported iron oxide.

Ca(2+) -independent phospholipase A2 (iPLA2 ) is hypothesized to control mitochondrial reactive oxygen species (ROS) generation. Here, we modulated the influence of iPLA2 -induced liberation of non-esterified free fatty acids on ROS generation associated with the electron transport chain. We demonstrate enzymatic activity of membrane-associated iPLA2 in native, energized rat brain mitochondria (RBM). Theoretically, enhanced liberation of free fatty acids by iPLA2 modulates mitochondrial ROS generation, either attenuating the reversed electron transport (RET) or deregulating the forward electron transport of electron transport chain. For mimicking such conditions, we probed the effect of docosahexaenoic acid (DHA), a major iPLA2 product on ROS generation. We demonstrate that the adenine nucleotide translocase partly mediates DHA-induced uncoupling, and that low micromolar DHA concentrations diminish RET-dependent ROS generation. Uncoupling proteins have no effect, but the adenine nucleotide translocase inhibitor carboxyatractyloside attenuates DHA-linked uncoupling effect on RET-dependent ROS generation. Under physiological conditions of forward electron transport, low micromolar DHA stimulates ROS generation. Finally, exposure of RBM to the iPLA2 inhibitor bromoenol lactone (BEL) enhanced ROS generation. BEL diminished RBM glutathione content. BEL-treated RBM exhibits reduced Ca(2+) retention capacity and partial depolarization. Thus, we rebut the view that iPLA2 attenuates oxidative stress in brain mitochondria. However, the iPLA2 inhibitor BEL has detrimental activities on energy-dependent mitochondrial functions. The Ca(2+) -independent phospholipase A2 (iPLA2 ), a FFA (free fatty acids)-generating membrane-attached mitochondrial phospholipase, is potential to regulate ROS (reactive oxygen species) generation by mitochondria. FFA can either decrease reversed electron transport (RET)-linked or enhance forward electron transport (FET)-linked ROS generation. In the physiological mode of FET, iPLA2 activity increases ROS generation. The iPLA2 inhibitor BEL exerts detrimental effects on energy-dependent mitochondrial functions.

Emerging Designs of Aggregation-Induced Emission Agents for Enhanced Phototherapy Applications

UVB Radiation Induces Apoptosis in Keratinocytes by Activating a Pathway Linked to “BLT2-Reactive Oxygen Species”

Heterogeneous catalytic ozonation (HCO) processes have been widely studied for water purification. The reaction mechanisms of these processes are very complicated because of the simultaneous involvement of gas, solid, and liquid phases. Although typical reaction mechanisms have been established for HCO, some of them are only appropriate for specific systems. The divergence and deficiency in mechanisms hinders the development of novel active catalysts. This critical review compares the various existing mechanisms and categorizes the catalytic oxidation of HCO into radical-based oxidation and nonradical oxidation processes with an in-depth discussion. The catalytic active sites and adsorption behaviors of O3 molecules on the catalyst surface are regarded as the key clues for further elucidating the O3 activation processes, evolution of reactive oxygen species (ROS) or organic oxidation pathways. Moreover, the detection methods of the ROS produced in both types of oxidations and their roles in the destruction of organics are reviewed with discussion of some specific problems among them, including the scavengers selection, experiment results analysis as well as some questionable conclusions. Finally, alternative strategies for the systematic investigation of the HCO mechanism and the prospects for future studies are envisaged.

Explore synergistic catalytic ozonation by dual active sites of oxygen vacancies and defects in MgO/biochar for atrazine degradation

Electron transfer enhancing the Mn(II)/Mn(III) cycle in MnO/CN towards catalytic ozonation of atrazine via a synergistic effect between MnO and CN

Single-step methane to methanol over lanthanum cerium oxide: The crucial role of surface reactive oxygen and carbonate species

Oxygen vacancies are crucial to the production of reactive oxygen species (ROS) in the metal oxide electrocatalytic membrane (MOx EM) process. Here, using cathodic TiOx EM as a model, we thoroughly reveal the roles of oxygen vacancies in ROS generation and transformation. Oxygen vacancies significantly promote H2O2 and •OH production at low concentrations (increment <35%) but inhibit their production at high concentrations (increment >35%). Electrochemical analysis discloses that the enhancement of ROS production profits from the acceleration of charge transfer kinetics by both bulk and surface oxygen vacancies, whereas we attribute the decline in ROS production to the strong adsorption of ROS by surface oxygen vacancies. It is strongly supported by theoretical calculations that reveal the promoted adsorption of *OOH and *OH by oxygen vacancies, which intensifies the capture and scavenging of H2O2 and •OH. Moreover, the gradual increase of interaction time between ROS and oxygen vacancies (from ∼1 to ∼5 s) notably reduces the generation and transformation efficiency of ROS, further highlighting the detrimental impact of oxygen vacancies. In summary, oxygen vacancies show "two faces" toward ROS generation and transformation, acting as ROS promoters at low concentrations but inhibitors at high concentrations. A medium oxygen vacancy concentration is preferred for ROS production, thus causing impressive pollutant removal (>95% removal of bisphenol A within 1.2-1.5 s at 360-440 LMH). This study provides guidance on regulating ROS generation and transformation by manipulating the oxygen vacancy concentration to enhance the decontamination efficiency of MOx EMs.