Construction of Embedded Sulfur-Doped g-C3N4/BiOBr S-Scheme Heterojunction for Highly Efficient Visible Light Photocatalytic Degradation of Organic Compound Rhodamine B.

Constructing S-scheme heterojunction catalysts is a key challenge in visible-light catalysed degradation of organic pollutants. Most heterojunction materials are reported to face significant obstacles in the separation of photogenerated electron-hole pairs owing to differences in the material size and energy barriers. In this study, sulfur-doped g-C3N4 oxidative-type semiconductor materials are synthesized and then coupled with BiOBr reductive-type semiconductor to form S-g-C3N4/BiOBr S-scheme heterojunction. A strong and efficient internal electric field is established between the two materials, facilitating the separation of photogenerated electron-hole pairs. Notably, in situ XPS proved that after visible light irradiation, Bi3+ is converted into Bi(3+ɑ)+, and a large number of photogenerated holes are produced on the surface of BiOBr, which oxidized and activated H2O into •OH.  â€¢OH cooperated with •O2 - and 1O2 to attack Rhodamine B (RhB) molecules to achieve deep oxidation mineralization. The composite material is designed with a LUMO energy level higher than that of RhB, promoting the sensitization of RhB by injecting photogenerated electrons into the heterojunction, thereby enhancing the photocatalytic performance to 22.44 times that of pure g-C3N4. This study provides a new perspective on the efficient degradation of organic molecules using visible light catalysis.

Treatment of Oxidative Stress with Exosomes in Myocardial Ischemia.

A thrombus in a coronary artery causes ischemia, which eventually leads to myocardial infarction (MI) if not removed. However, removal generates reactive oxygen species (ROS), which causes ischemia-reperfusion (I/R) injury that damages the tissue and exacerbates the resulting MI. The mechanism of I/R injury is currently extensively understood. However, supplementation of exogenous antioxidants is ineffective against oxidative stress (OS). Enhancing the ability of endogenous antioxidants may be a more effective way to treat OS, and exosomes may play a role as targeted carriers. Exosomes are nanosized vesicles wrapped in biofilms which contain various complex RNAs and proteins. They are important intermediate carriers of intercellular communication and material exchange. In recent years, diagnosis and treatment with exosomes in cardiovascular diseases have gained considerable attention. Herein, we review the new findings of exosomes in the regulation of OS in coronary heart disease, discuss the possibility of exosomes as carriers for the targeted regulation of endogenous ROS generation, and compare the advantages of exosome therapy with those of stem-cell therapy. Finally, we explore several miRNAs found in exosomes against OS.

Modifying Effect of Autotransfusion of Mesenchymal Stromal Cells on the Production of Reactive Oxygen Species and Cytokines by Mononuclear Cells in Patients with Chronic Heart Failure.

We studied in vivo modifying effect of autotransfusion of human bone marrow mesenchymal stromal cells on ROS generation and production of cytokines (TNFα,TNFß, IL-1α, IL-10, IFNγ, and GM-CSF) and PGE2 by mononuclear cells of patients (N=21) with chronic heart failure. These parameters were evaluated prior to (control) and after (immediately and on day 14) intravenous administration of stromal cells in doses of 100-200×106. Immediately after autotransfusion, significant increase of in vitro zymosan-induced chemiluminescence of blood mononuclear cells from 10 patients was observed. At later terms after autotransfusion (day 14), inhibition of chemiluminescent activity of blood mononuclear cells was revealed in 50% patients. We discuss possible mechanisms of involvement of transplanted autologous bone marrow mesenchymal stromal cells in reprogramming of blood mononuclear phagocytes from the pro- to anti-inflammatory phenotype under conditions of their in vivo interaction manifesting in transition from activation to inhibition of ROS-producing activity of macrophages and significant suppression of in vitro LPS-induced production of TNFα and GM-CSF by blood mononuclears against the background of significantly elevated TNFß, IL-10, and IL-1α concentrations.

Advances on the Role of Ferroptosis in Ionizing Radiation Response.

Ferroptosis is an iron-dependent programmed cell death mode that is distinct from other cell death modes, and radiation is able to stimulate cellular oxidative stress and induce the production of large amounts of reactive oxygen radicals, which in turn leads to the accumulation of lipid peroxide and the onset of ferroptosis. In this review, from the perspective of the role of ferroptosis in generating a radiation response following cellular irradiation, the relationship between ferroptosis induced by ionizing radiation stress and the response to ionizing radiation is reviewed, including the roles of MAPK and Nrf2 signaling pathways in ferroptosis, resulting from the oxidative stress response to ionizing radiation, the metabolic regulatory role of the p53 gene in ferroptosis, and regulatory modes of action of iron metabolism and iron metabolism-related regulatory proteins in promoting and inhibiting ferroptosis. It provides some ideas for the follow-up research to explore the specific mechanism and regulatory network of ferroptosis in response to ionizing radiation.

Vitamin D-Dimer: A Possible Biomolecule Modulator in Cytotoxic and Phagocytosis Processes?

Background: Vitamin D3 complexed to deglycosylated vitamin D binding protein (VitD-dgVDBP) is a water-soluble vitamin D dimeric compound (VitD-dgVDBP). It is not clear how VitD-dgVDBP affects circulating monocytes, macrophages, other immune cell systems, including phagocytosis and apoptosis, and the generation of reactive oxygen species (ROS) compared to dgVDBP. Methods: Flow cytometry was used to measure superoxide anion radical (O2*−) levels and macrophage activity in the presence of VitD-dgVDBP or dgVDBP. VitD-dgVDBP was incubated with normal human lymphocytes (nPBMCs), and several clusters of determination (CDs) were estimated. dgVDBP and VitD-dgVDBP apoptosis was estimated on malignant prostatic cells. Results: The macrophage activity was 2.8-fold higher using VitD-dgVDBP (19.8·106 counts) compared to dgVDBP (7.0·106 counts), but O2*− production was 1.8-fold lower in favor of VitD-dgVDBP (355·103 counts) compared to dgVDBP (630·106 counts). The calculated ratio of the radical/macrophage activity was 5-fold lower compared to that of dgVDBP. Only VitD-dgVDBP activated caspase-3 (8%), caspase-9 (13%), and cytochrome-C (11%) on prostatic cancer cells. PE-Cy7-labeled VitD-dgVDBP was found to bind to cytotoxic suppressor cells, monocytes/macrophages, dendritic and natural killer cells (CD8+), and helper cells (CD4+). After 12 h of co-incubation of nPBMCs with VitD-dgVDBP, significant activation and expression were measured for CD16++/CD16 (0.6 ± 0.1% vs. 0.4 ± 0.1%, p < 0.05), CD45k+ (96.0 ± 6.0% vs. 84.7 ± 9.5%, p < 0.05), CD85k+ (24.3 ± 13.2% vs. 3.8 ± 3.2%, p < 0.05), and CD85k+/CD123+ (46.8 ± 8.1% vs. 3.5 ± 3.7%, p < 0.001) compared to the control experiment. No significant difference was found using CD3+, CD4+, CD8+, CD4/CD8, CD4/CD8, CD16+, CD16++, CD14+, or CD123+. A significant decline in CD14+/CD16+ was obtained in the presence of VitD-dgVDBP (0.7 ± 0.2% vs. 3.1 ± 1.7%; p < 0.01). Conclusion: The newly developed water-soluble VitD3 form VitD-dgVDBP affected cytotoxic suppressor cells by activating the low radical-dependent CD16 pathway and seemed to induce apoptosis in malignant prostatic cells.

Nanosilver Targets the Bacterial Cell Envelope: The Link with Generation of Reactive Oxygen Radicals.

The work describes the interactions of nanosilver (NAg) with bacterial cell envelope components at a molecular level and how this associates with the reactive oxygen species (ROS)-mediated toxicity of the nanoparticle. Major structural changes were detected in cell envelope biomolecules as a result of damages in functional moieties, such as the saccharides, amides, and phosphodiesters. NAg exposure disintegrates the glycan backbone in the major cell wall component peptidoglycan, causes complete breakdown of lipoteichoic acid, and disrupts the phosphate-amine and fatty acid groups in phosphatidylethanolamine, a membrane phospholipid. Consistent with the oxidative attacks, we propose that the observed cell envelope damages are inflicted, at least in part, by the reactive oxygen radicals being generated by the nanoparticle during its leaching process, abiotically, without cells. The cell envelope targeting, especially those on the inner membrane phospholipid, is likely to then trigger the rapid generation of lethal levels of cellular superoxide (O2•-) and hydroxyl (OH•) radicals herein seen with a model bacterium. The present study provides a better understanding of the antibacterial mechanisms of NAg, whereby ROS generation could be both the cause and consequence of the toxicity, associated with the initial cell envelope targeting by the nanoparticle.

Heterogeneous Electro-Fenton catalysis with HKUST-1-derived Cu@C decorated in 3D graphene network.

Transition metal and nanocarbon-based composites with high activity and stability draw great attention in electro-Fenton system for organic pollutants removal. In this study, HKUST-1-derived Cu@C nanoparticles embedded within three-dimensional reduced graphene oxide (rGO) network (denoted as 3DG/Cu@C) is synthesized through a simple strategy. The prepared catalyst shows ordered 3D porous carbon structure and Cu@C NPs are uniformly dispersed in the matrix. The 3DG/Cu@C is used as heterogeneous electro-Fenton (hetero-EF) catalyst and shows outstanding performance in various persistent organic pollutants removal. High concentration Rhodamine B (RhB) (40 mg L-1) can achieve a complete decolorization within 150 min with 25 mg L-1 3DG/Cu@C catalyst, which is one of the lowest catalyst dosages in hetero-EF for RhB removal. More importantly, the 3DG/Cu@C achieves high RhB mineralization efficiency of 81.5% and exhibits high catalytic performance in a wide pH window from 3 to 9. The 3DG/Cu@C also remains high efficiency after five successive reaction cycles. The working mechanism study shows that RhB is mainly oxidized by •OH and O2•- radicals through hetero-EF and anodic oxidation processes. The high stability and outstanding performance of 3DG/Cu@C provide new insights in organic pollutants removal by hetero-EF process with transition metal and nanocarbon-based catalysts.

Study on oxidative lipid and DNA damages in the malignant transformed BEP2D cells induced by α-particle exposure / 中华放射医学与防护杂志

Objective To investigate the mechanism of malignant transformation in human bronchial epithelial cell line BEP2D exposed to α-particles.Methods The levels of intracellular ROS and malonaldehyde (MDA) in BEP2D,RH22 (passage 22 of α-particle-irradiated BEP2D cells) and BERP35T-1 cells (derived from nude mice bearing malignant transformed cells generated from the passage 35 of α-particle-irradiated BEP2D cells) were assayed with DCFH-DA and MDA kit,respectively.The expressions of 8-OH-dG and γ-H2AX in BEP2D,RH23 (passage 23 of α-particle-irradiated BEP2D cells)and BERP35T-1 cells were also measured with immunocytochemistry and immunofluorescence staining.Results Compared to BEP2D cells,the levels of ROS ( t =4.30 and 3.94,P ＜ 0.05 ) and MDA ( t =4.89 and 15.10,P ＜0.05) increased in RH22 and BERP35T-1 cells.The expressions of 8-OH-dG (t =3.80 and 2.92,P ＜ 0.05 ) and γ-H2AX ( t =7.61 and 12.67,P ＜ 0.05 ) in RH23 and BERP35T-1 cells were also higher than those in BEP2D cells.Conclusions Oxidative stress induces lipid peroxidation and DNA damage leading to genomic instability,which could contribute to cellular malignant transforming process in the human bronchial epithelial cell line BEP2D with α-particle exposure.

Effects of Reactive Oxygen Species on Hyperactivation of Human Sperms / 대한비뇨기과학회지

capacitation of human sperm is essential for fertilization and is characterized visually by hyperactivated motility. There is a controversy whether reactive oxygen radicals cause infertility or stimulate sperm-zona interaction. We investigated the exact role of reactive oxygen radicals on hyperactivation (HA) of human sperm which could be a part of the capacitation process. Hyperactivation of human sperm was compared to the Ham's F-10 controls by the addition of superoxide anion and hydrogen peroxide generating enzymes on the percale treated sperms. The motility parameters of human sperms were estimated by computer assisted semen analysis system. The addition of xanthine + xanthine oxidase + catalase (generating system of superoxide anion and removal of hydrogen peroxide) on the sperms induced levels of HA (10.5% at 2 hour, 11.3% at 5 hour) which were about 2 times higher than those of controls (HA: 5.4% at 2 hour, 5.6% at 5 hour). The addition of glucose + glucose oxidase (generation of hydrogen peroxide) decreased the levels of HA (0.0% at 2 and 5 hour) significantly. Superoxide dismutase, the scavenger of superoxide anion inhibited HA significantly, whereas catalase, the scavenger of hydrogen peroxide promoted HA significantly These results suggest that the reactive oxygen radicals may be involved in hyperactivation of human sperms by the way that superoxide anion promotes and hydrogen peroxide inhibits hyperactivation of the fertile human sperms. It may be very important in the process of fertilization that promotion or inhibition of hyperactivation occurs at the proper time and location of female genital organ.