Primary Reactive Oxygen Species Research Articles

Хемилюминесцентные характеристики периферической крови при облучении in vitro в диапазоне доз 100–500 мГр

Abstract. Nowadays a lot of examinations are dedicated to determination of radiobiological effects under low doses of ionising radiation. It is known that ionising radiation in the cells of an organism increases generation of reactive oxygen species (ROS). The purpose of the work is to determine basic parameters of chemiluminescent kinetics of ROS in peripheral blood under in vitro radiation in the range of 100–500 mGy doses. The research will extend the knowledge of the impact degree of ionising radiation in low doses on organism tissue of farm animals. Scientific novelty is that the results of the research will allow to predict radiobiological effects of low doses in a multicellular organism. The research is included in practical and fundamental directions of radiobiology. Research methods. In vitro radiation of blood samples in the range of 100–500 mGy doses. The kinetics of generation of ROS is registered on 36-channel chemiluminometer 3604-PC. Results. The doses in the range of 100–300 mGy accelerated the time of the first peak of spontaneous and activated generation of radicals, under 500 mGy dose the formation of the first peak of spontaneous and activated generation of primary ROS decelerated. Under the impact of low absorbed doses maximum intensity of primary and secondary radicals generation decreased. The inhibition of primary radicals spontaneous production occurred under 100–300 mGy doses, the inhibition of antigen activated generation of primary ROS was under 400 mGy. The reduction of the amount of spontaneous secondary ROS was registered under 100 mGy dose. The decrease of antigen activated secondary radicals production occurred under 100–300 mGy doses. 500 mGy dose inhibited a reaction ability of blood cells to generate primary radicals. The external in vitro gamma radiation in the range of 100–500 mGy had a negative impact on peripheral blood cells showing an acceleration of chemiluminescent reaction as well as decrease of maximum intensity of the first peak of spontaneous and antigen activated primary and secondary radicals production. As a consequence, a decrease of the amount of primary and secondary radicals production was revealed.

The level of blood neutrophils primary reactive oxygen species production in Graves’ disease patients undergoing conservative therapy with thiamazole.

Background. Conservative therapy with thiamazole in Graves’ disease helps to reduce the level of oxidative stress by restoring euthyroidism and the total reactive antioxidant potential of plasma. However, until now, in patients with Graves’ disease, the radical-producing ability of neutrophils remains unexplored at the initial stage of free radical conversion at different durations of drug-induced euthyroidism, which seems significant in revealing the mechanisms of disease recurrence. The aim is to study the level of production of primary reactive oxygen species in peripheral blood neutrophils depending on the duration of drug — induced euthyroidism in patients with Graves’ disease. Materials and methods. A single-center, prospective, controlled study was conducted with the participation of patients with laboratory-confirmed Graves’ disease. Subgroups of patients with Graves’ disease were formed depending on the duration of achieved drug-induced euthyroidism with continuous conservative therapy with thiamazole. The level of ROS production in peripheral blood neutrophils was determined by chemiluminescence. The assessment of spontaneous and zymosan-induced chemiluminescence was carried out for 90 minutes on a 36-channel chemiluminescence analyzer BLM-3607 (Medbiotech LLC, Krasnoyarsk). Results. The study included 102 Graves’ disease women with an average age of 47.54 ± 15.47 years. Of these, 75 (73.5 %) with relapse and 27 (26.47 %) with newly diagnosed disease. The total synthesis of (S) primary ROS increased statistically significantly relative to the control values in the examined patients with a duration of the euthyroid state of 5–8 and 9–12 months. It was found that in patients with Graves’ disease with stable drug-induced euthyroidism for 5–8 and 9–12 months, the S index of zymosan-induced lucigenin-dependent chemiluminescence of neutrophils increased statistically significantly, respectively, by 10.7 and 7.4 times relative to the control values. Conclusion. The restoration and maintenance of drug-induced euthyroidism for more than 12 months against the background of conservative thiamazole therapy in patients with Graves’ disease reduces the load of systemic oxidative stress on the immune system. However, the high total production of primary ROS in neutrophils of patients with Graves’ disease in a state of drug-induced euthyroidism with conservative thiamazole therapy may play a significant role in disconnecting the functioning of the NADPH oxidase complex and determine the functional capabilities of neutrophils in case of disease recurrence.

Ternary metal conjugated ZIF-67 coordination with Ag and Ce for the efficient Fenton-like remediation of dyes under visible light

The dye pollution of wastewater has resulted in substantial disturbances in the aquatic environment and photosynthetic activity. Here, ZIF-67, Ag, and Ce were employed to design a metal-organic framework (AgCe@ZIF-67) by one pot and post auto-combustion method for efficient degradation of Rhodamine B (RhB) and Crystal violet (CV) dyes from water. The fabricated materials were affirmed by X-rays diffraction (XRD), Scanning electron microscopy (SEM), Energy dispersive spectroscopy (EDS), Fourier transform infrared (FTIR), Photoluminescence (PL) and Electrochemical impedance spectroscopy (EIS). The Fenton assisted composite, AgCe@ZIF-67. b displays extraordinary catalytic performance to degrade 94% of RhB and 96% of CV dye solutions within 50 and 109 min, respectively. The boosted degradation efficiency is ascribed to the promulgation of metallic nodes of Ag and Ce material, promoting accessible active sites that result in production .OH and .O2 are primary reactive oxygen species. Besides, the AgCe@ZIF-67 also showed better reusability and stability even after multiple degradation cycles. The optimized material AgCe@ZIF-67 is expected to provide a better alternative for Fenton assisted photocatalytic degradation of dye from water.

Abstract 5325: Cytokine CCL9, new downstream target of oncogene Kras to modulate acinar-to-ductal metaplasia during pancreatic cancer initiation

Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of cancer with a current five-year survival rate at 12% in the US, and is dominated by oncogenic Kras mutations. Accumulating evidence showed that PDAC can be originated from acinar-to-ductal metaplasia (ADM). In this process, pancreatic acini harboring oncogenic Kras mutations are transdifferentiated to a duct-like phenotype that further progresses to become pancreatic intraepithelial neoplasia (PanIN) lesions, giving rise to PDAC. Although ADM formation is commonly observed in KrasG12D transgenic mouse models of PDAC, the exact mechanisms of how oncogenic KrasG12D modulates this process remain unclear. Here, we unveil a new downstream target of oncogenic Kras, cytokine CCL9 during ADM formation. Either exogenously treating primary pancreatic acini with recombinant CCL9 or ectopically expressing CCL9 in primary pancreatic acini resulted in ADM formation in a 3D organoid culture system. Furthermore, knockdown of CCL9 in KrasG12D-expressed acini reduced KrasG12D-induced ADM. Higher levels of reactive oxygen species (ROS) were detected in the KrasG12D-expressed pancreatic acini, and knockdown of CCL9 in these acini decreased ROS levels. Overexpression of CCL9 in primary pancreatic acini elevated cellular ROS of pancreatic acinar cells. Furthermore, depletion of ROS in 3D organoid culture of CCL9-expressed acini reduced CCL9-induced ADM formation. In transgenic mice of p48cre:KrasG12D, blockade of CCL9 through its specific neutralizing antibody attenuated ADM formation as well as PanIN structures. Altogether, our results indicated oncogenic KrasG12D initiates PDAC through a new downstream target molecule, CCL9, to enhance ROS levels of pancreatic acinar cells. Citation Format: Geou-Yarh (Stancy) Liou, Justin K. Messex, Crystal J. Byrd. Cytokine CCL9, new downstream target of oncogene Kras to modulate acinar-to-ductal metaplasia during pancreatic cancer initiation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5325.

Efficient removal of 17α-ethinylestradiol by algae-based red mud catalyst activated persulfate: Removal mechanism and defect of quenching

The synthesis and optimization of carbon-based materials, derived from various solid waste sources to activate peroxydisulfate (PDS), offer a practical approach that addresses both the recycling of solid waste resources and the removal of recalcitrant organic pollutants. In this study, stacked algae sludge and discarded red mud solid waste were repurposed to synthesize an algae-based red mud catalyst (AR-BC) using the carbon-thermal reduction technique. The obtained AR-BC catalyst exhibited efficient adsorption and degradation capabilities for 17α-ethinylestradiol (EE2). The results showed that AR-BC can adsorb 42.67 % of EE2 at equilibrium, with a maximum capacity of 8.0 mg/g. After the activation of PDS by the AR-BC catalyst, it was observed that EE2 was completely degraded within 20 min. The superior activation ability is mainly attributed to the presence of Fe3O4 and oxygen-containing functional groups in AR-BC. Both free radicals and non-free radicals coexisted in the AR-BC/PDS system, with the former predominantly influencing the EE2 degradation process. And hydroxyl radical was identified as the primary reactive oxygen species. Moreover, AR-BC exhibited robust adaptability and reusability in real water for efficient adsorption and degradation of EE2. This study presents a viable solution by seamlessly integrating resource recycling with pollutant removal, offering an innovation approach.

Efficient degradation of phenol in water by ball-milling modulated nitrogen-doped structured biochar

Presently, most kinds of biochar rely on the addition of transition metals to improve their electron transport capacity, thereby boosting the activation of oxidants. However, challenges such as the precipitation of transition metals and the chemical inertness of biochar are commonly encountered. Biochar with nitrogen-containing functional groups has emerged as a promising solution as oxidant activators. The nitrogen doping of biochar through ball milling is a straightforward, cost-effective, and efficient preparation method. To optimize the activation properties, a multi-step process involving roasting, ball milling, and tempering was employed to produce biochar. Sesame dregs was chosen as the precursor for this biochar. By optimizing the roasting temperature to 900 °C and using urea as the nitrogen source, biochar derived from sesame residue was successfully prepared. This biochar featured pyridine nitrogen as the primary functional group, exhibiting improved crystallinity and aromaticity. The activation of sodium persulfate (3.0 mM) with biochar eliminated phenol from wastewater with an initial concentration of 50 mg/L in just 15 minutes, achieving a remarkable mineralization rate of 96.77%. Even after undergoing six cycles of repeated use, the system consistently removed 97.73% of phenol within the same timeframe, maintaining a high mineralization rate of 86.77%. Notably, it was found that N-CN, N-6, and N-q were instrumental in stimulating reactive oxygen species (ROS), while ·OH, SO4·-, and 1O2 served as the primary ROS responsible for degrading phenol. The research also revealed a linear relationship between active oxygen sites and oxidized substances, offering insights into the mechanism of phenol degradation.

Electrochemical oxidation degradation of xanthate and its mechanism: Effects of carbon chain length and electrolyte type

There are a lot of residual flotation reagents such as xanthate remaining in the mineral processing wastewater, which must be deeply removed for recycling or discharge. However, there are few studies using electrochemical oxidation to remove xanthate. This article employs the electrochemical oxidation method to treat simulated xanthate-containing wastewater, which investigates the mechanisms involved in removing four xanthate homologues under different electrolyte conditions. Results show that under 1 g/L of Na2SO4, current density of 40 mA/cm2, initial pH of 7.0, and initial concentration of xanthates 1 mM, four alkyl xanthates can be completely removed within 60 min. The COD removal and TOC removal can reach 71.42%–88.61% and 54.23%–81.50%, respectively. By contrast, NaCl electrolyte is more favorable for xanthate degradation. The generated SO42− concentration can reach 145.4 mg/L at 60min, resulting in the sulfur mineralization ratio (ηs) of 75.72%. Regardless of the electrolyte type, as the carbon chain length increases, the xanthate degradation rate accelerates, accompanied by higher COD and TOC removal. The results of UV–vis spectra and LC–MS indicate that intermediate substances such as xanthate peroxides and alcohols are first formed in the process, ultimately leading to the complete mineralization of small molecule substances such as SO42−, CO2, and H2O. The fate of S and Cl elements confirms it. EPR and probe fluorescence spectroscopy results indicate that in Na2SO4 electrolyte, the main active substances are ·OH and a small amount of SO4∙–. Additionally, the production of ·OH increases as the electrolysis time is prolonged. In NaCl electrolyte, ·OH undergoes a series of reactions with Cl− to convert into Cl∙ and active chlorine, which constitute the primary reactive oxygen species.

Hepatocellular carcinoma cells downregulate NADH:Ubiquinone Oxidoreductase Subunit B3 to maintain reactive oxygen species homeostasis.

HCC is a leading cause of cancer-related death. The role of reactive oxygen species (ROS) in HCC remains elusive. Since a primary ROS source is the mitochondrial electron transport chain complex Ι and the NADH:ubiquinone Oxidoreductase Subunit B3 (NDUFB3), a complex I subunit, is critical for complex I assembly and regulates the associated ROS production, we hypothesize that some HCCs progress by hijacking NDUFB3 to maintain ROS homeostasis. NDUFB3 in human HCC lines was either knocked down or overexpressed. The cells were then analyzed in vitro for proliferation, migration, invasiveness, colony formation, complex I activity, ROS production, oxygen consumption, apoptosis, and cell cycle. In addition, the in vivo growth of the cells was evaluated in nude mice. Moreover, the role of ROS in the NDUFB3-mediated changes in the HCC lines was determined using cellular and mitochondrion-targeted ROS scavengers. HCC tissues showed reduced NDUFB3 protein expression compared to adjacent healthy tissues. In addition, NDUFB3 knockdown promoted, while its overexpression suppressed, HCC cells' growth, migration, and invasiveness. Moreover, NDUFB3 knockdown significantly decreased, whereas its overexpression increased complex I activity. Further studies revealed that NDUFB3 overexpression elevated mitochondrial ROS production, causing cell apoptosis, as manifested by the enhanced expressions of proapoptotic molecules and the suppressed expression of the antiapoptotic molecule B cell lymphoma 2. Finally, our data demonstrated that the apoptosis was due to the activation of the c-Jun N-terminal kinase (JNK) signaling pathway and cell cycle arrest at G0/G1 phase. Because ROS plays essential roles in many biological processes, such as aging and cancers, our findings suggest that NDFUB3 can be targeted for treating HCC and other human diseases.

Fe-ZSM-5 zeolite catalyst for heterogeneous Fenton oxidation of 1,4-dioxane: effect of Si/Al ratios and contributions of reactive oxygen species.

Heterogeneous Fenton oxidation using traditional catalysts with H2O2 for the degradation of 1,4-dioxane (1,4-DX) still presents challenge. In this study, we explored the potential of Fe-ZSM-5 zeolites (Fe-zeolite) with three Si/Al ratios (25, 100, 300) as heterogeneous Fenton catalysts for the removal of 1,4-DX from aqueous solution. Fe2O3 or ZSM-5 alone provided ineffective in degrading 1,4-DX when combined with H2O2. However, the efficient removal of 1,4-DX using H2O2 was observed when Fe2O3 was loaded on ZSM-5. Notably, the Brønsted acid sites of Fe-zeolite played a crucial role during the degradation of 1,4-DX. Fe-zeolites, in combination with H2O2, effectively removed 1,4-DX via a combination of adsorption and oxidation. Initially, Fe-zeolites demonstrated excellent affinity for 1,4-DX, achieving adsorption equilibrium rapidly in about 10min, followed by effective catalytic oxidative degradation. Among the Fe-ZSM-5 catalysts, Fe-ZSM-5 (25) exhibited the highest catalytic activity and degraded 1,4-DX the fastest. We identified hydroxyl radicals (·OH) and singlet oxygen (1O2) as the primary reactive oxygen species (ROS) responsible for 1,4-DX degradation, with superoxide anions (HO2·/O2·-) mainly converting into 1O2 and ·OH. The degradation primarily occurred at the Fe-zeolite interface, with the degradation rate constants proportional to the amount of Brønsted acid sites on the Fe-zeolite. Fe-zeolites were effective over a wide working pH range, with alkaline pH conditions favoring 1,4-DX degradation. Overall, our study provides valuable insights into the selection of suitable catalysts for effective removal of 1,4-DX using a heterogeneous Fenton technology.

Influence mechanism of anions on iron doping into swine bone char: Promoting non-radical oxidation of acetaminophen in a Fenton-like system

The application of iron-doped biochar in peroxymonosulfate (PMS) activation systems has gained increasing attention due to their effectiveness and environmental friendliness in addressing environmental issues. However, the behavioral mechanism of iron doping and the detailed 1O2 generation mechanism in PMS activation systems remain ambiguous. Here, we investigated the effects of three anions (Cl−, NO3−and SO42−) on the process of iron doping into bone char, leading to the synthesis of three iron-doped bone char (Fe-ClBC, Fe-NBC and Fe -SBC). These iron-doped bone char were used to catalyze PMS to degrade acetaminophen (APAP) and exhibited the following activity order: Fe-ClBC > Fe-NBC > Fe-SBC. Characterization results indicated that iron doping primarily occurred through the substitution of calcium in hydroxyapatite within BC. In the course of the impregnation, the binding of SO42− and Ca2+ hindered the exchange of iron ions, resulting in lower catalytic activity of Fe-SBC. The primary reactive oxygen species in the Fe-ClBC/PMS and Fe-NBC/PMS systems were both 1O2. 1O2 is produced through O2•− conversion and PMS self-dissociation, which involves the generation of metastable iron intermediates and electron transfer within iron species. The presence of oxygen vacancies and more carbon defects in the Fe-ClBC catalyst facilitates 1O2 generation, thereby enhancing APAP degradation within the Fe-ClBC/PMS system. This study is dedicated to in-depth exploration of the mechanisms underlying iron doping and defect materials in promoting 1O2 generation.

Structural Fe(II)-induced generation of reactive oxygen species on magnetite surface for aqueous As(III) oxidation during oxygen activation

Magnetite is a reductive Fe(II)-bearing mineral, and its reduction property is considered important for degradation of contaminants in groundwater and anaerobic subsurface environments. However, the redox condition of subsurface environments frequently changes from anaerobic to aerobic owing to natural and anthropogenic disturbances, generating reactive oxygen species (ROS) from the interaction between Fe(II)-bearing minerals and O2. Despite this, the mechanism of ROS generation induced by magnetite under aerobic conditions is poorly understood, which may play a crucial role in As(III) oxidation. Herein, we found that magnetite could activate O2 and induce the oxidative transformation of As(III) under aerobic conditions. As(III) oxidation was attributed to the ROS generated via structural Fe(II) within the magnetite octahedra oxygenation. The electron paramagnetic resonance and quenching tests confirmed that O2•−, H2O2, and •OH were produced by magnetite. Moreover, density function theory calculations combined with experiments demonstrated that O2•− was initially formed via single electron transfer from the structural Fe(II) to the adsorbed O2; O2•− was then converted to •OH and H2O2 via a series of free radical reactions. Among them, O2•−and H2O2 were the primary ROS responsible for As(III) oxidation, accounting for approximately 52 % and 19 % of As(III) oxidation. Notably, As(III) oxidation mainly occurred on the magnetite surface, and As was immobilized further within the magnetite structure. This study provides solid evidence regarding the role of magnetite in determining the fate and transformation of As in redox-fluctuating subsurface environments.

Synergistic redox and adsorption for enhanced Roxarsone removal: Heterogeneous Fenton-Like reaction with a novel composite of nanoscale zero-valent iron supported on γ-aluminum oxide

Roxarsone (ROX), a livestock growth enhancer, poses environmental and health hazards due to its remarkable stability, making traditional degradation methods ineffective. To tackle this issue, a novel Fenton-like composite, composed of nanoscale zero-valent iron supported on γ-aluminum oxide (nZVI/γ-Al2O3), was synthesized to boost ROX degradation. Results demonstrated nearly complete mineralization of the ROX organic matrix within just 180 min, facilitated by the Lewis acidity sites of γ-Al2O3. Significantly, this composite exhibited selective adsorption of released AsO43− ions on its surface, forming FeAsO4 and Fe-As-Al complexes. It also established an internal redox cycle involving Fe(0), Fe(II), and Fe(III), ensuring a continuous and efficient generation of primary reactive oxygen species (·OH and O2·−). Thus, a simultaneous redox process occurred on the composite surface can be attributed to the synergy of the reducibility of nZVI and the oxidation catalyzed by ·OH and O2·−. Initially, the nitro group of ROX was reduced by nZVI, forming more hydrophilic o-aminophenol, favoring subsequent oxidation and mineralization. Simultaneously, the As-C bonds in ROX were oxidized, yielding AsO43−, which was subsequently adsorbed over extended reaction times. This innovative approach offers a potential solution for treating wastewater contaminated with metalloid-organic composite pollutants, addressing the environmental and health concerns associated with ROX residues.

Boosted Photocatalytic Degradation of Atrazine Using Oxygen-Modified g-C3N4: Investigation of the Reactive Oxygen Species Interconversion.

Elaborating the specific reactive oxygen species (ROS) involved in the photocatalytic degradation of atrazine (ATZ) is of great significance for elucidating the underlying mechanism. This study provided conclusive evidence that hydroxyl radicals (·OH) were the primary ROS responsible for the efficient photocatalytic degradation of ATZ, thereby questioning the reliability of widely adopted radical quenching techniques in discerning authentic ROS species. As an illustration, oxygen-modified g-C3N4 (OCN) was prepared to counteract the limitations of pristine g-C3N4 (CN). Comparative assessments between CN and OCN revealed a remarkable 10.44-fold improvement in the photocatalytic degradation of ATZ by OCN. This enhancement was ascribed to the increased content of C-O functional groups on the surface of the OCN, which facilitated the conversion of superoxide radicals (·O2-) into hydrogen peroxide (H2O2), subsequently leading to the generation of ·OH. The increased production of ·OH contributed to the efficient dealkylation, dechlorination, and hydroxylation of ATZ. Furthermore, toxicity assessments revealed a significant reduction in ATZ toxicity following its photocatalytic degradation by OCN. This study sheds light on the intricate interconversion of ROS and offers valuable mechanistic insights into the photocatalytic degradation of ATZ.

Enhanced efficiency of refractory organic pollutant degradation over a wide pH range by peroxymonosulfate activated by cobalt-doped FeS

A series of cobalt-doped FeS (x% Co–FeS) nanoparticles, prepared via a hydrothermal method, were introduced as catalysts for generating radicals from peroxymonosulfate (PMS) to degrade the endocrine disrupter bisphenol S (BPS) in wastewater. The kinetic results revealed that only a small amount of Co doping (7% At.) could greatly improve the efficiency of PMS activation by FeS, leading to the rapid degradation of BPS (0.21min−1 vs. 0.0046 min−1), and no secondary pollution caused by Co leaching. Notably, exceptional activation was observed over a wide pH range from 4 to 11. Moreover, various background ions (NO3−, Cl−, CO32−) and temperatures (10.0–55.0 °C) minimally affected BPS degradation, suggesting excellent applicability in different sewage environments. Furthermore, quenching experiments, coupled with electron paramagnetic resonance technology, identified singlet oxygen (1O2) and sulfate radicals (SO4•-) as the primary reactive oxygen species responsible for BPS degradation. Due to the selectivity of 1O2 and the high redox potential of SO4•-, this technology had excellent anti-interference and degradation ability. In six repeated batch experiments, the catalysts showed favorable cyclability and stability due to Co(II)/Co(III) cycling mediated by structural S2−. These results provided insights into the potential applications of modifying natural FeS-type minerals as a promising heterogeneous catalyst for environmental restoration.

Fe electrocoagulation technology for highly-efficient p-arsanilic acid removal from water: Feasibility and mechanisms

Conventional oxidation methods are effective for the removal of p-arsanilic acid (p-ASA) in water but are limited by complicated process. Herein, Fe electrocoagulation with Fe as anodes was used to efficiently remove p-ASA with 100% total arsenic removal within 60 min (1.75–20 A/m2). Current density significantly influenced sludge production, anode loss, and energy consumption (p-value < 0.05). Kinetic analyses showed a decline in arsenic removal rate with increasing initial pH (4.0–10.0). The changes in main elements of p-ASA (As and N) were analyzed to identify intermediate products using UPLC-Q-TOF-MS, HPLC-ICP-MS, and spectrometry. Hydroxyl radicals were confirmed as the primary reactive oxygen species. The active sites of p-ASA molecules were predicted by theoretical calculations and reaction paths were proposed. The toxicity of Fe-EC effluent was effectively reduced according to the analyses of ECOSAR and E. coli colonies method. The possible mechanisms of p-ASA removal, including oxidative degradation, electrostatic attraction, and ligand complexation, were proposed. Real water containing a p-ASA concentration of 250 μg/L was treated for 48 h using continuous-flow Fe-EC and arsenic concentrations of 2–30 μg/L in effluent were obtained. Overall, Fe-EC was a simple, cost-effective, and eco-friendly technology for the removal of p-ASA.

Sources of Reactive Oxygen Species in Normoxic and Hypoxic Naked Mole-Rat Brain

Oxygen availability dictates the rate of reactive oxygen species production from various cellular sources; excessive ROS accumulation can be cytotoxic. Mitochondria are usually the primary contributors to basal reactive oxygen species generation in the brain; however, xanthine oxidoreductase and nicotinamide adenine dinucleotide phosphate oxidase can also produce considerable reactive oxygen species during hypoxia/reoxygenation. In the brains of most mammals, cellular death accompanies hypoxia-mediated surges in reactive oxygen species production, but this is avoided in the cortex of hypoxia-tolerant naked mole-rats (Heterocephalus glaber). However, the contributions of various reactive oxygen species generators towards total reactive oxygen species homeostasis in naked mole-rat brain is unknown. We hypothesized that mitochondria remain the primary reactive oxygen species generators in naked mole-rat cortex and predicted that pharmacological inhibition of mitochondrial complex I would induce greater fluctuations in superoxide (O2•-) and hydrogen peroxide (H2O2) than inhibition of xanthine oxidoreductase or nicotinamide adenine dinucleotide phosphate oxidase. To test this, we used fluorescence microscopy to measure H2O2 and O2•- production from cortical slices during normoxia and hypoxia while pharmacologically inhibiting mitochondrial complex I, xanthine oxidoreductase, or nicotinamide adenine dinucleotide phosphate oxidase. Unexpectedly, we found xanthine oxidoreductase inhibition induced the greatest increase in O2•- during normoxia and hypoxia (~100% and 70%, respectively). Hypoxic inhibition of nicotinamide adenine dinucleotide phosphate oxidase induced the greatest decrease in H2O2 by ~35% below baseline. Finally, although inhibition of mitochondrial complex I during hypoxia yielded significant fluctuations in O2•- and H2O2, these changes were considerably smaller than fluctuations induced by inhibiting xanthine oxidoreductase or nicotinamide adenine dinucleotide phosphate oxidase. Together, and unlike in other rodent brain, our results suggest that xanthine oxidoreductase is the primary contributor to reactive oxygen species production in naked mole-rat cortex.

Assembly of MOF derived composite catalyst on the PVDF membrane matrix for high-efficient phenol removal

Integrating the heterogeneous catalysts with the membrane matrix is a promising approach for wastewater decontamination. In this study, a ZIF-67 derived cobalt‑manganese spinel catalyst MnCo2O4.5@Carbon (MCOC) was prepared using a one-pot pyrolysis process and was then blended with a polyvinylidene fluoride (PVDF) membrane through the phase inversion method. The introduction of the MCOC catalyst not only improved the permeance of the membrane but also constructed active reaction sites within the membrane matrix. As a result, the PVDF/MCOC membranes exhibited both satisfactory degradation capabilities by activating peroxymonosulfate and favorable permeation performance. Remarkably, about 99 % of phenol (20 mg/L) can be removed within 30 min, with a water flux of 649.0 L/m2∙h. Besides, the PVDF/MCOC catalytic membrane possessed favorable anti-fouling properties and stability. The flux recovery rate of the PVDF/MCOC membrane reached 85 % after three fouling/washing cycles, while the phenol removal efficiency remained consistent at 95 % after 5 consecutive cycles. Radical quenching tests and electron paramagnetic resonance analysis further indicated that sulfate radicals and singlet oxygen were the primary reactive oxygen species in the phenol degradation processes. Consequently, this work highlights an effective method to fabricate a catalytic membrane with high permeance and catalytic efficiency, potentially expanding the application of heterogeneous catalysts in wastewater decontamination.

Undaria pinnatifida (wakame)-derived Fe, N co-doped graphene-like hierarchical porous carbon as highly efficient catalyst for activation of peroxymonosulfate (PMS) toward degradation of tetracycline (TC)

The use of biomass as a catalyst offers a cost-effective and efficient approach for various processes, including the activation of peroxymonosulfate (PMS) to degrade contaminants. In this study, we successfully obtained Fe and N co-doped graphene-like hierarchical porous structure carbon (Fe-N/BC) by using undaria pinnatifida (wakame) as the precursor. The Fe-N/BC catalyst was utilized to activate PMS and degrade tetracycline (TC). Characterization results demonstrated an even distribution of Fe and N on the surface of the porous structure carbon. Compared to BC@PMS and N/BC@PMS, the Fe-N/BC@PMS system exhibited excellent degradation performance, achieving an 83.9 % degradation of TC in just 5 min with an ultralow catalyst dosage (Ca = 0.05 g/L) and a high TC concentration (TC = 0.03 g/L). Furthermore, experiments on radicals quenching and electron paramagnetic resonance (EPR) analysis indicated that singlet oxygen (1O2), a non-radical species, was demonstrated as the primary reactive oxygen species (ROS). The degradation mechanical analysis suggested that zero-valent iron (Fe0), pyridinic N, graphitic N, and Fe-Nx in the Fe-N/BC were the reason for the high catalytic activity. Moreover, the degradation pathways of TC were suggested through the use of LC-MS. Additionally, the ECOSAR system was employed to assess the toxicity of the intermediate products. This study reveals the active site and its mechanism in Fe-N composite biocarbon catalysts, providing a new method for synthesizing algal biocarbon catalysts.

Electrochemical oxidation of reverse osmosis concentrate using a pilot-scale reactive electrochemical membrane filtration system: Performance and mechanisms

Scale-up treatment of real wastewater holds the key to promoting the practical application of electrochemical filtration technology. This work used a pilot-scale Ti/Pd reactive electrochemical membrane (REM) system (12 REM modules with a total REM area of 0.144 m2) to treat high-salinity reverse osmosis concentrate (ROC) from a chemical industry park. The pilot-scale Ti/Pd REM system demonstrated effective electrochemical degradation of ROC wastewater, achieving removal efficiencies of 82.3 ± 1.9% for COD and 46.7 ± 5.6% for TN at a membrane flux of 90 L/(m2·h) and a cell voltage of 5 V, with an energy consumption of 0.045 kWh/g-COD. Singlet oxygen (1O2) and reactive chlorine species were identified as the two primary reactive oxygen species generated in the Ti/Pd REM system. Fluorescence spectroscopy and Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS) analysis indicated that the pilot-scale Ti/Pd REM treatment effectively oxidized humic acid-like substance and unsaturated aromatic compounds. Overall, the Ti/Pd REM technology shows a promising application potential for the treatment of high-salinity ROC from the chemical industry.

Mitochondrial H2O2 Is a Central Mediator of Diclofenac-Induced Hepatocellular Injury.

Nonsteroidal anti-inflammatory drug (NSAID) use is associated with adverse consequences, including hepatic injury. The detrimental hepatotoxicity of diclofenac, a widely used NSAID, is primarily connected to oxidative damage in mitochondria, which are the primary source of reactive oxygen species (ROS). The primary ROS responsible for inducing diclofenac-related hepatocellular toxicity and the principal antioxidant that mitigates these ROS remain unknown. Peroxiredoxin III (PrxIII) is the most abundant and potent H2O2-eliminating enzyme in the mitochondria of mammalian cells. Here, we investigated the role of mitochondrial H2O2 and the protective function of PrxIII in diclofenac-induced mitochondrial dysfunction and apoptosis in hepatocytes. Mitochondrial H2O2 levels were differentiated from other types of ROS using a fluorescent H2O2 indicator. Upon diclofenac treatment, PrxIII-knockdown HepG2 human hepatoma cells showed higher levels of mitochondrial H2O2 than PrxIII-expressing controls. PrxIII-depleted cells exhibited higher mitochondrial dysfunction as measured by a lower oxygen consumption rate, loss of mitochondrial membrane potential, cardiolipin oxidation, and caspase activation, and were more sensitive to apoptosis. Ectopic expression of mitochondrially targeted catalase in PrxIII-knockdown HepG2 cells or in primary hepatocytes derived from PrxIII-knockout mice suppressed the diclofenac-induced accumulation of mitochondrial H2O2 and decreased apoptosis. Thus, we demonstrated that mitochondrial H2O2 is a key mediator of diclofenac-induced hepatocellular damage driven by mitochondrial dysfunction and apoptosis. We showed that PrxIII loss results in the critical accumulation of mitochondrial H2O2 and increases the harmful effects of diclofenac. PrxIII or other antioxidants targeting mitochondrial H2O2 could be explored as potential therapeutic agents to protect against the hepatotoxicity associated with NSAID use.