Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut.

The view that sleep is essential for survival is supported by the ubiquity of this behavior, the apparent existence of sleep-like states in the earliest animals, and the fact that severe sleep loss can be lethal. The cause of this lethality is unknown. Here we show, using flies and mice, that sleep deprivation leads to accumulation of reactive oxygen species (ROS) and consequent oxidative stress, specifically in the gut. ROS are not just correlates of sleep deprivation but drivers of death: their neutralization prevents oxidative stress and allows flies to have a normal lifespan with little to no sleep. The rescue can be achieved with oral antioxidant compounds or with gut-targeted transgenic expression of antioxidant enzymes. We conclude that death upon severe sleep restriction can be caused by oxidative stress, that the gut is central in this process, and that survival without sleep is possible when ROS accumulation is prevented. VIDEO ABSTRACT.

Harmonizing the cyano-group and Na to enhance selective photocatalytic O2 activation on carbon nitride for refractory pollutant degradation.

Manipulating exciton dissociation and charge-carrier transfer processes to selectively generate free radicals of more robust photocatalytic oxidation capacity for mineralizing refractory pollutants remains challenging. Herein, we propose a strategy by simultaneously introducing the cyano-group and Na into graphitic carbon nitride (CN) to obtain CN-Cy-Na, which makes the charge-carrier transfer pathways the dominant process and consequently achieves the selective generation of free radicals. Briefly, the cyano-group intensifies the local charge density of CN, offering a potential well to attract the hole of exciton, which accelerates the exciton dissociation. Meanwhile, the separated electron transfers efficiently under the robust built-in electric field induced by the cyano-group and Na, and eventually accumulates in the heptazine ring of CN for the following O2 reduction due to the reinforced electron sink effect caused by Na. As a result, CN-Cy-Na exhibits 4.42 mmol L-1 h-1 productivity with 97.6% selectivity for free radicals and achieves 82.1% total organic carbon removal efficiency in the tetracycline photodegradation within 6 h. Additionally, CN-Cy-Na also shows outstanding photodegradation efficiency of refractory pollutants, including antibiotics, pesticide plastic additives, and dyes. This work presents an innovative approach to manipulating the exciton effect and enhancing charge-carrier mobility within two-dimensional photocatalysts, opening an avenue for precise control of free radical generation.

Nicotine inhalation and metabolism triggers AOX-mediated superoxide generation with oxidative lung injury.

With the increasing use of vaping devices that deliver high levels of nicotine (NIC) to the lungs, sporadic lung injury has been observed. Commercial vaping solutions can contain high NIC concentrations of 150 mM or more. With high NIC levels, its metabolic products may induce toxicity. NIC is primarily metabolized to form NIC iminium (NICI) which is further metabolized by aldehyde oxidase (AOX) to cotinine. We determine that NICI in the presence of AOX is a potent trigger of superoxide generation. NICI stimulated superoxide generation from AOX with Km = 2.7 µM and Vmax = 794 nmol/min/mg measured by cytochrome-c reduction. EPR spin-trapping confirmed that NICI in the presence of AOX is a potent source of superoxide. AOX is expressed in the lungs and chronic e-cigarette exposure in mice greatly increased AOX expression. NICI or NIC stimulated superoxide production in the lungs of control mice with an even greater increase after chronic e-cigarette exposure. This superoxide production was quenched by AOX inhibition. Furthermore, e-cigarette-mediated NIC delivery triggered oxidative lung damage that was blocked by AOX inhibition. Thus, NIC metabolism triggers AOX-mediated superoxide generation that can cause lung injury. Therefore, high uncontrolled levels of NIC inhalation, as occur with e-cigarette use, can induce oxidative lung damage.

Severe hypoxaemic hypercapnia compounds cerebral oxidative-nitrosative stress during extreme apnoea: Implications for cerebral bioenergetic function.

We examined the extent to which apnoea-induced extremes of oxygen demand/carbon dioxide production impact redox regulation of cerebral bioenergetic function. Ten ultra-elite apnoeists (six men and four women) performed two maximal dry apnoeas preceded by normoxic normoventilation, resulting in severe end-apnoea hypoxaemic hypercapnia, and hyperoxic hyperventilation designed to ablate hypoxaemia, resulting in hyperoxaemic hypercapnia. Transcerebral exchange of ascorbate radicals (by electron paramagnetic resonance spectroscopy) and nitric oxide metabolites (by tri-iodide chemiluminescence) were calculated as the product of global cerebral blood flow (by duplex ultrasound) and radial arterial (a) to internal jugular venous (v) concentration gradients. Apnoea duration increased from 306 ± 62 s during hypoxaemic hypercapnia to 959 ± 201 s in hyperoxaemic hypercapnia (P ≤ 0.001). Apnoea generally increased global cerebral blood flow (all P ≤ 0.001) but was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose (P = 0.015-0.044). This was associated with a general net cerebral output (v > a) of ascorbate radicals that was greater in hypoxaemic hypercapnia (P = 0.046 vs. hyperoxaemic hypercapnia) and coincided with a selective suppression in plasma nitrite uptake (a > v) and global cerebral blood flow (P = 0.034 to <0.001 vs. hyperoxaemic hypercapnia), implying reduced consumption and delivery of nitric oxide consistent with elevated cerebral oxidative-nitrosative stress. In contrast, we failed to observe equidirectional gradients consistent with S-nitrosohaemoglobin consumption and plasma S-nitrosothiol delivery during apnoea (all P ≥ 0.05). Collectively, these findings highlight a key catalytic role for hypoxaemic hypercapnia in cerebral oxidative-nitrosative stress. KEY POINTS: Local sampling of blood across the cerebral circulation in ultra-elite apnoeists determined the extent to which severe end-apnoea hypoxaemic hypercapnia (prior normoxic normoventilation) and hyperoxaemic hypercapnia (prior hyperoxic hyperventilation) impact free radical-mediated nitric oxide bioavailability and global cerebral bioenergetic function. Apnoea generally increased the net cerebral output of free radicals and suppressed plasma nitrite consumption, thereby reducing delivery of nitric oxide consistent with elevated oxidative-nitrosative stress. The apnoea-induced elevation in global cerebral blood flow was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose. Cerebral oxidative-nitrosative stress was greater during hypoxaemic hypercapnia compared with hyperoxaemic hypercapnia and coincided with a lower apnoea-induced elevation in global cerebral blood flow, highlighting a key catalytic role for hypoxaemia. This applied model of voluntary human asphyxia might have broader implications for the management and treatment of neurological diseases characterized by extremes of oxygen demand and carbon dioxide production.

Multiple oxidative post-translational modifications of human glutamine synthetase mediate peroxynitrite-dependent enzyme inactivation and aggregation.

Glutamine synthetase (GS), which catalyzes the ATP-dependent synthesis of L-glutamine from L-glutamate and ammonia, is a ubiquitous and conserved enzyme that plays a pivotal role in nitrogen metabolism across all life domains. In vertebrates, GS is highly expressed in astrocytes, where its activity sustains the glutamate-glutamine cycle at glutamatergic synapses and is thus essential for maintaining brain homeostasis. In fact, decreased GS levels or activity have been associated with neurodegenerative diseases, with these alterations attributed to oxidative post-translational modifications of the protein, in particular tyrosine nitration. In this study, we expressed and purified human GS (HsGS) and performed an in-depth analysis of its oxidative inactivation by peroxynitrite (ONOO-) in vitro. We found that ONOO- exposure led to a dose-dependent loss of HsGS activity, the oxidation of cysteine, methionine, and tyrosine residues and also the nitration of tryptophan and tyrosine residues. Peptide mapping by LC-MS/MS through combined H216O/H218O trypsin digestion identified up to 10 tyrosine nitration sites and five types of dityrosine cross-links; these modifications were further scrutinized by structural analysis. Tyrosine residues 171, 185, 269, 283, and 336 were the main nitration targets; however, tyrosine-to-phenylalanine HsGS mutants revealed that their sole nitration was not responsible for enzyme inactivation. In addition, we observed that ONOO- induced HsGS aggregation and activity loss. Thiol oxidation was a key modification to elicit aggregation, as it was also induced by hydrogen peroxide treatment. Taken together, our results indicate that multiple oxidative events at various sites are responsible for the inactivation and aggregation of human GS.

Constructing Nano-Heterostructure with Dual-Site to Boost H2O2 Activation and Regulate the Transformation of Free Radicals.

A major issue with Fenton-like reaction is the excessive consumption of H2O2 caused by the sluggish regeneration rate of low-valent metal, and how to improve the activation efficiency of H2O2 has become a key in current research. Herein, a nano-heterostructure catalyst (1.0-MnCu/C) based on nano-interface engineering is constructed by supporting Cu and MnO on carbon skeleton, and its kinetic rate for the degradation of tetracycline hydrochloride is 0.0436 min-1, which is 2.9 times higher than that of Cu/C system (0.0151 min-1). The enhancement of removal rate results from the introduced Mn species can aggregate and transfer electrons to Cu sites through the electron bridge Mn-N/O-Cu, thus preventing Cu2+ from oxidizing H2O2 to form O2 •-, and facilitating the reduction of Cu2+ and generating more reactive oxygen species (1O2 and ·OH) with stronger oxidation ability, resulting in H2O2 utilization efficiency is 1.9 times as much as that of Cu/C. Additionally, the good and stable practical application capacity in different bodies demonstrates that it has great potential for practical environmental remediation.

The white rot basidiomycete Gelatoporia subvermispora produces fatty aldehydes that enable fungal manganese peroxidases to degrade recalcitrant lignin structures.

The ability of some white rot basidiomycetes to remove lignin selectively from wood indicates that low molecular weight oxidants have a role in ligninolysis. These oxidants are likely free radicals generated by fungal peroxidases from compounds in the biodegrading wood. Past work supports a role for manganese peroxidases (MnPs) in the production of ligninolytic oxidants from fungal membrane lipids. However, the fatty acid alkylperoxyl radicals initially formed during this process are not reactive enough to attack the major structures in lignin. Here, we evaluate the hypothesis that the peroxidation of fatty aldehydes might provide a source of more reactive acylperoxyl radicals. We found that Gelatoporia subvermispora produced trans-2-nonenal, trans-2-octenal, and n-hexanal (a likely metabolite of trans-2,4-decadienal) during the incipient decay of aspen wood. Fungal fatty aldehydes supported the in vitro oxidation by MnPs of a nonphenolic lignin model dimer, and also of the monomeric model veratryl alcohol. Experiments with the latter compound showed that the reactions were partially inhibited by oxalate, the chelator that white rot fungi employ to detach Mn3+ from the MnP active site, but nevertheless proceeded at its physiological concentration of 1 mM. The addition of catalase was inhibitory, which suggests that the standard MnP catalytic cycle is involved in the oxidation of aldehydes. MnP oxidized trans-2-nonenal quantitatively to trans-2-nonenoic acid with the consumption of one O2 equivalent. The data suggest that when Mn3+ remains associated with MnP, it can oxidize aldehydes to their acyl radicals, and the latter subsequently add O2 to become ligninolytic acylperoxyl radicals.IMPORTANCEThe biodegradation of lignin by white rot fungi is essential for the natural recycling of plant biomass and has useful applications in lignocellulose bioprocessing. Although fungal peroxidases have a key role in ligninolysis, past work indicates that biodegradation is initiated by smaller, as yet unidentified oxidants that can infiltrate the substrate. Here, we present evidence that the peroxidase-catalyzed oxidation of naturally occurring fungal aldehydes may provide a source of ligninolytic free radical oxidants.

Deciphering the Potential Therapeutic Effects of Hydnocarpus wightianus Seed Extracts using in vitro and in silico approaches.

Phytocompounds possess the potential to treat a broad spectrum of disorders due to their remarkable bioactivity. Naturally occurring compounds possess lower toxicity profiles, which making them attractive targets for drug development. Hydnocarpus wightianus seeds were extracted using ethanol, acetone, and hexane solvents. The extracts were evaluated for phytochemicals screening and other therapeutic characteristics, such as free radicals scavenging, anti α-amylase, anti α-glucosidase, and anti-bacterial activities. The ethanolic extract exhibited noteworthy antibacterial characteristics and demonstrated considerable antioxidant, and anti-diabetic effects. The IC50 value of the ethanolic extract for Dpph, α-amylase, and α-glucosidase were found to be 77.299 ± 3.381 µg/mL, 165.56 2.56 µg/mL, and 136.58 ± 5.82 µg/mL, respectively. The ethanolic extract was effective against Methicillin resistant Staphylococcus aureus (26 mm zone of inhibition at 100 µL concentration). Molecular docking investigations revealed the phytoconstituent's inhibitory mechanisms against diabetic, free radicals, and bacterial activity. Docking score for phytocompounds against targeted protein varies from -7.2 to -5.1 kcal/mol. The bioactive compounds present in the ethanolic extract were identified by Gas chromatography/Mass spectrometry analysis, followed by molecular docking and molecular dynamic simulation studies to further explore the phytoconstituent's inhibitory mechanism of α-glucosidase, ∝-amylase, radical scavenging, and bacterial activity. The electronic structure and possible pharmacological actions of the phytocompound were revealed through the use of Density Functional Theory (DFT) analysis. Computational and in vitro studies revealed that these identified compounds have anti-diabetic, anti-oxidant, and anti-bacterial activities against antibiotic-resistant strain of Staphylococcus aureus.

Radiation-Induced Defects in Uranyl Trinitrate Solids.

Actinides are inherently radioactive; thus, ionizing radiation is emitted by these elements can have profound effects on its surrounding chemical environment through the formation of free radical species. While previous work has noted that the presence of free radicals in the system impacts the redox state of the actinides, there is little atomistic understanding of how these metal cations interact with free radicals. Herein, we explore the effects of radiation (UV and γ) on three U(VI) trinitrate complexes, M[UO2(NO3)3] (where M=K+, Rb+, Cs+), and their respective nitrate salts in the solid state via electron paramagnetic resonance (EPR) and Raman spectroscopy paired with Density Functional Theory (DFT) methods. We find that the alkali salts form nitrate radicals under UV and γ irradiation, but also note the presence of additional degradation products. M[UO2(NO3)3] solids also form nitrate radicals and additional DFT calculations indicate the species corresponds to a change from the bidentate bound nitrate anion into a monodentate NO3 • radical. Computational studies also highlight the need to include the second sphere coordination environment around the [UO2(NO3)3]0,1 species to gain agreement between the experimental and predicted EPR signatures.

Unravelling the Role of Free Radicals in Photocatalysis.

Free radicals are increasingly recognized as active intermediate reactive species that can participate in various redox processes, significantly influencing the mechanistic pathways of reactions. Numerous researchers have investigated the generation of one or more distinct photogenerated radicals, proposing various hypotheses to explain the reaction mechanisms. Notably, recent research has demonstrated the emergence of photogenerated radicals in innovative processes, including organic chemical reactions and the photocatalytic dissolution of precious metals. To harness the potential of these free radicals more effectively, it is imperative to consolidate and analyze the processes and action modes of these photogenerated radicals. This conceptual paper delves into the latest advancements in understanding the mechanics of photogenerated radicals.

3-bromopyruvate induces morphological alteration and may initiate programmed cell death in Cryptococcus neoformans cells.

3-Bromopyruvate (3BP), known for its potent anticancer properties, also exhibits remarkable efficacy against the pathogenic fungus Cryptococcus neoformans. So far it has been proven that the main fungicidal activity of 3BP is based on ATP depletion and a reduction of intracellular level of glutathione. The presented study includes a broad range of methods to further investigate the mechanistic effects of 3BP on C. neoformans cells. The use of flow cytometry allowed a thorough examination of their survival during 3BP treatment, while observations using electron microscopy made it possible to note the changes in cellular morphology. Utilizing ruthenium red, the study suggests a mitochondrial pathway may initiate programmed cell death in response to 3BP. Analysis of free radical generation and gene expression changes supports this hypothesis. These findings enhance comprehension of 3BP's mechanisms in fungal cells, paving the way for its potential application as a therapeutic agent against cryptococcosis.

Application of electron paramagnetic resonance spectroscopy for determining the relative nanoenvironment fluidity of polymeric micelles.

Polymeric micelles are nanocarriers for drug, protein and gene delivery due to their unique core/shell structure, which encapsulates and protects therapeutic cargos with diverse physicochemical properties. However, information regarding the micellar nanoenvironment's fluidity can provide unique insight into their makeup. In this study, we used electron paramagnetic resonance (EPR) spectroscopy to study free radical spin probe (5-doxylstearate methyl ester, 5-MDS, and 16-doxylstearic acid, 16-DS) behaviour in methoxy-poly(ethylene oxide)-poly(α-benzyl carboxylate-ε-caprolactone) (PEO-PBCL) and methoxy-poly(ethylene oxide)-poly(ε-caprolactone) (PEO-PCL) polymeric micelles. Spin probes provided information about the spectroscopic rotational correlation time (τ, s) and the spectroscopic partition parameter F. We hypothesized that spin probes would partition into the polymeric micelles, and these parameters would be calculated. The results showed that both 5-MDS and 16-DS spectra were modulated in the presence of polymeric micelles. Based on τ values, 5-MDS revealed that PEO-PCL (τ = 3.92 ± 0.26 × 10-8 s) was more fluid than PEO-PBCL (τ = 7.15 ± 0.63 × 10-8 s). The F parameter, however, could not be calculated due to the rotational hindrance of the probe within the micelles. With 16-DS, more probe rotation was observed, and although the F parameter could be calculated, it was not helpful to distinguish the micelles' fluidity. Also, doxorubicin-loading interfered with the spin probes, particularly for 16-DS. However, using simulations, we could distinguish the hydrophilic and hydrophobic components of the 16-DS probe. The findings suggest that EPR spectroscopy is a valuable method for determining core fluidity in polymeric micelles.

Implications of COVID-19 in Parkinson's disease: the purinergic system in a therapeutic-target perspective to diminish neurodegeneration.

The pathophysiology of Parkinson's disease (PD) is marked by degeneration of dopaminergic neurons in the substantia nigra. With advent of COVID-19, which is closely associated with generalized inflammation and multiple organ dysfunctions, the PD patients may develop severe conditions of disease leading to exacerbated degeneration. This condition is caused by the excessive release of pro-inflammatory markers, called cytokine storm, that is capable of triggering neurodegenerative conditions by affecting the blood-brain barrier (BBB). A possible SARS-CoV-2 infection, in serious cases, may compromise the immune system by triggering a hyperstimulation of the neuroimmune response, similar to the pathological processes found in PD. From this perspective, the inflammatory scenario triggers oxidative stress and, consequently, cellular dysfunction in the nervous tissue. The P2X7R seems to be the key mediator of the neuroinflammatory process, as it acts by increasing the concentration of ATP, allowing the influx of Ca2+ and the occurrence of mutations in the α-synuclein protein, causing activation of this receptor. Thus, modulation of the purinergic system may have therapeutic potential on the effects of PD, as well as on the damage caused by inflammation of the BBB, which may be able to mitigate the neurodegeneration caused by diseases. Considering all the processes of neuroinflammation, oxidative stress, and mitochondrial dysfunction that PD propose, we can conclude that the P2X7 antagonist acts in the prevention of viral diseases, and it also controls purinergic receptors formed by multi-target compounds directed to self-amplification circuits and, therefore, may be a viable strategy to obtain the desired disease-modifying effect. Thus, purinergic system receptor modulations have a high therapeutic potential for neurodegenerative diseases such as PD.

Oxidative stress disrupts vascular microenvironmental homeostasis affecting the development of atherosclerosis.

Atherosclerosis is primarily an inflammatory reaction of the cardiovascular system caused by endothelial damage, leading to progressive thickening and hardening of the vessel walls, as well as extensive necrosis and fibrosis of the surrounding tissues, the most necessary pathological process causing cardiovascular disease. When the body responds to harmful internal and external stimuli, excess oxygen free radicals are produced causing oxidative stress to occur in cells and tissues. Simultaneously, the activation of inflammatory immunological processes is followed by an elevation in oxygen free radicals, which directly initiates the release of cytokines and chemokines, resulting in a detrimental cycle of vascular homeostasis abnormalities. Oxidative stress contributes to the harm inflicted upon vascular endothelial cells and the decrease in nitric oxide levels. Nitric oxide is crucial for maintaining vascular homeostasis and is implicated in the development of atherosclerosis. This study examines the influence of oxidative stress on the formation of atherosclerosis, which is facilitated by the vascular milieu. It also provides an overview of the pertinent targets and pharmaceutical approaches for treating this condition.

Residential Wood Burning and Vehicle Emissions as Major Sources of Environmentally Persistent Free Radicals in Fairbanks, Alaska.

Environmentally persistent free radicals (EPFRs) play an important role in aerosol effects on air quality and public health, but their atmospheric abundance and sources are poorly understood. We measured EPFRs contained in PM2.5 collected in Fairbanks, Alaska, in winter 2022. We find that EPFR concentrations were enhanced during surface-based inversion and correlate strongly with incomplete combustion markers, including carbon monoxide and elemental carbon (R2 > 0.75). EPFRs exhibit moderately good correlations with PAHs, biomass burning organic aerosols, and potassium (R2 > 0.4). We also observe strong correlations of EPFRs with hydrocarbon-like organic aerosols, Fe and Ti (R2 > 0.6), and single-particle mass spectrometry measurements reveal internal mixing of PAHs, with potassium and iron. These results suggest that residential wood burning and vehicle tailpipes are major sources of EPFRs and nontailpipe emissions, such as brake wear and road dust, may contribute to the stabilization of EPFRs. Exposure to the observed EPFR concentrations (18 ± 12 pmol m-3) would be equivalent to smoking ∼0.4-1 cigarette daily. Very strong correlations (R2 > 0.8) of EPFR with hydroxyl radical formation in surrogate lung fluid indicate that exposure to EPFRs may induce oxidative stress in the human respiratory tract.

Photoaged Tire Wear Particles Leading to the Oxidative Damage on Earthworms (Eisenia fetida) by Disrupting the Antioxidant Defense System: The Definitive Role of Environmental Free Radicals.

Tire wear particles (TWPs) have caused increasing concerns due to their detrimental effects on the soil ecosystem. However, the role of weathering in altering the toxicity of TWP to soil organisms is poorly understood. In this study, the toxicity of original and photoaged TWP was compared using earthworms (Eisenia fetida) as soil model organisms. The obtained results indicated that photoaging of TWP resulted in an increase of environmentally persistent free radicals (EPFRs) from 3.69 × 1017 to 5.20 × 1017 spin/g. Meanwhile, photoaged TWP induced the changes of toxic endpoint in E. fetide, i.e., the increase of the weight loss and death ratio from 0.0425 to 0.0756 g/worm and 23.3 to 50% compared to original TWP under a 10% concentration, respectively. Analyses of transcriptomics, antioxidant enzyme activity, and histopathology demonstrated that the enhanced toxicity was mainly due to oxidative damage, which was induced by disruption in the antioxidant defense system. Free-radical quenching and correlation analysis further suggested that the excessive production of ex vivo reactive oxygen species, induced by EPFRs, led to the exhaustion of the antioxidant defense system. Overall, this work provides new insights into the potential hazard of the weathered TWP in a soil environment and has significant implications for the recycling and proper disposal of spent tire particles.

Unclassical Radical Generation Mechanisms in the Troposphere: A Review.

Hydroxyl (OH) and hydroperoxyl (HO2) radicals, collectively known as HOx radicals, are crucial in removing primary pollutants, controlling atmospheric oxidation capacity, and regulating global air quality and climate. An imbalance between radical observations and simulations has been identified based on radical closure experiments, a valuable tool for accessing the state-of-the-art chemical mechanisms, demonstrating a deviation between the existing and actual tropospheric mechanisms. In the past decades, researchers have attempted to explain this deviation and proposed numerous radical generation mechanisms. However, these newly proposed unclassical radical generation mechanisms have not been systematically reviewed, and previous radical-related reviews dominantly focus on radical measurement instruments and radical observations in extensive field campaigns. Herein, we overview the unclassical generation mechanisms of radicals, mainly focusing on outlining the methodology and results of radical closure experiments worldwide and systematically introducing the mainstream mechanisms of unclassical radical generation, involving the bimolecular reaction of HO2 and organic peroxy radicals (RO2), RO2 isomerization, halogen chemistry, the reaction of H2O with O2 over soot, epoxide formation mechanism, mechanism of electronically excited NO2 and water, and prompt HO2 formation in aromatic oxidation. Finally, we highlight the existing gaps in the current studies and suggest possible directions for future research. This review of unclassical radical generation mechanisms will help promote a comprehensive understanding of the latest radical mechanisms and the development of additional new mechanisms to further explain deviations between the existing and actual mechanisms.

Overlooked Roles and Transformation of Carbon-Centered Radicals Produced from Natural Organic Matter in a Thermally Activated Persulfate System.

The presence and induced secondary reactions of natural organic matter (NOM) significantly affect the remediation efficacy of in situ chemical oxidation (ISCO) systems. However, it remains unclear how this process relates to organic radicals generated from reactions between the NOM and oxidants. The study, for the first time, reported the vital roles and transformation pathways of carbon-centered radicals (CCR•) derived from NOM in activated persulfate (PS) systems. Results showed that both typical terrestrial/aquatic NOM isolates and collected NOM samples produced CCR• by scavenging activated PS and greatly enhanced the dehalogenation performance under anoxic conditions. Under oxic conditions, newly formed CCR• could be oxidized by O2 and generate organic peroxide intermediates (ROO•) to catalytically yield additional •OH without the involvement of PS. Nuclear magnetic resonance (NMR) and Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS) results indicated that CCR• predominantly formed from carboxyl and aliphatic structures instead of aromatics within NOM through hydrogen abstraction and decarboxylation reactions by SO4•- or •OH. Specific anoxic reactions (i.e., dehalogenation and intramolecular cross-coupling reactions) further promoted the transformation of CCR• to more unsaturated and polymerized/condensed compounds. In contrast, oxic propagation of ROO• enhanced bond breakage/ring cleavage and degradation of CCR• due to the presence of additional •OH and self-decomposition. This study provides novel insights into the role of NOM and O2 in ISCO and the development of engineered strategies for creating organic radicals capable of enhancing the remediation of specific contaminants and recovering organic carbon.

Reactive Oxygen Species Formation and Peroxide and Carbonyl Decomposition in Aqueous Photolysis of Secondary Organic Aerosols.

The mechanism and kinetics of reactive oxygen species (ROS) formation when atmospheric secondary organic aerosol (SOA) is exposed to solar radiation are poorly understood. In this study, we combined an in situ UV-vis irradiation system with electron paramagnetic resonance (EPR) spectroscopy to characterize the photolytic formation of ROS in aqueous extracts of SOA formed by the oxidation of isoprene, α-pinene, α-terpineol, and toluene. We observed substantial formation of free radicals, including •OH, superoxide (HO2•), and organic radicals (R•/RO•) upon irradiation. Compared to dark conditions, the radical yield was enhanced by a factor of ∼30 for •OH and by a factor of 2-10 for superoxide radicals, and we observed the emergence of organic radicals. Total peroxide measurements showed substantial decreases of peroxide contents after photoirradiation, indicating that organic peroxides can be an important source of the observed radicals. A liquid chromatography interfaced with high-resolution mass spectrometry was used to detect a number of organic radicals in the form of adducts with a spin trap, BMPO. The types of detected radicals and aqueous photolysis of model compounds indicated that photolysis of carbonyls by Norrish type I mechanisms plays an important role in the organic radical formation. The photolytic ROS formation serves as the driving force for cloud and fog processing of SOA.

Investigation of the Mechanism of Oxidative Potential Increase in Atmospheric Particulate Matter during Photoaging: Important Role of Aromatic Nitrogenous Compounds.

Particulate matter (PM) undergoing various aging processes in the atmosphere changes its toxicity. However, the mechanism of toxicity evolution is not fully clarified currently. This study demonstrates that photoaging promotes an increase in the oxidative potential (OP) of atmospheric PM by about 30%, and the increased OP is mainly attributed to the production of secondary organic compounds, while water-soluble metal ions contribute only 11%. The OP of nonextractable matters (NEMs) of atmospheric PM was mostly increased after photoaging, followed by water-soluble matters (WSMs). NEM can produce quinone-like functional groups and secondary persistent free radicals during photoaging, which are most likely to produce reactive oxygen species (ROS). For WSM, the conversion of low-oxidation humic-like substances (HULIS) to high-oxidation HULIS is the main reason for the increase in OP. Quinones, nitrophenols, and N-containing heterocycles are the OP contributors produced during the conversion process. Among them, quinones are the main secondary oxidizing active compounds, while nitro-phenolic compounds and N-containing heterocyclic compounds may play a catalyst-like role, facilitating the production of oxidizing active compounds and ROS in the newly converted high-oxidation HULIS. This study clarifies the secondary OP generation mechanism and provides new insights into the uncertainty of PM toxicity during atmospheric aging.