-
Circulation Journal : Official Journal... 2012Reactive oxygen species (ROS) have long been viewed as deleterious chemicals that lead to oxidative stress. More recently, ROS, especially the stable ROS hydrogen... (Review)
Review
Reactive oxygen species (ROS) have long been viewed as deleterious chemicals that lead to oxidative stress. More recently, ROS, especially the stable ROS hydrogen peroxide (H(2)O(2)), have been shown to have roles in normal physiological responses in vascular cells. Endothelial nitric oxide synthase (eNOS) is dynamically targeted to plasmalemmal caveolae, and represents the principal enzymatic source of nitric oxide (NO(•)) in the vascular wall. eNOS maintains normal vascular tone and inhibits the clinical expression of many cardiovascular diseases. Increases in oxidative stress are associated with eNOS dysfunction. In a paradigm shift in the conceptual framework linking redox biochemistry and vascular function, H(2)O(2) has been established as a physiological mediator in signaling pathways, yet the intracellular sources of H(2)O(2) and their regulation remain incompletely understood. The subcellular distributions of ROS and of ROS-modified proteins critically influence the redox-sensitive regulation of eNOS-dependent pathways. ROS localization in specific subcellular compartments can lead to selective oxidative modifications of eNOS and eNOS-associated proteins. Likewise, the dynamic targeting of eNOS and other signaling proteins influences their interactions with reactive nitrogen species and ROS that are also differentially distributed within the cell. Thus, the subcellular distribution both of eNOS and redox-active biomolecules serves as a critical basis for the control of the "redox switch" that influences NO(•)- and oxidant-regulated signaling pathways. Here we discuss the biochemical factors, cellular determinants, and molecular mechanisms that modulate redox-sensitive regulation of eNOS and NO(•) signaling under normal and pathological conditions.
Topics: Animals; Cardiovascular Diseases; Caveolae; Gene Expression Regulation, Enzymologic; Humans; Hydrogen Peroxide; Nitric Oxide; Nitric Oxide Synthase Type III; Oxidants; Oxidation-Reduction; Signal Transduction
PubMed: 23075817
DOI: 10.1253/circj.cj-12-1207 -
Archives of Biochemistry and Biophysics Sep 2022Humans have widespread exposure to both oxidants, and soft electrophilic compounds such as alpha,beta-unsaturated aldehydes and quinones. Electrophilic motifs are... (Review)
Review
Humans have widespread exposure to both oxidants, and soft electrophilic compounds such as alpha,beta-unsaturated aldehydes and quinones. Electrophilic motifs are commonly found in a drugs, industrial chemicals, pollutants and are also generated via oxidant-mediated degradation of biomolecules including lipids (e.g. formation of 4-hydroxynonenal, 4-hydroxyhexenal, prostaglandin J2). All of these classes of compounds react efficiently with Cys residues, and the particularly the thiolate anion, with this resulting in Cys modification via either oxidation or adduct formation. This can result in deleterious or beneficial effects, that are either reversible (e.g. in cell signalling) or irreversible (damaging). For example, acrolein is a well-established toxin, whereas dimethylfumarate is used in the treatment of multiple sclerosis and psoriasis. This short review discusses the targets of alpha,beta-unsaturated aldehydes, and particularly two prototypic cases, acrolein and dimethylfumarate, and the factors that control the selectivity and kinetics of reaction of these species. Comparison is made between the reactivity of oxidants versus soft electrophiles. These rate constants indicate that electrophiles can be significant thiol modifying agents in some situations, as they have rate constants similar to or greater than species such as HO, can be present at higher concentrations, and are less efficiently removed by protective systems when compared to HO. They may also induce similar or higher levels of modification than highly reactive oxidants, due to the very low concentrations of oxidants formed in most in vivo situations.
Topics: Acrolein; Aldehydes; Cysteine; Dimethyl Fumarate; Humans; Hydrogen Peroxide; Kinetics; Oxidants
PubMed: 35777524
DOI: 10.1016/j.abb.2022.109344 -
Clinical Microbiology Reviews Jan 1997Reactive oxidant species (superoxide, hydrogen peroxide, hydroxyl radical, hypohalous acid, and nitric oxide) are involved in many of the complex interactions between... (Review)
Review
Reactive oxidant species (superoxide, hydrogen peroxide, hydroxyl radical, hypohalous acid, and nitric oxide) are involved in many of the complex interactions between the invading microorganism and its host. Regardless of the source of these compounds or whether they are produced under normal conditions or those of oxidative stress, these oxidants exhibit a broad range of toxic effects to biomolecules that are essential for cell survival. Production of these oxidants by microorganisms enables them to have a survival advantage in their environment. Host oxidant production, especially by phagocytes, is a counteractive mechanism aimed at microbial killing. However, this mechanism may be contribute to a deleterious consequence of oxidant exposure, i.e., inflammatory tissue injury. Both the host and the microorganism have evolved complex adaptive mechanisms to deflect oxidant-mediated damage, including enzymatic and nonenzymatic oxidant-scavenging systems. This review discusses the formation of reactive oxidant species in vivo and how they mediate many of the processes involved in the complex interplay between microbial invasion and host defense.
Topics: Animals; Bacteria; Bacterial Infections; Fungi; Humans; Hydrogen Peroxide; Immunity, Innate; Iron; Mycoses; Nitric Oxide; Oxidants; Parasites; Parasitic Diseases; Peroxidase; Phagocytosis; Superoxides; Virus Diseases; Viruses
PubMed: 8993856
DOI: 10.1128/CMR.10.1.1 -
TheScientificWorldJournal 2015The use of optical radiation for the activation of bleaching products has not yet been completely elucidated. Laser light is suggested to enhance the oxidizing effect of... (Review)
Review
The use of optical radiation for the activation of bleaching products has not yet been completely elucidated. Laser light is suggested to enhance the oxidizing effect of hydrogen peroxide. Different methods of enhancing hydrogen peroxide based bleaching are possible. They can be classified into six groups: alkaline pH environment, thermal enhancement and photothermal effect, photooxidation effect and direct photobleaching, photolysis effect and photodissociation, Fenton reaction and photocatalysis, and photodynamic effect.
Topics: Animals; Dental Enamel; Humans; Hydrogen Peroxide; Lasers, Solid-State; Low-Level Light Therapy; Oxidants; Tooth Bleaching; Tooth Bleaching Agents
PubMed: 25874251
DOI: 10.1155/2015/650492 -
Brain Pathology (Zurich, Switzerland) Jan 1999Fifty years after the advent of antibiotics for clinical use, the rates of morbidity and mortality associated with bacterial meningitis remain high. The unfavourable... (Review)
Review
Fifty years after the advent of antibiotics for clinical use, the rates of morbidity and mortality associated with bacterial meningitis remain high. The unfavourable clinical outcome is often due to intracranial complications including cerebrovascular insults, raised intracranial pressure, hydrocephalus, and brain edema. Reactive oxygen species (ROS) are known effector molecules in the antimicrobial armature of polymorphonuclear and mononuclear phagocytes. However, over the last decade, there has been a substantial body of work implicating a central role of ROS in the development of intracranial complications and brain damage in bacterial meningitis. Recently, it also became evident that reactive nitrogen species (RNS), especially nitric oxide, are important mediators of meningitis-associated pathophysiological changes, at least during the early phase of the disease. There is now substantial evidence that much of the oxidative injury associated by simultaneous production of superoxide and nitric oxide is mediated by the strong oxidant peroxynitrite. ROS and peroxynitrite can be cytotoxic via a number of independent mechanisms. Their cytotoxic effects include initiation of lipid peroxidation and induction of DNA single strand breakage. Damaged DNA activates poly(ADP-ribose) polymerase (PARP). Recent experimental data propose a role of lipid peroxidation and PARP activation in the development of meningitis-associated intracranial complications and brain injury. Agents which interfere with the production of ROS and peroxynitrite, as well as with PARP activation and lipid peroxidation may represent novel, therapeutic strategies to limit meningitis-associated brain damage, and, thus, to improve the outcome of this serious disease.
Topics: Animals; Brain Injuries; Host-Parasite Interactions; Humans; Lipid Peroxidation; Meningitis, Bacterial; Nitrates; Nitric Oxide; Oxidants; Oxidative Stress; Poly(ADP-ribose) Polymerases; Reactive Oxygen Species
PubMed: 9989452
DOI: 10.1111/j.1750-3639.1999.tb00211.x -
Journal of Environmental Management Nov 2023Disinfection and decontamination of water by application of oxidisers is an essential treatment step across numerous industrial sectors including potable supply and... (Review)
Review
Disinfection and decontamination of water by application of oxidisers is an essential treatment step across numerous industrial sectors including potable supply and industry waste management, however, could be greatly enhanced if operated as advanced oxidation processes (AOPs). AOPs destroy contaminants including pathogens by uniquely harnessing radical chemistry. Despite AOPs offer great practical opportunities, no reviews to date have highlighted the critical AOP virtues that facilitate AOPs' scale up under growing industrial demand. Hence, this review analyses the critical AOP parameters such as oxidant conversion efficiency, batch mode vs continuous-flow systems, location of radical production, radical delivery by advanced micro-/mesoporous structures and AOP process costs to assist the translation of progressing developments of AOPs into their large-scale applications. Additionally, the state of the art is analysed for various AOP inducing radical/oxidiser measurement techniques and their half-lives with a view to identify radicals/oxidisers that are suitable for in-situ production. It is concluded that radicals with short half-lives such as hydroxyl (10 μsec) and sulfate (30-40 μsec) need to be produced in-situ via continuous-flow reactors for their effective transport and dosing. Meanwhile, radicals/oxidisers with longer half-lives such as ozone (7-10 min), hydrogen peroxide (stable for several hours), and hypochlorous acid (10 min -17 h) need to be applied through batch reactor systems due to their relatively longer stability during transportation and dosing. Complex and costly synthesis as well as cytotoxicity of many micro-/mesoporous structures limit their use in scaling up AOPs, particularly to immobilising and delivering the short-lived hydroxyl and sulfate radicals to their point of applications. Overall, radical delivery using safe and advanced biocompatible micro-/mesoporous structures, radical conversion efficiency using advanced reactor design and portability of AOPs are priority areas of development for scaling up to industry.
Topics: Oxidation-Reduction; Oxidants; Disinfection; Hydrogen Peroxide; Hydroxyl Radical; Sulfates
PubMed: 37651902
DOI: 10.1016/j.jenvman.2023.118861 -
Brain Pathology (Zurich, Switzerland) Jan 1999This review summarises the role that reactive oxygen and nitrogen species play in demyelination, such as that occurring in the inflammatory demyelinating disorders... (Review)
Review
This review summarises the role that reactive oxygen and nitrogen species play in demyelination, such as that occurring in the inflammatory demyelinating disorders multiple sclerosis and Guillain-Barré syndrome. The concentrations of reactive oxygen and nitrogen species (e.g. superoxide, nitric oxide and peroxynitrite) can increase dramatically under conditions such as inflammation, and this can overwhelm the inherent antioxidant defences within lesions. Such oxidative and/or nitrative stress can damage the lipids, proteins and nucleic acids of cells and mitochondria, potentially causing cell death. Oligodendrocytes are more sensitive to oxidative and nitrative stress in vitro than are astrocytes and microglia, seemingly due to a diminished capacity for antioxidant defence, and the presence of raised risk factors, including a high iron content. Oxidative and nitrative stress might therefore result in vivo in selective oligodendrocyte death, and thereby demyelination. The reactive species may also damage the myelin sheath, promoting its attack by macrophages. Damage can occur directly by lipid peroxidation, and indirectly by the activation of proteases and phospholipase A2. Evidence for the existence of oxidative and nitrative stress within inflammatory demyelinating lesions includes the presence of both lipid and protein peroxides, and nitrotyrosine (a marker for peroxynitrite formation). The neurological deficit resulting from experimental autoimmune demyelinating disease has generally been reduced by trial therapies intended to diminish the concentration of reactive oxygen species. However, therapies aimed at diminishing reactive nitrogen species have had a more variable outcome, sometimes exacerbating disease.
Topics: Animals; Antioxidants; Demyelinating Diseases; Humans; Inflammation; Lipid Peroxidation; Nervous System; Nitrates; Nitric Oxide; Oxidants; Oxidative Stress; Reactive Oxygen Species
PubMed: 9989453
DOI: 10.1111/j.1750-3639.1999.tb00212.x -
Nature Communications May 2022Removal of organic micropollutants from water through advanced oxidation processes (AOPs) is hampered by the excessive input of energy and/or chemicals as well as the...
Removal of organic micropollutants from water through advanced oxidation processes (AOPs) is hampered by the excessive input of energy and/or chemicals as well as the large amounts of residuals resulting from incomplete mineralization. Herein, we report a new water purification paradigm, the direct oxidative transfer process (DOTP), which enables complete, highly efficient decontamination at very low dosage of oxidants. DOTP differs fundamentally from AOPs and adsorption in its pollutant removal behavior and mechanisms. In DOTP, the nanocatalyst can interact with persulfate to activate the pollutants by lowering their reductive potential energy, which triggers a non-decomposing oxidative transfer of pollutants from the bulk solution to the nanocatalyst surface. By leveraging the activation, stabilization, and accumulation functions of the heterogeneous catalyst, the DOTP can occur spontaneously on the nanocatalyst surface to enable complete removal of pollutants. The process is found to occur for diverse pollutants, oxidants, and nanocatalysts, including various low-cost catalysts. Significantly, DOTP requires no external energy input, has low oxidant consumption, produces no residual byproducts, and performs robustly in real environmental matrices. These favorable features render DOTP an extremely promising nanotechnology platform for water purification.
Topics: Decontamination; Environmental Pollutants; Oxidants; Water; Water Pollutants, Chemical
PubMed: 35637224
DOI: 10.1038/s41467-022-30560-9 -
F1000Research 2019Hypochlorous acid (HOCl; bleach) is a powerful weapon used by our immune system to eliminate invading bacteria. Yet the way HOCl actually kills bacteria and how they... (Review)
Review
Hypochlorous acid (HOCl; bleach) is a powerful weapon used by our immune system to eliminate invading bacteria. Yet the way HOCl actually kills bacteria and how they defend themselves from its oxidative action have only started to be uncovered. As this molecule induces both protein oxidation and aggregation, bacteria need concerted efforts of chaperones and antioxidants to maintain proteostasis during stress. Recent advances in the field identified several stress-activated chaperones, like Hsp33, RidA, and CnoX, which display unique structural features and play a central role in protecting the bacterial proteome during HOCl stress.
Topics: Bacteria; Bacterial Infections; Bacterial Proteins; Humans; Hypochlorous Acid; Molecular Chaperones; Oxidants; Oxidation-Reduction; Proteolysis; Stress, Physiological
PubMed: 31583082
DOI: 10.12688/f1000research.19517.1 -
Biochimica Et Biophysica Acta May 1995Reactive oxygen species (ROS: superoxide radical, O2.-; hydrogen peroxide, H2O2; hydroxyl radical, OH.), which arise from the univalent reduction of dioxygen are formed... (Review)
Review
Reactive oxygen species (ROS: superoxide radical, O2.-; hydrogen peroxide, H2O2; hydroxyl radical, OH.), which arise from the univalent reduction of dioxygen are formed in mitochondria. We summarize here results which indicate that ROS, and also the radical nitrogen monoxide ('nitric oxide', NO), act as physiological modulators of some mitochondrial functions, but may also damage mitochondria. Hydrogen peroxide, which originates in mitochondria predominantly from the dismutation of superoxide, causes oxidation of mitochondrial pyridine nucleotides and thereby stimulates a specific Ca2+ release from intact mitochondria. This release is prevented by cyclosporin A (CSA). Hydrogen peroxide thus contributes to the maintenance of cellular Ca2+ homeostasis. A stimulation of mitochondrial ROS production followed by an enhanced Ca2+ release and re uptake (Ca2+ 'cycling') by mitochondria causes apoptosis and necrosis, and contributes to hypoxia/reperfusion injury. These kinds of cell injury can be attenuated at the mitochondrial level by CSA. When ROS are produced in excessive amounts in mitochondria nucleic acids, proteins, and lipids are extensively modified by oxidation. Physiological (sub-micromolar) concentrations of NO potently and reversibly deenergize mitochondria at oxygen tensions that prevail in cells by transiently binding to cytochrome oxidase. This is paralleled by mitochondrial Ca2+ release and uptake. Higher NO concentrations or prolonged exposure of cells to NO causes their death. It is concluded that ROS and NO are important physiological reactants in mitochondria and become toxic only when present in excessive amounts.
Topics: Animals; Apoptosis; Calcium; Cell Survival; Disease; Glutathione; Humans; Liver; Mitochondria; Nitric Oxide; Nitroso Compounds; Oxidants; Oxidative Stress; Reactive Oxygen Species; Reference Values; S-Nitrosoglutathione
PubMed: 7599228
DOI: 10.1016/0925-4439(95)00012-s