Modeling Peroxidase-Oxidase Interactions

2011 ◽  
Author(s):  
W. M. Schaffer ◽  
T. V. Bronnikova
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Low Concentrations ◽  
Wide Range ◽  
Regulatory Capacity ◽  
Episodic Nature ◽  
High Concentrations

Reactive oxygen species (ROS) and peroxidase-oxidase (PO) reactions are Janus-faced contributors to cellular metabolism. At low concentrations, reactive oxygen species serve as signaling molecules; at high concentrations, as destroyers of proteins, lipids and DNA. Correspondingly, PO reactions are both sources and consumers of ROS. In the present paper, we study a well-tested model of the PO reaction based on horseradish peroxidase chemistry. Our principal predictions are these: 1. Under hypoxia, the PO reaction can emit pulses of hydrogen peroxide at apparently arbitrarily long intervals. 2. For a wide range of input rates, continuing infusions of ROS are transduced into bounded dynamics. 3. The response to ROS input is hysteretic. 4. With sufficient input, regulatory capacity is exceeded and hydrogen peroxide, but not superoxide, accumulates. These results are discussed with regard to the episodic nature of neurodevelopmental and neurodegenerative diseases that have been linked to oxidative stress and to downstream interactions that may result in positive feedback and pathology of increasing severity.

scholarly journals Novel Antioxidant Properties of Doxycycline

2018 ◽  
Vol 19 (12) ◽  
pp. 4078 ◽  
Author(s):  
Dahn Clemens ◽  
Michael Duryee ◽  
Cleofes Sarmiento ◽  
Andrew Chiou ◽  
Jacob McGowan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Chronic Inflammation ◽  
Antioxidant Properties ◽  
Antibacterial Properties ◽  
Reactive Oxygen ◽  
Protein Adducts ◽  
Oxygen Species ◽  
Free System

Doxycycline (DOX), a derivative of tetracycline, is a broad-spectrum antibiotic that exhibits a number of therapeutic activities in addition to its antibacterial properties. For example, DOX has been used in the management of a number of diseases characterized by chronic inflammation. One potential mechanism by which DOX inhibits the progression of these diseases is by reducing oxidative stress, thereby inhibiting subsequent lipid peroxidation and inflammatory responses. Herein, we tested the hypothesis that DOX directly scavenges reactive oxygen species (ROS) and inhibits the formation of redox-mediated malondialdehyde-acetaldehyde (MAA) protein adducts. Using a cell-free system, we demonstrated that DOX scavenged reactive oxygen species (ROS) produced during the formation of MAA-adducts and inhibits the formation of MAA-protein adducts. To determine whether DOX scavenges specific ROS, we examined the ability of DOX to directly scavenge superoxide and hydrogen peroxide. Using electron paramagnetic resonance (EPR) spectroscopy, we found that DOX directly scavenged superoxide, but not hydrogen peroxide. Additionally, we found that DOX inhibits MAA-induced activation of Nrf2, a redox-sensitive transcription factor. Together, these findings demonstrate the under-recognized direct antioxidant property of DOX that may help to explain its therapeutic potential in the treatment of conditions characterized by chronic inflammation and increased oxidative stress.

scholarly journals Caffeic Acid - Potential Antioxidant in Cultured Human Retinal Pigment Epithelial Cells

1970 ◽  
Vol 66 (2) ◽  
Author(s):  
Dumitriţa RUGINǍ ◽  
Adela PINTEA ◽  
Raluca PÂRLOG ◽  
Andreea VARGA
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Caffeic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Defence ◽  
Rpe Cells ◽  
In Cells

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.

scholarly journals Impacts of Oxidative Stress and Antioxidants on Semen Functions

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Amrit Kaur Bansal ◽  
G. S. Bilaspuri
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Sperm Quality ◽  
Reactive Oxygen ◽  
The Body ◽  
Atp Depletion ◽  
Contributory Factor ◽  
Ros Generation ◽  
Oxygen Species ◽  
High Concentrations

Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.

scholarly journals Distinct Signaling Pathways Respond to Arsenite and Reactive Oxygen Species in Schizosaccharomyces pombe

2005 ◽  
Vol 4 (8) ◽  
pp. 1396-1402 ◽  
Author(s):  
Miguel A. Rodríguez-Gabriel ◽  
Paul Russell
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Schizosaccharomyces Pombe ◽  
Stress Responses ◽  
Biological Effects ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Increased Risk ◽  
Risk Of Cancer

ABSTRACT Exposure to certain metal and metalloid species, such as arsenic, cadmium, chromium, and nickel, has been associated with an increased risk of cancer in humans. The biological effects of these metals are thought to result from induction of reactive oxygen species (ROS) and inhibition of DNA repair enzymes, although alterations in signal transduction pathways may also be involved in tumor development. To better understand metal toxicity and its connection to ROS, we have compared the effects of arsenite and hydrogen peroxide in wild-type and mutant strains of the fission yeast Schizosaccharomyces pombe. An atf1Δ pap1Δ strain, which is defective in two transcription factors that control stress responses, is extremely sensitive to hydrogen peroxide but not to arsenite. A strain that lacks the transcription factor Zip1 has the opposite relationship. Spc1 (Sty1) mitogen-activated protein kinase (MAPK), a homologue of mammalian p38 MAPK, and the upstream MAPK kinase (MAPKK) Wis1 are essential for survival of both arsenite and hydrogen peroxide. Inactivation of two MAPKK kinases, Win1 and Wis4, almost completely eliminates Spc1 activation by arsenite, yet these cells survive arsenite treatment. The two-component phosphorelay protein Mcs4, which acts upstream of Win1 and Wis4 and is required for Spc1 activation in response to oxidative stress, is not required for Spc1 activation in response to arsenite. We conclude that the toxic effects of arsenic are not strongly connected to oxidative stress and that although Spc1 is activated by arsenic exposure, the basal activity of Spc1 is largely sufficient for the survival of arsenic.

scholarly journals The antimicrobial action of polyaniline involves production of oxidative stress while functionalisation of polyaniline introduces additional mechanisms

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5135 ◽  
Author(s):  
Julia Robertson ◽  
Marija Gizdavic-Nikolaidis ◽  
Michel K. Nieuwoudt ◽  
Simon Swift
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Atp Synthase ◽  
Acid Stress ◽  
Reactive Oxygen ◽  
Antimicrobial Action ◽  
Oxygen Species ◽  
E Coli ◽  
Production Of Hydrogen

Polyaniline (PANI) and functionalised polyanilines (fPANI) are novel antimicrobial agents whose mechanism of action was investigated.Escherichia colisingle gene deletion mutants revealed that the antimicrobial mechanism of PANI likely involves production of hydrogen peroxide while homopolymer poly(3-aminobenzoic acid), P3ABA, used as an example of a fPANI, disrupts metabolic and respiratory machinery, by targeting ATP synthase and causes acid stress. PANI was more active againstE. coliin aerobic, compared to anaerobic, conditions, while this was apparent for P3ABA only in rich media. Greater activity in aerobic conditions suggests involvement of reactive oxygen species. P3ABA treatment causes an increase in intracellular free iron, which is linked to perturbation of metabolic enzymes and could promote reactive oxygen species production. Addition of exogenous catalase protectedE. colifrom PANI antimicrobial action; however, this was not apparent for P3ABA treated cells. The results presented suggest that PANI induces production of hydrogen peroxide, which can promote formation of hydroxyl radicals causing biomolecule damage and potentially cell death. P3ABA is thought to act as an uncoupler by targeting ATP synthase resulting in a futile cycle, which precipitates dysregulation of iron homeostasis, oxidative stress, acid stress, and potentially the fatal loss of proton motive force.

Reactive oxygen species induce reversible PECAM-1 tyrosine phosphorylation and SHP-2 binding

2003 ◽  
Vol 285 (6) ◽  
pp. H2336-H2344 ◽  
Author(s):  
Matthias Maas ◽  
Ronggang Wang ◽  
Cathy Paddock ◽  
Srigiridhar Kotamraju ◽  
Balaraman Kalyanaraman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Tyrosine Phosphorylation ◽  
Tyrosine Phosphatase ◽  
Reactive Oxygen ◽  
Protein Tyrosine Phosphatases ◽  
Sh2 Domain ◽  
Oxygen Species ◽  
Protein Tyrosine ◽  
High Concentrations

Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) functions to control the activation and survival of the cells on which it is expressed. Many of the regulatory functions of PECAM-1 are dependent on its tyrosine phosphorylation and subsequent recruitment of the Src homology (SH2) domain containing protein tyrosine phosphatase SHP-2. The recent demonstration that PECAM-1 tyrosine phosphorylation occurs in cells exposed to the reactive oxygen species hydrogen peroxide (H2O2) suggested that this form of oxidative stress may also support PECAM-1/SHP-2 complex formation. In the present study, we show that PECAM-1 tyrosine phosphorylation in response to exposure of cells to H2O2 is reversible, involves a shift in the balance between kinase and phosphatase activities, and supports binding of SHP-2 and recruitment of this phosphatase to cell-cell borders. We speculate, however, that the unique ability of H2O2 to reversibly oxidize the reactive site cysteine residues of protein tyrosine phosphatases may result in transient inactivation of the SHP-2 that is bound to PECAM-1 under these conditions. Finally, we provide evidence that PECAM-1 tyrosine phosphorylation and SHP-2 binding in endothelial cells requires exposure to an “oxidative burst” of H2O2, but that exposure of these cells to sufficiently high concentrations of H2O2 for a sufficiently long period of time abrogates binding of SHP-2 to tyrosine-phosphorylated PECAM-1. These findings support a role for PECAM-1 as a sensor of oxidative stress, perhaps most importantly during the process of inflammation.

Induction ofPseudomonas aeruginosafhpandfhpRby reactive oxygen species

2009 ◽  
Vol 55 (6) ◽  
pp. 657-663 ◽  
Author(s):  
Taija S. Koskenkorva-Frank ◽  
Pauli T. Kallio
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Promoter Activity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Low Oxygen ◽  
Butyl Hydroperoxide ◽  
Tert Butyl Hydroperoxide ◽  
Oxygen Conditions

In Pseudomonas aeruginosa , flavohemoglobin (Fhp) and its cognate regulator FhpR (PA2665) form a protective regulatory circuit, which responds to reactive nitrogen species and is also capable of protecting cells against nitrosative stress. Recently, it has been shown that the expression of the fhp promoter is regulated not only by FhpR, but also by two new regulators, PA0779 and PA3697. It has also been suggested that the bacterial flavohemoglobins (flavoHbs) could play a crucial role in the protection of cells against reactive oxygen species (ROS). Therefore, the role and function of the Fhp/FhpR system during oxidative stress were studied by assessing the viability and membrane integrity of P. aeruginosa cells and by analyzing the promoter activities of fhp and fhpR upon exposure to paraquat, hydrogen peroxide, and tert-butyl hydroperoxide, under both aerobic and low-oxygen conditions. The results showed that under aerobic conditions, both fhp and fhpR promoters are induced by ROS generated by the stressors. Thus, the Fhp/FhpR system is implicated in the oxidative stress response. ROS-induced fhp promoter activity was dependent on FhpR, PA0779, and PA3697 regulators. Tert-butyl hydroperoxide-induced fhpR promoter activity was found to be highly repressed by PA0779, and FhpR showed negative autoregulation of its own promoter. Under low-oxygen conditions, the activity of the fhp promoter was not inducible by ROS, but fhpR promoter activity was induced by paraquat, and hydrogen peroxide was repressed in both cases by the regulators PA0779 and PA3697.

scholarly journals Extracellular Reactive Oxygen Species (ROS) Production in Fresh Donkey Sperm Exposed to Reductive Stress, Oxidative Stress and NETosis

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1367
Author(s):  
Iván Yánez-Ortiz ◽  
Jaime Catalán ◽  
Yentel Mateo-Otero ◽  
Marta Dordas-Perpinyà ◽  
Sabrina Gacem ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Selection Process ◽  
Reactive Oxygen ◽  
Polymorphonuclear Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Oxidative Stresses ◽  
Stress Oxidative

Jenny shows a large endometrial reaction after semen influx to the uterus with a large amount of polymorphonuclear neutrophils (PMN) migrating into the uterine lumen. PMN act as a sperm selection mechanism through phagocytosis and NETosis (DNA extrudes and, together with proteins, trap spermatozoa). While a reduced percentage of spermatozoa are phagocytosed by PMN, most are found to be attached to neutrophil extracellular traps (NETs). This selection process together with sperm metabolism produces a large amount of reactive oxygen species (ROS) that influence the reproductive success. The present study aimed to determine the extracellular ROS production in both sperm and PMN. With this purpose, (1) donkey sperm were exposed to reductive and oxidative stresses, through adding different concentrations of reduced glutathione (GSH) and hydrogen peroxide (H2O2), respectively; and (2) PMN were subjected to NETosis in the presence of the whole semen, sperm, seminal plasma (SP) or other activators such as formyl-methionyl-leucyl-phenylalanine (FMLP). Extracellular ROS production (measured as H2O2 levels) was determined with the Amplex® Red Hydrogen Peroxide/Peroxidase Assay Kit. Donkey sperm showed more resilience to oxidative stress than to the reductive one, and GSH treatments led to greater H2O2 extracellular production. Moreover, not only did SP appear to be the main inducer of NETosis in PMN, but it was also able to maintain the extracellular H2O2 levels produced by sperm and NETosis.

scholarly journals Oxidative stress and antioxidant mechanisms in human body

2019 ◽  
Vol 6 (1) ◽  
pp. 43-47
Author(s):  
Azab Elsayed Azab ◽  
 Almokhtar A Adwas ◽  
Ata Sedik Ibrahim Elsayed ◽  
Almokhtar A Adwas ◽  
 Ata Sedik Ibrahim Elsayed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Liver Diseases ◽  
Biological Activities ◽  
Heart Diseases ◽  
Reactive Oxygen ◽  
Ischemic Heart ◽  
Oxygen Species ◽  
Ischemic Heart Diseases ◽  
Wide Range

The present review aims to high light on the oxidative stress, and prevention by internal antioxidants and external antioxidants by some natural products possessing antioxidant properties. Oxidative stress occurs when the balance between reactive oxygen species (ROS) formation and detoxification favors an increase in ROS levels, leading to disturbed cellular function. ROS causes damage to cellular macromolecules causing lipid peroxidation, nucleic acid, and protein alterations. Their formation is considered as a pathobiochemical mechanism involved in the initiation or progression phase of various diseases such as atherosclerosis, ischemic heart diseases, diabetes, and initiation of carcinogenesis or liver diseases. In order to maintain proper cell signaling, it is likely that a number of radical scavenging enzymes maintain a threshold level of ROS inside the cell. However, when the level of ROS exceeds this threshold, an increase in ROS production may lead to excessive signals to the cell, in addition to direct damage to key components in signaling pathways. ROS can also irreversibly damage essential macromolecules. Protein-bound thiol and non-protein-thiol are the major cytosolic low molecular weight sulfhydryl compound that acts as a cellular reducing and a protective reagent against numerous toxic substances including most inorganic pollutants, through the –SH group. Hence, thiol is often the first line of defense against oxidative stress. Flavonoids have been found to play important roles in the non-enzymatic protection against oxidative stress, especially in the case of cancer. Flavonoids have occurred widely in tea, fruit, red wine, vegetables, and cocoas. Flavonoids, including flavones, flavanone, flavonols, and isoflavones, are polyphenolic compounds which are widespread in foods and beverages, and possess a wide range of biological activities, of which anti-oxidation has been extensively explored. It can be concluded that oxidative stress causes irreversible damage in cellular macromolecules that leads to initiation of various diseases such as atherosclerosis, ischemic heart diseases, liver diseases, diabetes, and initiation of carcinogenesis. Antioxidants inhibit reactive oxygen species production and scavenging of free radicals. Therefore, the review recommends that high consumption of natural foods that are rich in antioxidants will provide more protection against toxic agents and related diseases.

scholarly journals Resistance of nerve cells to oxidative injury

2011 ◽  
Vol 64 (7-8) ◽  
pp. 386-391 ◽  
Author(s):  
Zorica Jovanovic ◽  
Svetlana Jovanovic
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Neuronal Damage ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Brain Cell ◽  
Nerve Cells ◽  
Oxygen Species ◽  
The Brain

Introduction. Reactive oxygen species are particularly active in the brain and neuronal tissue, and they are involved in numerous cellular functions, including cell death and survival. Brain and oxidative stress. A high metabolic rate and an abundant supply of the transition metals make the brain an ideal target for a free radical attack. In addition, the brain has a high susceptibility to oxidative stress due to the high lipid content and relatively lower regenerative capacity in comparison with other tissues. Vulnerability of nerve cells to oxidative stress. The neurons are more vulnerable to oxidative stress than other brain cell types. In addition to the two conventional enzymes, catalase and glutathione peroxidase, peroxiredoxins remove intracellular hydrogen peroxide by reducing it to water. The recent work increasingly supports the hypothesis that peroxiredoxins are not only antioxidant proteins, but they also play a role in cell signaling by controlling hydrogen peroxide and alkyl hydroperoxide levels. The accumulating evidence demonstrates that microglia can become deleterious and damage neurons. The overactivated microglia release reactive oxygen species that cause neuronal damage in neurodegenerative diseases. Conclusion. The defense of nerve cells against reactive oxygen species - mediated oxidative damage is essential for maintaining the functionality of nerve cells. The ongoing studies show that neuron-glial compartmentalization of antioxidants is critical for the neuronal signaling by hydrogen peroxide as well as the neuronal protection.

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