scholarly journals Peroxidase activity of hemoglobin and heme destruction in the presence of hydrogen peroxide and CT-DNA

2020 ◽  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Peroxidase Activity ◽  
Hypochlorous Acid ◽  
Iron Ion ◽  
Acid Effect ◽  
High Concentrations ◽  
Ct Dna ◽  
Heme Destruction ◽  
Protein Environment

The aim of this study was to investigate the peroxidase activity of Hb with different concentrations of hydrogen peroxide and compare it with hypochlorous acid effect on Hb. Hypochlorous acid at higher concentrations decomposed Hb and heme, releasing fee iron ion from the metal center. High concentrations of hydrogen peroxide switched the peroxidase activity of Hb towards the partial Hb and heme destruction. Heme alone was degraded showing that the Hb conformation and protein environment protects Hb from the distraction in the presence of highly increased hydrogen peroxide concentration that occurs as a result of oxidative stress. In the presence of CT-DNA acted inhibition of the peroxidase activity of Hb was observed signaling inhibited hydrogen peroxide consumption.

scholarly journals Antioxidant Protection by American Ginseng in Pancreatic ß-Cells

2008 ◽  
Vol 36 (05) ◽  
pp. 981-988 ◽  
Author(s):  
Elaine Lin ◽  
Yong Wang ◽  
Sangeeta Mehendale ◽  
Shi Sun ◽  
Chong-Zhi Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
American Ginseng ◽  
Antioxidant Protection ◽  
Ginsenoside Re ◽  
Peripheral Tissues ◽  
Glucose Levels ◽  
Reduce Blood Glucose ◽  
Dichlorofluorescin Diacetate ◽  
High Concentrations

Hyperglycemia in diabetic conditions may cause oxidative stress in pancreatic ß-cells, leading to their dysfunction and insulin resistance within peripheral tissues. Previous studies suggest that American ginseng berry extract may have hypoglycemic effects, as well as offer antioxidant protection. We examined effects of American ginseng berry extract and ginsenoside Re in a pancreatic ß-cell line, MIN-6, to determine if these two properties are related. Cells were exposed to oxidative stress via hydrogen peroxide incubation and oxidative stress was measured by oxidation of 2′,7′-dichlorofluorescin diacetate. These cells showed a concentration-related response to hydrogen peroxide at 100–500 μM. In acute conditions where cells were treated with the extract for 10 min, we observed reduced oxidant injury suggesting direct scavenging effects. Chronic incubation of cells with the extract for 48 hours also demonstrated attenuation of oxidative stress. At high concentrations, Re showed a mild antioxidant effect in MIN-6 cells. Our insulin release observations also showed that the extract may help to increase insulin secretions from the cells. Our data suggest that the observed ability of ginseng to reduce blood glucose levels may be linked to its antioxidant effects on pancreatic ß-cells.

ROLE OF PREGNAN-X-RECEPTOR IN CELL RESISTANCE TO NITROSATIVE AND OXIDATIVE STRESS

2021 ◽  
Author(s):  
Yulia Abalenikhina ◽  
◽  
Elena A. Sudakova ◽  
Pelageya Erokhina ◽  
Aleksey Shchulkin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Nitrosative Stress ◽  
Pregnane X Receptor ◽  
Cell Resistance ◽  
Oxidative And Nitrosative Stress ◽  
High Concentrations ◽  
And Oxidative Stress

The article discusses the new role of pregnane X receptor (PXR) under conditions of oxidative and nitrosative stress. The results showed that the effect of hydrogen peroxide and S-nitrosoglu-tathione in high concentrations on Caco-2 cells leads to a decrease in cell viability, which is accompanied by an increase in the amount of PXR. These changes are offset by the addition of ketoconazole (inhibitor of PXR) to the medium.

scholarly journals The antioxidant action of taurine, hypotaurine and their metabolic precursors

1988 ◽  
Vol 256 (1) ◽  
pp. 251-255 ◽  
Author(s):  
O I Aruoma ◽  
B Halliwell ◽  
B M Hoey ◽  
J Butler
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Radical ◽  
Hypochlorous Acid ◽  
Cysteic Acid ◽  
Iron Ions ◽  
Antioxidant Action ◽  
Iron Ion ◽  
Metabolic Precursors ◽  
Sufficient Concentration

It has been suggested that taurine, hypotaurine and their metabolic precursors (cysteic acid, cysteamine and cysteinesulphinic acid) might act as antioxidants in vivo. The rates of their reactions with the biologically important oxidants hydroxyl radical (.OH), superoxide radical (O2.-), hydrogen peroxide (H2O2) and hypochlorous acid (HOCl) were studied. Their ability to inhibit iron-ion-dependent formation of .OH from H2O2 by chelating iron ions was also tested. Taurine does not react rapidly with O2.-, H2O2 or .OH, and the product of its reaction with HOCl is still sufficiently oxidizing to inactivate alpha 1-antiproteinase. Thus it seems unlikely that taurine functions as an antioxidant in vivo. Cysteic acid is also poorly reactive to the above oxidizing species. By contrast, hypotaurine is an excellent scavenger of .OH and HOCl and can interfere with iron-ion-dependent formation of .OH, although no reaction with O2.- or H2O2 could be detected within the limits of our assay techniques. Cysteamine is an excellent scavenger of .OH and HOCl; it also reacts with H2O2, but no reaction with O2.- could be measured within the limits of our assay techniques. It is concluded that cysteamine and hypotaurine are far more likely to act as antioxidants in vivo than is taurine, provided that they are present in sufficient concentration at sites of oxidant generation.

scholarly journals Carnosine, homocarnosine and anserine: could they act as antioxidants in vivo?

1989 ◽  
Vol 264 (3) ◽  
pp. 863-869 ◽  
Author(s):  
O I Aruoma ◽  
M J Laughton ◽  
B Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Hypochlorous Acid ◽  
Thiobarbituric Acid ◽  
Structural Similarity ◽  
Iron Ion ◽  
Inhibitory Effects ◽  
Inhibit Lipid Peroxidation ◽  
High Concentrations ◽  
Radical Damage

Carnosine, homocarnosine and anserine have been proposed to act as antioxidants in vivo. Our studies show that all three compounds are good scavengers of the hydroxyl radical (.OH) but that none of them can react with superoxide radical, hydrogen peroxide or hypochlorous acid at biologically significant rates. None of them can bind iron ions in ways that interfere with ‘site-specific’ iron-dependent radical damage to the sugar deoxyribose, nor can they restrict the availability of Cu2+ to phenanthroline. Homocarnosine has no effect on iron ion-dependent lipid peroxidation; carnosine and anserine have weak inhibitory effects when used at high concentrations in some (but not all) assay systems. However, the ability of these compounds to interfere with a commonly used version of the thiobarbituric acid (TBA) test may have led to an overestimate of their ability to inhibit lipid peroxidation in some previous studies. By contrast, histidine stimulated iron ion-dependent lipid peroxidation. It is concluded that, because of the high concentrations present in vivo, carnosine and anserine could conceivably act as physiological antioxidants by scavenging .OH, but that they do not have a broad spectrum of antioxidant activity, and their ability to inhibit lipid peroxidation is not well established. It may be that they have a function other than antioxidant protection (e.g. buffering), but that they are safer to accumulate than histidine, which has a marked pro-oxidant action upon iron ion-dependent lipid peroxidation. The inability of homocarnosine to react with HOCl, interfere with the TBA test or affect lipid peroxidation systems in the same way as carnosine is surprising in view of the apparent structural similarity between these two molecules.

scholarly journals Use of H2O2 to Cause Oxidative Stress, the Catalase Issue

2020 ◽  
Vol 21 (23) ◽  
pp. 9149
Author(s):  
Céline Ransy ◽  
Clément Vaz ◽  
Anne Lombès ◽  
Frédéric Bouillaud
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Oxygen Concentration ◽  
H2o2 Concentration ◽  
High Concentrations ◽  
Polarographic Measurement ◽  
H2o2 Addition

Addition of hydrogen peroxide (H2O2) is a method commonly used to trigger cellular oxidative stress. However, the doses used (often hundreds of micromolar) are disproportionally high with regard to physiological oxygen concentration (low micromolar). In this study using polarographic measurement of oxygen concentration in cellular suspensions we show that H2O2 addition results in O2 release as expected from catalase reaction. This reaction is fast enough to, within seconds, decrease drastically H2O2 concentration and to annihilate it within a few minutes. Firstly, this is likely to explain why recording of oxidative damage requires the high concentrations found in the literature. Secondly, it illustrates the potency of intracellular antioxidant (H2O2) defense. Thirdly, it complicates the interpretation of experiments as subsequent observations might result from high/transient H2O2 exposure and/or from the diverse possible consequences of the O2 release.

scholarly journals The antioxidant action of human extracellular fluids. Effect of human serum and its protein components on the inactivation of α1-antiproteinase by hypochlorous acid and by hydrogen peroxide

1987 ◽  
Vol 243 (1) ◽  
pp. 219-223 ◽  
Author(s):  
M Wasil ◽  
B Halliwell ◽  
D C S Hutchison ◽  
H Baum
Keyword(s):  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Hydroxyl Radicals ◽  
Hypochlorous Acid ◽  
Antioxidant Action ◽  
Serum Samples ◽  
Inhibitory Capacity ◽  
Low Concentrations ◽  
High Concentrations ◽  
Protein Components

The elastase-inhibitory capacity of purified human alpha 1-antiproteinase is inactivated by low concentrations of the myeloperoxidase-derived oxidant hypochlorous acid, but much higher concentrations are required to inhibit the elastase-inhibitory capacity of serum samples. The protective effect of serum appears to be largely due to albumin. High concentrations of H2O2 also inactivate the elastase-inhibitory capacity of alpha 1-antiproteinase, by a mechanism not involving formation of hydroxyl radicals. Serum offers protection against H2O2 inactivation of alpha 1-antiproteinase. The relevance of these results to the tissue damage produced by activated phagocytes is discussed.

scholarly journals The impact of oxidative stress on the neurotoxic effect of acetaminophen

2019 ◽  
Vol 59 (9) ◽  
pp. 106-109
Author(s):  
Ksenia A. Zagorodnikova ◽  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Neurotoxic Effect ◽  
Mtt Method ◽  
Culture Viability ◽  
Negative Effect ◽  
High Concentrations ◽  
Pharmacologically Active ◽  
The Impact

Paracetamol (acetaminophen, APAP) is a commonly-used antipyretic and analgesic. However, there have been reports indicating possible link between its use in pregnancy and impaired neuropsychic development in children. A number of prospective studies of the possible negative effect of acetaminophen on the development of a child after his mother took this drug during pregnancy, as well as the results of studies on glioma cells and neurons in murine cortex, may indicate presence of the neurotoxic effect of acetaminophen. It is currently unclear if paracetamol itself being pharmacologically active neurotropic substance, or its metabolites, one of which – NAPQI (N-acetyl-p-benzoquinone imine) known by its toxic effects in mitochindria, play the most significant role in proposed neurotoxicity. Therefore it seems important to study each metabolite separately. The ability of acetaminophen(paracetamol) in concentrations of 1 mg/ml and 2 mg/ml to reduce cell viability was shown on cells of the PC12 neuronal line using MTT-method, which is based on the ability of mitochondria of viable cells to restore formazan 3-(4,5-dimethylthiazole)-2,5-diphenyl-2-tetrazolium bromide (MTT). Concentrations of 0.125 mg/ml, 0.25 mg/ml and 0.5 mg/ml had no similar impact on cell culture viability. In addition, the impact of hydrogen peroxide (as an inducer of oxidative stress) on the neurotoxic effect of acetaminophen was studied. We demonstrated that in the presence of 0.3 mM or 0.5 mM hydrogen peroxide and acetaminophen in concentrations of 1 mg/ml and 2 mg/ml reliably reduced the percentage of surviving cells. We showed that the decrease of the viability of the cells of the PC12 neuronal line is obvious only after exposure to high concentrations of acetaminophen, especially in the presence of hydrogen peroxide, which means that neurotoxic effect is not likely to occur in vivo.

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.

Abstract 239: Parthanatos is Involved in Hydrogen Peroxide Induced Vascular Smooth Muscle Cell Death

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Conner C Feldman ◽  
Ting Zhou ◽  
Noel Phan ◽  
Bo Liu
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
High Concentrations ◽  
Parp 1 ◽  
Necrotic Response

Objectives: Oxidative stress underlies major vascular diseases including atherosclerosis and abdominal aortic aneurysm. Hydrogen peroxide (H2O2) is widely used to trigger oxidative stress in vitro for the study of apoptosis. However, we have previously shown that vascular smooth muscle cells (SMCs) respond to high concentrations (>1 mM) of H2O2 with necrosis. Traditionally regarded as incidental form of cell death, necrosis can occur through different mechanisms mediated by distinct intracellular signaling networks. The precise knowledge of death pathway is essential to the design of therapeutic strategy targeting cell death. The goal of the current study is to determine how H2O2 induces necrosis in SMCs. Methods: Mouse vascular aortic smooth muscle cell line, MOVAS, were treated with 3mM H2O2 for 2 hours, after which cell death was analyzed using flow cytometry and protein expression determined via western blot. Results: SMCs underwent apoptosis and necrosis in response to 0.3 and 3 mM H2O2, respectively. The 3mM H2O2 group died via a caspase-independent mechanism. Expression of common autophagy-associated proteins were unaffected. Additionally, different autophagy activators and inhibitors only moderately facilitated the pro-necrotic effect of H2O2. The H2O2-induced necrosis was not affected by necroptosis inhibitors including necrostatin-1s or by SiRNA silencing of necroptosis mediators RIP1, RIP3 and MLKL. Furthermore, ferroptosis and CypD inhibitors did not provide protection from necrosis induced by H2O2. In contrast, the necrotic response was attenuated by the PARP-1 inhibitor 3-aminobenzamide (37.10±13.72% vs 82.05±0.64%). Moreover, an PARP1 siRNA also reduced necrosis. PARP-1 is the central mediator of a necroptosis mechanism called parthanatos. Conclusions: Our data demonstrates that parthanatos constitutes a major mechanism underlying the necrotic response to high concentrations of H2O2. Current studies delineate the involvement of parthanatos in myocardial ischemia/reperfusion injury, cardiovascular ailments, and atherosclerosis. The present study may provide a new perspective on targeting PARP-1 for the protection of SMCs and likely cardiac myocytes against oxidative stress.

Visualizing hypochlorous acid production by human neutrophils with fluorescent graphene quantum dots

2021 ◽  
Author(s):  
Lena Golubewa ◽  
Tatsiana Kulahava ◽  
Aliona Klimovich ◽  
Danielis Rutkauskas ◽  
Ieva Matulaitiene ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Quantum Dots ◽  
Biomedical Applications ◽  
Fluorescence Spectra ◽  
Hypochlorous Acid ◽  
Graphene Quantum Dots ◽  
Cellular Systems ◽  
Human Neutrophils ◽  
High Concentrations ◽  
Living Organisms

Abstract In living organisms, redox reactions play a crucial role in the progression of disorders accompanied by the overproduction of reactive oxygen and reactive chlorine species, such as hydrogen peroxide and hypochlorous acid, respectively. We demonstrate that green fluorescence graphene quantum dots (GQDs) can be employed for revealing the presence of the hypochlorous acid in aqueous solutions and cellular systems. Hypochlorous acid modifies the oxygen-containing groups of the GQD, predominantly opens epoxide rind C–O–C, forms excessive C=O bonds and damages the carbonic core of GQDs. These changes, which depend on the concentration of the hypochlorous acid and exposure time, manifest themselves in the absorbance and fluorescence spectra of the GQD, and in the fluorescence lifetime. We also show that the GQD fluorescence is not affected by hydrogen peroxide. This finding makes GQDs a promising sensing agent for selective detecting reactive chlorine species produced by neutrophils. Neutrophils actively accumulate GQDs allowing to visualize cells and to examine the redox processes via GQDs fluorescence. At high concentrations GQDs induce neutrophil activation and myeloperoxidase release, leading to the disruption of GQD structure by the produced hypochlorous acid. This makes the GQDs a biodegradable material suitable for various biomedical applications.

Sign in / Sign up

Export Citation Format

Share Document