Production of superoxide anion and hydrogen peroxide by KB cells in an anoxia-reoxygenation model, and role of allopurinol

This paper presents an experimental study of biocorrosion of D16T and AMg6 aluminum alloys. The determining role of reactive oxygen species in aluminum biocorrosion by a consortium of molds has been shown. A model is proposed, according to which the initiators of corrosion damage to the metal surface are superoxide anion radical and hydrogen peroxide released during the life of micromycetes. It is assumed that the initiation and development of biocorrosion occurs, among other things, as a result of the process of reductive activation of oxygen and the Fenton decomposition of hydrogen peroxide. A conclusion is made about the mechanism of the occurrence of intergranular and pitting corrosion of aluminum alloys interacting with microscopic fungi.

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The Antioxidant Machinery of Young and Senescent Human Umbilical Vein Endothelial Cells and Their Microvesicles

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/7094781 ◽

2017 ◽

Vol 2017 ◽

pp. 1-12 ◽

Cited By ~ 9

Author(s):

Guillermo Bodega ◽

Matilde Alique ◽

Lourdes Bohórquez ◽

Sergio Ciordia ◽

María C. Mena ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Endothelial Cells ◽

Superoxide Anion ◽

Umbilical Vein ◽

Redox Status ◽

Human Umbilical Vein ◽

Umbilical Vein Endothelial Cells ◽

Ros Scavengers ◽

Antioxidant Machinery

We examine the antioxidant role of young and senescent human umbilical vein endothelial cells (HUVECs) and their microvesicles (MVs). Proteomic and Western blot studies have shown young HUVECs to have a complete and well-developed antioxidant system. Their MVs also contain antioxidant molecules, though of a smaller and more specific range, specialized in the degradation of hydrogen peroxide and the superoxide anion via the thioredoxin-peroxiredoxin system. Senescence was shown to be associated with a large increase in the size of the antioxidant machinery in both HUVECs and their MVs. These responses might help HUVECs and their MVs deal with the more oxidising conditions found in older cells. Functional analysis confirmed the antioxidant machinery of the MVs to be active and to increase in size with senescence. No glutathione or nonpeptide antioxidant (ascorbic acid and vitamin E) activity was detected in the MVs. Endothelial cells and MVs seem to adapt to higher ROS concentrations in senescence by increasing their antioxidant machinery, although this is not enough to recover completely from the senescence-induced ROS increase. Moreover, MVs could be involved in the regulation of the blood plasma redox status by functioning as ROS scavengers.

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Resistance to the Nitric Oxide/Cyclic Guanosine 5′-Monophosphate/Protein Kinase G Pathway in Vascular Smooth Muscle Cells from the Obese Zucker Rat, a Classical Animal Model of Insulin Resistance: Role of Oxidative Stress

Endocrinology ◽

10.1210/en.2007-0920 ◽

2007 ◽

Vol 149 (4) ◽

pp. 1480-1489 ◽

Cited By ~ 33

Author(s):

I. Russo ◽

P. Del Mese ◽

G. Doronzo ◽

L. Mattiello ◽

M. Viretto ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Hydrogen Peroxide ◽

Smooth Muscle ◽

Superoxide Anion ◽

Zucker Rats ◽

No Donor ◽

Vasp Phosphorylation ◽

Donor Ability

Some in vivo and ex vivo studies demonstrated a resistance to the vasodilating effects of nitric oxide (NO) in insulin-resistant states and, in particular, obese Zucker rats (OZR). To evaluate the biochemical basis of this phenomenon, we aimed to identify defects of the NO/cGMP/cGMP-dependent protein kinase (PKG) pathway in cultured vascular smooth muscle cells (VSMCs) from OZR and lean Zucker rats (LZR) by measuring: 1) NO donor ability to increase cGMP in the absence and presence of inhibitors of soluble guanylate cyclase (sGC) and phosphodiesterases (PDEs); 2) NO and cGMP ability to induce, via PKG, vasodilator-stimulated phosphoprotein (VASP) phosphorylation at serine 239 and PDE5 activity; 3) protein expression of sGC, PKG, total VASP, and PDE5; 4) superoxide anion concentrations and ability of antioxidants (superoxide dismutase+catalase and amifostine) to influence the NO/cGMP/PKG pathway activation; and 5) hydrogen peroxide influence on PDE5 activity and VASP phosphorylation. VSMCs from OZR vs. LZR showed: 1) baseline cGMP concentrations higher, at least in part owing to reduced catabolism by PDEs; 2) impairment of NO donor ability to increase cGMP, even in the presence of PDE inhibitors, suggesting a defect in the NO-induced sGC activation; 3) reduction of NO and cGMP ability to activate PKG, indicated by the impaired ability to phosphorylate VASP at serine 239 and to increase PDE5 activity via PKG; 4) similar baseline protein expression of sGC, PKG, total VASP, and PDE5; and 5) higher levels of superoxide anion. Antioxidants partially prevented the defects of the NO/cGMP/PKG pathway observed in VSMCs from OZR, which were reproduced by hydrogen peroxide in VSMCs from LZR, suggesting the pivotal role of oxidative stress.

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The homeostatic role of hydrogen peroxide, superoxide anion and nitric oxide in the vasculature

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2020.11.021 ◽

2020 ◽

Author(s):

Tiago J. Costa ◽

Paula Rodrigues Barros ◽

Cristina Arce ◽

Jeimison Duarte Santos ◽

Júlio da Silva-Neto ◽

...

Keyword(s):

Nitric Oxide ◽

Hydrogen Peroxide ◽

Superoxide Anion

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Role of xanthine oxidase and granulocytes in ischemia-reperfusion injury

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.6.h1269 ◽

1988 ◽

Vol 255 (6) ◽

pp. H1269-H1275 ◽

Cited By ~ 75

Author(s):

D. N. Granger

Keyword(s):

Hydrogen Peroxide ◽

Xanthine Oxidase ◽

Superoxide Anion ◽

Cell Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Microvascular Endothelium ◽

Ischemic Period ◽

Membrane Components

In this lecture, evidence is presented to support the following hypothesis regarding the roles of xanthine oxidase-derived oxidants and granulocytes in ischemia-reperfusion-induced microvascular injury. During the ischemic period, ATP is catabolized to yield hypoxanthine. The hypoxic stress also triggers the conversion of NAD-reducing xanthine dehydrogenase to the oxygen radical-producing xanthine oxidase. During reperfusion, molecular oxygen is reintroduced into the tissue where it reacts with hypoxanthine and xanthine oxidase to produce a burst of superoxide anion and hydrogen peroxide. In the presence of iron, superoxide anion and hydrogen peroxide react via the Haber-Weiss reaction to form hydroxyl radicals. This highly reactive and cytotoxic radical then initiates lipid peroxidation of cell membrane components and the subsequent release of substances that attract, activate, and promote the adherence of granulocytes to microvascular endothelium. The adherent granulocytes then cause further endothelial cell injury via the release of superoxide and various proteases.

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An ESR study of UV-irradiated solutions of tetramethylammonium mercaptoundecahydro-closo-dodecaborate(2-) at 77 K

Collection of Czechoslovak Chemical Communications ◽

10.1135/cccc19910657 ◽

1991 ◽

Vol 56 (3) ◽

pp. 657-662 ◽

Cited By ~ 3

Author(s):

Pavel Stopka ◽

Oldřich Štrouf

Keyword(s):

Hydrogen Peroxide ◽

Aqueous Solutions ◽

Ultraviolet Irradiation ◽

Superoxide Anion ◽

Oxygen Molecule ◽

Superoxide Anion Radicals ◽

Anion Radicals

The superoxide anion-radicals O2·- are generated by the ultraviolet irradiation of air- or oxygen-saturated aqueous solutions of tetramethylammonium mercaptoundecahydro-closo-dodecaborate(2-) at 77 K. The superoxide anion-radicals are formed from the oxygen molecule coordinated on the mercaptoundecahydro-closo-dodecaborate dianion. In the absence of this dianion no O2·- are generated. By the irradiation in the presence of hydrogen peroxide the formation of the superoxide anion-radicals is more intensive than in the presence of oxygen only. Simultaneously with O2·- generation the corresponding thiol radicals are formed. These radicals give the disulfide compound [B12H11S]24-. A possible role of sulfur-centered radicals in the autoxidation transformations of the mercaptoundecahydro-closo-dodecaborate dianion is discussed.

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Reactive forms of oxygen and chemiluminescence in phagocytizing rabbit alveolar macrophages

AJP Cell Physiology ◽

10.1152/ajpcell.1978.235.3.c103 ◽

1978 ◽

Vol 235 (3) ◽

pp. C103-C108 ◽

Cited By ~ 63

Author(s):

P. R. Miles ◽

V. Castranova ◽

P. Lee

Keyword(s):

Hydrogen Peroxide ◽

Superoxide Dismutase ◽

Hydroxyl Radical ◽

Alveolar Macrophages ◽

Superoxide Anion ◽

Extracellular Fluid ◽

Particle Uptake ◽

O2 Production

Chemiluminescence (CL), superoxide anion (O2-) production, and particle uptake were measured to determine the role of antibacterial substances in the chemiluminescent response associated with phagocytosis in rabbit alveolar macrophages (AM). Exposure of AM to zymosan particles induced both CL and the production of extracellular O2-. CL is inhibited by superoxide dismutase, an enzyme which catalyzes the conversion of O2- to hydrogen peroxide (H2O2), by catalase, an enzyme which destroys H2O2, and by the hydroxyl radical (.OH) scavengers, benzoate and ethanol. Superoxide dismutase and catalase probably exert their effects in the extracellular fluid. CL can also be produced by the addition of NaO2 or H2O2 to zymosan in a noncellular system. The chemiluminescent response occurs before particle uptake is complete, which also indicates that CL occurs in the extracellular fluid. These results suggest that CL induced by zymosan in AM is due to the extracellular reaction between various reactive forms of oxygen and zymosan.

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The response of Azotobacter chroococcum to oxygen: superoxide-mediated effects

Canadian Journal of Microbiology ◽

10.1139/m77-228 ◽

1977 ◽

Vol 23 (11) ◽

pp. 1548-1553 ◽

Cited By ~ 10

Author(s):

Alfred G. Buchanan

Keyword(s):

Hydrogen Peroxide ◽

Superoxide Dismutase ◽

Oxygen Uptake ◽

Superoxide Anion ◽

Azotobacter Chroococcum ◽

Continuous Cultures ◽

Whole Cells ◽

Mediated Effects ◽

Nitrogenase Inhibition

Nitrogenase in Azotobacter chroococcum whole cells was inhibited by enzymically generated superoxide anion (O2−), hydrogen peroxide, and ethyl hydrogen peroxide. The degree of inhibition produced by O2− was related to the quantity of oxygen supplied to the organisms in continuous cultures. O2− also inhibited oxygen uptake by whole cells. These O2−-mediated inhibitions were prevented by bovine superoxide dismutase. The quantities of superoxide dismutase (SOD), and catalase associated with cells grown under varying oxygen concentrations were determined. The role of hydrogen peroxide, and of the hydroxyl radical (∙OH) in nitrogenase inhibition was examined. The response of Azotobacter chroococcum to oxygen was evaluated with respect to the observed effects of O2− on the organism, and some explanation is given to account for nitrogenase sensitivity to oxygen.

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