In vitro effects of reactive oxygen metabolites, with and without flunixin meglumine, on equine colonic mucosa

2007 ◽  
Vol 68 (3) ◽  
pp. 305-312 ◽  
Author(s):  
Olivia J. Inoue ◽  
David E. Freeman ◽  
Matthew A. Wallig ◽  
Robert B. Clarkson
Keyword(s):  
Colonic Mucosa ◽  
Reactive Oxygen ◽  
Reactive Oxygen Metabolites ◽  
Flunixin Meglumine ◽  
In Vitro Effects ◽  
Oxygen Metabolites

Oxidant Mechanisms in Glomerular Injury

Physiology ◽  
1988 ◽  
Vol 3 (6) ◽  
pp. 254-257
Author(s):  
SV Shah
Keyword(s):  
Reactive Oxygen ◽  
In Vivo Studies ◽  
Reactive Oxygen Metabolites ◽  
Glomerular Injury ◽  
Oxygen Metabolites

An increasing body of evidence derived from both in vitro and in vivo studies utilizing leukocyte-dependent and leukocyte-independent models of glomerulonephritis suggests an important role for reactive oxygen metabolites in glomerular pathophysiology.

Nitric oxide enhances hydrogen peroxide-mediated endothelial permeability in vitro

1997 ◽  
Vol 273 (5) ◽  
pp. C1581-C1587 ◽  
Author(s):  
Naotsuka Okayama ◽  
Christopher G. Kevil ◽  
Loisann Correia ◽  
David Jourd’Heuil ◽  
Makoto Itoh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Permeability ◽  
Reactive Oxygen ◽  
Iron Chelator ◽  
Reactive Oxygen Metabolites ◽  
No Donor ◽  
Spermine Nonoate ◽  
Oxygen Metabolites

The objective of this study was to evaluate the effects of nitric oxide (NO) on H2O2-mediated endothelial permeability. H2O2(0.1 mM) increased permeability at 90 min to 298% of baseline. Spermine NONOate (SNO), an NO donor, at 0.1 or 1 mM did not alter permeability. However, 0.1 mM H2O2+ 1 mM SNO increased permeability to 764%, twice that of 0.1 mM H2O2alone. These treatments were not directly toxic to endothelial cells. This NO effect was concentration dependent, inasmuch as 0.1 mM SNO did not significantly change H2O2-mediated permeability. The NO-enhanced, H2O2-dependent permeability required the simultaneous presence of NO and H2O2, inasmuch as preincubation with SNO for 30 min followed by 0.1 mM H2O2did not alter permeability. Staining of endothelial junctions showed widening of the intercellular space only in junctions of cells exposed to H2O2(0.1 mM) + SNO (1 mM). Furthermore, NO did not affect H2O2metabolism by endothelial cells but significantly depleted intracellular glutathione. This reduction of cell glutathione produced by NO exposure recovered 15–30 min after removal of the NO donor. NO-enhanced permeability was completely blocked by methionine (1 mM), a scavenger of reactive oxygen species, and by the iron chelator desferrioxamine (0.1 mM). These results suggest that NO may exacerbate the effects of H2O2-dependent increase in endothelial monolayer permeability via the iron-catalyzed formation of reactive oxygen metabolites.

Circulating xanthine oxidase: potential mediator of ischemic injury

1990 ◽  
Vol 258 (4) ◽  
pp. G564-G570 ◽  
Author(s):  
Y. Yokoyama ◽  
J. S. Beckman ◽  
T. K. Beckman ◽  
J. K. Wheat ◽  
T. G. Cash ◽  
...  
Keyword(s):  
Xanthine Oxidase ◽  
Tissue Injury ◽  
Reactive Oxygen ◽  
Systemic Circulation ◽  
Reactive Oxygen Metabolites ◽  
Vascular Endothelial ◽  
Hepatic Ischemia ◽  
Oxygen Metabolites ◽  
Krebs Henseleit Buffer

Reactive oxygen metabolites generated from the enzyme xanthine oxidase (XO) play an important role in the pathogenesis of ischemia-induced tissue injury. The observation that intracellular proteins such as aspartate transaminase (AST) and alcohol dehydrogenase (ADH) are released from the ischemic liver during reperfusion led us to postulate that XO could be released into the systemic circulation. Livers from fasted rats were extirpated, perfused with oxygenated Krebs-Henseleit buffer, and subjected to 2 h ischemia followed by 2 h reperfusion. Reperfusion increased AST in the perfusate from 1 +/- 1 to 830 +/- 280 U/l, whereas ADH increased from 0.3 +/- 0.1 to 95 +/- 26 U/l. Concomitantly, xanthine dehydrogenase (XDH) + XO activity in the perfusate increased from 0 to 4.1 +/- 1.0 mU/ml. A 64% decrease in endogenous tissue XDH + XO activity paralleled release of XDH + XO. The XDH + XO activity predicted to appear in the circulation after hepatic ischemia was sufficient, when supplied with substrate, to produce severe vascular endothelial injury in vitro, even in the presence of serum or whole blood. These results suggest that massive quantities of XDH and XO are released into the circulation after hepatic ischemia and that the resulting reactive oxygen metabolites could produce widespread tissue injury.

The role of reactive oxygen metabolites in lymphocyte-mediated cytolysis

1987 ◽  
Vol 87 (3) ◽  
pp. 473-481
Author(s):  
C.J. Bishop ◽  
C.M. Rzepczyk ◽  
D. Stenzel ◽  
K. Anderson
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Xanthine Oxidase ◽  
Natural Killer ◽  
Reactive Oxygen ◽  
Tumour Cells ◽  
Reactive Oxygen Metabolites ◽  
Oxygen Metabolites

To examine the possible role of reactive oxygen metabolites in lymphocyte-mediated cytolysis, the morphology of cell death following the exposure of cells to reactive oxygen metabolites in vitro was compared with the morphology of cell-mediated killing in vitro of tumour cells by natural killer (NK) cells. Ultrastructural examination of human tumour cells that were dying following incubation for 60 min with the oxygen metabolite generating systems, xanthine-xanthine oxidase or t-butylhydroperoxide, showed that cell death in both instances was exclusively by necrosis. It was unclear which oxygen metabolites were involved in killing. Cell death was not decreased by the addition of superoxide dismutase, a scavenger of the superoxide anion, to the xanthine-xanthine oxidase mixture. Although the cells were not killed by incubation with 1 mM-hydrogen peroxide, the addition of catalase, a scavenger of hydrogen peroxide, to the xanthine-xanthine oxidase mixture significantly reduced cell death. The addition of scavengers for the hydroxyl radical to either the xanthine-xanthine oxidase mixture or t-butylhydroperoxide gave inconsistent protection. In contrast, tumour cell killing mediated by natural killer cells was by apoptosis, a morphologically distinct mode of cell death with a different basic mechanism, indicating that reactive oxygen metabolites are not directly involved in lymphocyte-mediated cytolysis.

scholarly journals Antiglomerular basement membrane nephritis in beige mice. Deficiency of leukocytic neutral proteinases prevents the induction of albuminuria in the heterologous phase.

1989 ◽  
Vol 169 (4) ◽  
pp. 1435-1448 ◽  
Author(s):  
G Schrijver ◽  
J Schalkwijk ◽  
J C Robben ◽  
K J Assmann ◽  
R A Koene
Keyword(s):  
Basement Membrane ◽  
Reactive Oxygen ◽  
Cathepsin G ◽  
Reactive Oxygen Metabolites ◽  
Glomerular Lesions ◽  
And Control ◽  
Dose Dependent ◽  
Oxygen Metabolites

Antiglomerular basement membrane (GBM) nephritis with massive albuminuria can be induced in mice by injection of heterologous antibodies against mouse GBM. The albuminuria and the glomerular lesions in this model are not mediated by complement, but are dependent on the presence of polymorphonuclear granulocytes (PMN) in the glomeruli. Neutral serine proteinases and reactive oxygen metabolites produced by activated PMN have been implicated as agents contributing to tissue damage. We examined the role of leukocytic neutral proteinases by comparing the glomerular damage and albuminuria after injection of rabbit anti-mouse GBM antibodies in normal control mice (C57BL/6J, +/+) and in beige mice (C57BL/6J,bg/bg) in which PMN are deficient of the neutral proteinases elastase and cathepsin G. The dose-dependent albuminuria that occurred in control mice after injection of 1.4-22 mg of anti-GBM antibodies was not observed in beige mice, despite a comparable influx of PMNs in the glomeruli. By electron microscopy both strains showed a similar attachment of PMN to the denuded GBM together with swelling and necrosis of endothelial cells. Elastase activity of extracts from PMN of beige mice was only 10-15% of the activity of control mice. In vitro, GBM degradation by PMN extracts of beige mice was 70% lower than that seen in control experiments. PMNs of beige and control mice showed no differences in superoxide production. In addition, administration of scavengers of reactive oxygen metabolites, such as catalase and desferrioxamine, did not prevent the albuminuria in this model. These findings support the important contribution of leukocytic neutral proteinases to the induction of albuminuria in the acute phase of anti-GBM nephritis in the mouse.

scholarly journals Effects of Non-Surgical Periodontal Treatment on Reactive Oxygen Metabolites and Glycemic Control in Diabetic Patients with Chronic Periodontitis

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1056
Author(s):  
Simone Marconcini ◽  
Enrica Giammarinaro ◽  
Saverio Cosola ◽  
Giacomo Oldoini ◽  
Annamaria Genovesi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glycemic Control ◽  
Systemic Inflammation ◽  
Glycated Hemoglobin ◽  
Reactive Oxygen ◽  
Periodontal Treatment ◽  
Diabetic Patients ◽  
Reactive Oxygen Metabolites ◽  
Periodontal Infection ◽  
Oxygen Metabolites

Background: Periodontal infection may contribute to poor glycemic control and systemic inflammation in diabetic patients. The aim of the present study is to evaluate the efficacy of non-surgical periodontal treatment in diabetic patients by measuring oxidative stress outcomes. Methods: Sixty diabetic patients with periodontitis were enrolled, treated with scaling and full-mouth disinfection, and randomly prescribed chlorhexidine mouthwash, antioxidant mouthwash, or ozone therapy. Reactive oxygen metabolites (ROMs), periodontal parameters, and glycated hemoglobin were measured at baseline and then at 1, 3, and 6 months after. Results: At baseline, all patients presented with pathologic levels of plasmatic ROM (388 ± 21.36 U CARR), higher than the normal population. Probing depth, plaque index, and bleeding on probing values showed significant clinical improvements after treatment, accompanied by significant reductions of plasma ROM levels (p < 0.05). At the 6-month evaluation, the mean ROM relapsed to 332 ± 31.76 U CARR. Glycated hemoglobin decreased significantly (∆ = −0.52 units) after treatment. Both the test groups showed longer-lasting improvements of periodontal parameters. Conclusion: In diabetic patients, periodontal treatment was effective at reducing plasma ROM, which is an indicator of systemic oxidative stress and inflammation. The treatment of periodontal infection might facilitate glycemic control and decrease systemic inflammation.

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