In-vivo measurement of oxygen free radical production correlates with pulmonary reperfusion injury

1999 ◽  
Vol 18 (1) ◽  
pp. 74
Keyword(s):  
Free Radical ◽  
Reperfusion Injury ◽  
Oxygen Free Radical ◽  
Free Radical Production ◽  
In Vivo Measurement ◽  
Radical Production

Production of reactive oxygen species after reperfusion in vitro and in vivo: protective effect of nitric oxide

2000 ◽  
Vol 93 (1) ◽  
pp. 99-107 ◽  
Author(s):  
R. Bryan Mason ◽  
Ryszard M. Pluta ◽  
Stuart Walbridge ◽  
David A. Wink ◽  
Edward H. Oldfield ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Reperfusion Injury ◽  
Oxygen Free Radical ◽  
Content Type ◽  
Free Radical Production ◽  
Radical Production ◽  
Fine Print

Object. Thrombolytic treatments for ischemic stroke can restore circulation, but reperfusion injury, mediated by oxygen free radicals, can limit their utility. The authors hypothesized that, during reperfusion, nitric oxide (NO) provides cytoprotection against oxygen free radical species.Methods. Levels of NO and oxygen free radicals were determined in both reoxygenation in vitro and reperfusion in vivo models using an NO electrochemical probe and high-performance liquid chromatography with the 2,3- and 2,5-dihydroxybenzoic acid trapping method, before and after addition of the NO donor diethanolamine nitric oxide (DEA/NO).Reoxygenation after anoxia produced a twofold increase in NO release by human fetal astrocytes and cerebral endothelial cells (p < 0.005). In both cell lines, there was also a two- to threefold increase in oxygen free radical production (p < 0.005). In human fetal astrocytes and cerebral endothelial cells given a single dose of DEA/NO, free radical production dropped fivefold compared with peak ischemic levels (p < 0.001). In a study in which a rat global cerebral ischemia model was used, NO production in a vehicle-treated group increased 48 ± 16% above baseline levels after reperfusion. After intravenous DEA/NO infusion, NO reached 1.6 times the concentration of the postischemic peak in vehicle-treated animals. In vehicle-treated animals during reperfusion, free radical production increased 4.5-fold over basal levels (p < 0.01). After intravenous DEA/NO infusion, free radical production dropped nearly 10-fold compared with peak levels in vehicle-treated animals (p < 0.006). The infarct volume in the vehicle-treated animals was 111 ± 16.9 mm3; after DEA/NO infusion it was 64.8 ± 23.4 mm3 (p < 0.01).Conclusions. The beneficial effect of early restoration of cerebral circulation after cerebral ischemia is limited by reperfusion injury. These results indicate that NO release and oxygen free radical production increase during reperfusion, and suggest a possible early treatment of reperfusion injury using NO donors.

Heparin-Binding EGF-Like Growth Factor (HB-EGF) Decreases Oxygen Free Radical Production In Vitro and In Vivo

2002 ◽  
Vol 4 (4) ◽  
pp. 639-646 ◽  
Author(s):  
M. Ann Kuhn ◽  
Guilang Xia ◽  
Veela B. Mehta ◽  
Sandra Glenn ◽  
Marc P. Michalsky ◽  
...  
Keyword(s):  
Free Radical ◽  
Growth Factor ◽  
Oxygen Free Radical ◽  
Heparin Binding ◽  
Free Radical Production ◽  
Radical Production

scholarly journals Direct evidence of iNOS-mediated in vivo free radical production and protein oxidation in acetone-induced ketosis

2008 ◽  
Vol 295 (2) ◽  
pp. E456-E462 ◽  
Author(s):  
Krisztian Stadler ◽  
Marcelo G. Bonini ◽  
Shannon Dallas ◽  
Danielle Duma ◽  
Ronald P. Mason ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Nadph Oxidase ◽  
Knockout Mice ◽  
Protein Oxidation ◽  
Ketone Bodies ◽  
Free Radical Production ◽  
Radical Production ◽  
Inos Knockout Mice

Diabetic patients frequently encounter ketosis that is characterized by the breakdown of lipids with the consequent accumulation of ketone bodies. Several studies have demonstrated that reactive species are likely to induce tissue damage in diabetes, but the role of the ketone bodies in the process has not been fully investigated. In this study, electron paramagnetic resonance (EPR) spectroscopy combined with novel spin-trapping and immunological techniques has been used to investigate in vivo free radical formation in a murine model of acetone-induced ketosis. A six-line EPR spectrum consistent with the α-(4-pyridyl-1-oxide)- N-t-butylnitrone radical adduct of a carbon-centered lipid-derived radical was detected in the liver extracts. To investigate the possible enzymatic source of these radicals, inducible nitric oxide synthase (iNOS) and NADPH oxidase knockout mice were used. Free radical production was unchanged in the NADPH oxidase knockout but much decreased in the iNOS knockout mice, suggesting a role for iNOS in free radical production. Longer-term exposure to acetone revealed iNOS overexpression in the liver together with protein radical formation, which was detected by confocal microscopy and a novel immunospin-trapping method. Immunohistochemical analysis revealed enhanced lipid peroxidation and protein oxidation as a consequence of persistent free radical generation after 21 days of acetone treatment in control and NADPH oxidase knockout but not in iNOS knockout mice. Taken together, our data demonstrate that acetone administration, a model of ketosis, can lead to protein oxidation and lipid peroxidation through a free radical-dependent mechanism driven mainly by iNOS overexpression.

Control of oxidative stress in microcirculation of spontaneously hypertensive rats

2005 ◽  
Vol 288 (2) ◽  
pp. H805-H812 ◽  
Author(s):  
F. A. DeLano ◽  
R. Balete ◽  
G. W. Schmid-Schönbein
Keyword(s):  
Free Radical ◽  
Spontaneously Hypertensive Rats ◽  
Oxygen Free Radical ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Free Radical Production ◽  
Wky Rats ◽  
Arterial Blood ◽  
Radical Production ◽  
Tetrazolium Reduction

One mechanism for organ damage in individuals with arterial hypertension may be due to oxygen free radical production. This study was designed to localize free radicals in a microvascular network of mature spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Because glucocorticoids play a role in pressure elevation of SHRs, we investigated their role in microvascular free radical formation. Oxygen radical production in mesentery was detected by tetranitroblue tetrazolium reduction to formazan aided by digital light-absorption measurements. Formazan deposits were observed in the endothelial cells and lumens of all microvessels and in lymphatic endothelia but were fewer in tissue parenchyma. The formazan distribution in younger (14–16 wk old) WKY rats and SHRs was heterogeneous with low values in capillaries and small arterioles/venules (<30 μm) but enhanced deposits in larger venules. Adrenalectomy served to reduce the formazan density in SHRs to the level of WKY rats, whereas dexamethasone supplementation of the adrenalectomized rats caused elevation in the larger venules of SHRs. In older (40 wk old) SHRs, formazan levels were elevated in all hierarchies of microvessels. After pressure reduction was employed with chronic hydralazine treatment, the formazan deposits were reduced in all locations of the microcirculation in both WKY rats and SHRs. Elevated formazan deposits were also found in lymphatic endothelium. These results suggest that oxygen free radical production is elevated in both high- and low-pressure regions of SHR microcirculation via a process that is controlled by glucocorticoids. Older SHRs have higher formazan levels than younger SHRs in all microvessels. Chronic hydralazine treatment, which serves to reduce arterial blood pressure, attenuates tetranitroblue tetrazolium reduction in WKY rats and SHRs even in venules of the microcirculation, which has no micropressure elevation. Free radical production may be a more global condition in SHRs and may not be limited to arteries and arterioles.

Amlodipine Decreases Iron Uptake and Oxygen Free Radical Production in the Heart of Chronically Iron Overloaded Mice

2002 ◽  
Vol 3 (4) ◽  
pp. 189-197 ◽  
Author(s):  
Sarah Crowe ◽  
Wally J. Bartfay
Keyword(s):  
Free Radical ◽  
Iron Metabolism ◽  
Iron Uptake ◽  
Hereditary Hemochromatosis ◽  
Antioxidant Properties ◽  
Oxygen Free Radical ◽  
Cardiac Complications ◽  
Channel Blockers ◽  
Free Radical Production ◽  
Radical Production

Hereditary hemochromatosis is a disorder of iron metabolism, which is currently the most prevalent autosomal recessive disorder in the world, with an expression of the homozygous form occurring in approximately 1 in 200 individuals of European descent. Approximately one third of patients with hemochromatosis die of iron-induced cardiac complications. Although the exact mechanism is not known, it is believed that the toxicity of excess iron in biological systems is due to its ability to catalyze the generation of harmful reactive oxygen free radical species (ROS), which can damage proteins, lipids, and DNA. There is preliminary evidence to suggest that nontransferrinbound iron uptake in the myocardium may occur through voltage-dependent L-type calcium channels, and that calcium channel blockers (CCBs) may possess antioxidant properties. Accordingly, the authors hypothesized that the administration of amlodipine besylate would (1) decrease iron uptake in the myocardium and (2) decrease oxygen free radical production as measured by cytotoxic aldehyde–derived peroxidation products in a murine model of iron overload cardiomyopathy. The findings show that the CCB amlodipine is partially effective in limiting iron uptake in the heart and significantly inhibits the production of ROS in chronically iron-loaded mice. These are important preliminary findings because they suggest that CCBs may have significance in the clinical management of genetic disorders of iron metabolism.

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