Effect of Aluminium on Superoxide Dismutase

1989 ◽  
Vol 77 (5) ◽  
pp. 463-466 ◽  
Author(s):  
Ruth Shainkin-Kestenbaum ◽  
Andrew J. Adler ◽  
Geoffrey M. Berlyne ◽  
C. Caruso
Keyword(s):  
Superoxide Dismutase ◽  
Free Radical ◽  
Elevated Serum ◽  
Oxygen Free Radical ◽  
Protective Role ◽  
Free Radical Production ◽  
Radical Production ◽  
Excessive Oxygen

1. The effect of Al3+ on superoxide dismutase in vitro was studied, since in uraemia there is excessive superoxide production and frequently an elevated serum Al3+ level. Thus, the protective role of superoxide dismutase is particularly important. 2. Al3+ in concentrations similar to those found in the serum of uraemic patients inhibits superoxide dismutase activity. The degree of inhibition is directly proportional to the Al3+ level. 3. The combination of excessive oxygen free radical production with an increased Al3+ level may contribute to a variety of complications, including aluminium dementia or initiation and promotion of carcinogenic processes, which are known to be more common in uraemic patients.

scholarly journals Role of Nitric Oxide Synthase Inhibition in Leukocyte-Endothelium Interaction in the Rat Pial Microvasculature

1996 ◽  
Vol 16 (6) ◽  
pp. 1143-1152 ◽  
Author(s):  
Ute Lindauer ◽  
Jens Dreier ◽  
Klemens Angstwurm ◽  
Inger Rubin ◽  
Arno Villringer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Oxygen Free Radical ◽  
Sodium Fluorescein ◽  
Free Radical Production ◽  
Physiological Conditions ◽  
Cranial Window ◽  
Radical Production ◽  
Bbb Permeability

We investigated the role of nitric oxide (NO) in leukocyte-endothelium interaction, blood-brain barrier (BBB) function and oxygen free-radical production in the rat pial microcirculation. In a closed cranial window preparation (dura removed) over the parietal cortex of pentobarbital-anesthetized Wistar rats, NO synthase (NOS) was inhibited by systemic and/or topical application of Nω-nitro-l-arginine (l-NNA) under physiological conditions and during leukotriene B4 (LTB4) activation. Circulating leukocytes were labeled by intravenous injection of rhodamine 6G. We used a confocal laser scanning microscope (CLSM) and studied leukocyte rolling and sticking in pial veins and arteries before and after NOS inhibition. At the end of the experiments, sodium-fluorescein was injected intravenously to test BBB integrity. Brain cortex oxygen free-radical production was investigated in the cranial window preparation using lucigenin-enhanced chemiluminescence (CL). l-NNA application did not lead to significant changes in leukocyte-endothelium interaction, BBB function, and oxygen free-radical production under physiological conditions [leukocyte-endothelium interaction: control (n = 5), l-NNA systemically (n = 5), l-NNA topically (n = 5): at baseline rollers/100 μm: 0.76 ± 0.55, 0.64 ± 0.94, 0.44 ± 0.55 and stickers/100 μm: 0.90 ± 0.28, 0.76 ± 0.24, 0.84 ± 0.42; at 60 min rollers/100 μm: 1.49 ± 0.66, 1.21 ± 0.99, 0.67 ± 0.66 and stickers/100 μm: 1.04 ± 0.20, 1.19 ± 0.23, 1.21 ± 0.54; oxygen free-radical production (n = 4): CL count before l-NNA application 35 ± 17 cps, after 1 h of topical superfusion of l-NNA 38 ± 14 cps; p < 0.05]. In contrast to the results achieved under physiological conditions, a significant further increase of rolling leukocytes and BBB permeability occurred due to NOS inhibition under LTB4-activated conditions [76 ± 47% significant ( p ≤ 0.01, n = 7) further increase of rollers/100 μm due to 60 min l-NNA application following the activation period of 120 min LTB4 superfusion]. Our results support a modulatory role for NO in leukocyte-endothelium interaction and BBB permeability in the pial microcirculation when this interaction is increased.

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.

Protective role of heme oxygenase-1 on trinitrobenzene sulfonic acid-induced colitis in rats

2001 ◽  
Vol 281 (2) ◽  
pp. G586-G594 ◽  
Author(s):  
W. P. Wang ◽  
X. Guo ◽  
M. W. L. Koo ◽  
B. C. Y. Wong ◽  
S. K. Lam ◽  
...  
Keyword(s):  
Free Radical ◽  
Heme Oxygenase ◽  
Sulfonic Acid ◽  
Protective Role ◽  
Inos Expression ◽  
Heme Oxygenase 1 ◽  
Trinitrobenzene Sulfonic Acid ◽  
Free Radical Production ◽  
Radical Production

Preliminary studies showed that the inducible form of heme oxygenase (HO-1) was induced and played a protective role in the process of inflammation. The present study investigated the possible role of HO-1 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. We measured HO-1 activity in TNBS-induced colitis in rats and analyzed the severity of colitis along with altered HO activity by assessing lesion area and myeloperoxidase activity. HO-1 mRNA and protein expressions were determined at different time points after TNBS induction. Free radical production and inducible nitric oxide synthase (iNOS), which participate in oxidative injury, were also assayed. HO activity and HO-1 gene expression increased markedly after TNBS induction. Administration with tin mesoporphyrin (SnMP), a HO inhibitor, potentiated the colonic damage along with a reduction in HO-1 activity. Furthermore, the reduction of HO-1 expression by SnMP also enhanced reactive oxygen species and iNOS expression, both of which were dramatically increased after the TNBS enema. l-Arginine preteatment further aggravated the injurious action of SnMP. Our results indicate that HO-1 plays a protective role in the colonic damage induced by the TNBS enema, and the preventive effects probably result from decreased free radical production and inhibition of iNOS expression in colonic tissues.

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

Glucomannan reduces neutrophil free radical production in vitro and in rats with adjuvant arthritis

2009 ◽  
Vol 59 (6) ◽  
pp. 399-403 ◽  
Author(s):  
Katarína Drábiková ◽  
Tomáš Perečko ◽  
Radomír Nosáľ ◽  
Katarína Bauerová ◽  
Silvester Poništ ◽  
...  
Keyword(s):  
Free Radical ◽  
Adjuvant Arthritis ◽  
Free Radical Production ◽  
Radical Production

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.

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