Showing papers on "Super oxide dismutase published in 1994"

The role of nitric oxide in the responses of equine digital veins to vasodilator and vasoconstrictor agents

Abstract: Summary Isolated equine digital veins were examined in vitro to study the importance of the endothelium in the responses to both vasodilator and vasoconstrictor agents and to characterise the endothelial-derived mediators involved. Carbachol (Cch; 1 μM) and bradykinin (Bk; 1 nM) caused relaxation of U44069-induced tone by 79.5 ± 0.35 % and 73.7 ± 4.0 % respectively. Mechanical removal of the endothelium completely prevented relaxant responses to Cch and to Bk showing they were mediated by the endothelium. Treatment of veins with NG-nitro-L-arginine methyl ester (L-NAME; 30 and 300 μM) inhibited vasorelaxant responses to both Cch and Bk whereas the cyclooxygenase inhibitor, ibuprofen (10 μM) had no inhibitory effect. The inhibitory action of L-NAME on the relaxations produced by Cch was partly reversed by L-arginine (3 and 10 mM). Cch-relaxations were potentiated in the presence of super oxide dismutase (15 units/ml) and inhibited by methylene blue (10 μM). The vasorelaxant effects of ATP (0.01 μM to 0.1 μM) were not dependent on the presence of the endothelium and the selective P2y receptor agonist, 2-methylthio-ATP proved to be ineffective as a vasodilator. Removal of the endothelium did not enhance the vasoconstrictor effects of the α1 adrenoceptor agonist phenylephrine (0.01 μM to 0.1 μM) and treatment with L-NAME (300 μM) did not change the vasoconstrictor responses to 5-HT (1 nM to 10 μM) or the α2 adrenoceptor agonist BHT-920 (1 nM to 1 μM). These data suggest the L-arginine nitric oxide pathway is of primary importance in mediating endothelium dependent relaxations to Cch and BK in equine digital veins but that basal release of nitric oxide is insufficient, under the conditions used in the present study, to modulate responses to vasoconstrictor agents. No functional evidence has been found for P2y-receptors, α2-adrenoceptors or 5-HT receptors on endothelial cells of equine digital veins linked to nitric oxide production.

Apoptotic cell death induced by serum and its prevention by thiols.

Abstract: We recently reported that serum contains low molecular weight factors that inhibit growth and cause cell death in vitro. The present study focused on identifying components of basal media that counteract the toxic effects of serum. Amino acids L-cyst(e)ine and L-tryptophan were found to prevent serum-induced cell death of TIG-1 human fetal lung fibroblasts and other cell types. In addition to L-cysteine, other thiol-bearing and dithiol-cleaving compounds showed a similar ability to rescue the cells. Various inhibitors of protein or RNA synthesis also prevented the cell death. By contrast, nonthiol-containing reducing agents and super oxide dismutase (SOD), an active oxygen-eliminating enzyme, were ineffective. Thiol compounds appeared to exert a supportive level in TIG-1 cells cultured in FBS, whereas protein synthesis inhibitors did not alter the reduced intracellular thiol content. Fragmentation of DNA occurred prior to the plasma membrane breakdown of dying cells. Taken together, these data suggest that serum-induced cell death represents a form of apoptosis in which molecules containing thiol groups are active participants.

Erythrocyte superoxide dismutase (eSOD) determination in positive moments of psychosis

Abstract: Dysregulation of free radical metabolism has been supposed to be involved in schizophrenia etiopathogeny. Recently, Wang et al. showed a red blood cell super oxide dismutase increase in positive schizophrenia (Crow's type I), but neither in negative schizophrenia (Crow's type II) nor in controls. The study included 28 in-patients suffering from acute positive psychosis who were compared with 15 controls. We confirmed the results of Wang. We found a significantly red blood cell Super oxide dismutase increase in positive psychosis, in comparison to negative psychosis and controls (p = 0.0001). This SOD increase was in relationship with the degree of clinical psychomotor excitement. After 21 days of neuroleptic treatment, SOD activity decreased and reached standard values. These results support the hypothesis of striking relationships between catecholaminergic hyper-metabolism and SOD increase, in positive psychosis. These could account for psychotic positive symptoms improvement with neuroleptic treatment, which blocks dopamine pathways.

Serum super oxide dismutase (SOD), malondialdehyde (MDA) levels in urinary disorders

Abstract: Evaluation of serum SOD and MDA level was done in 21 first episode renal stone formers, 9 recurrent stone formers, 20 patients with obstructive uropathy other than urolithiasis and 12 patients with urinary infection. Twenty-two healthy volunteers were taken as controls. The level of SOD in respective groups was 2.12±0.84, 2.78±0.85, 1.42±0.31, 1.98±0.70 and 2.32±0.62 units/ml and of MDA was 2.61±1.07, 2.69±1.15, 1.65±0.33, 1.33±0.34 and 1.55±0.48 n mol/ml respectively. The results indicate increased peroxidative stressin nephrolithiasis only. Since SOD level was normal in all groups, this increased peroxidative stress in nephrolithiasis should be due to factors other than this one.

Method for testing activity of super-oxide dismutase

Abstract: The present invention discloses a method for testing the activity of superoxide dismutase The said method uses free radicals O2 of the superoxide anion produced by a reaction system of XO and XOD for oxidizing hydroxylamine to form nitrite, which is then developed with a developer The present invention is characterized by dissolving XO in an alkali solution, dissolving hydroxylamine in a week acid and using a new buffer solution and a new developer The present invention has the advantages of accurate test result, fast test speed, high sensitivity and low cost as compared with the exisiting techniques