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T Cvetković

Publications and source records attributed to T Cvetković.

At least 19 recordsLinked to original sources
PubMed1998

The possible importance of the cation-binding site for the oxidative modification of liver 5'-nucleotidase.

The oxidative damage of proteins and lipid peroxidation of membrane lipoproteins has already been described as a possible pathogenic mechanism for liver injury. The aim of the present study was to examine the mechanism that could be responsible for the oxidative modification of rat liver 5'-nucleotidase during exposure to different free radical generating systems: FeCl2/ascorbate, xanthine/xanthine oxidase and H2O2. The level of lipid peroxidation products malondialdehyde (MDA), as well as the level of protein carbonyl groups formation was measured in cells and extracellular medium. The activity of 5'-nucleotidase was linearly decreased in both hepatocytes and extracellular medium after exposure to the FeCl2/ascorbate system indicating that the possible mechanism for oxidative modification could be a metal-binding site of the enzyme. In xanthine/xanthine oxidase system the enzyme activity of hepatocytes had decreased in hepatocytes but increased in the extracellular medium indicating that proteolysis of membrane proteins could he responsible for enzyme release in the extracellular medium. When hepatocytes were exposed to a H2O2 free-radical generating system, the activity of 5'-nucleotidase tended to be decreased in cells and decreased in extracellular medium too, indicating that H2O2 could be less reactive in producing an oxidative modification of the enzyme. In order to support the hypothesis that the cation-binding site can be responsible for oxidative modification of the enzyme, the isolated hepatocytes were preincubated with a Ca(2+)-channel blocker (Verapamil) and then exposed to different radical-generating systems. Verapamil had only a slight effect in potentiating the inhibition in the FeCl2/ascorbate system. This probably means that the cellular cation flux and cation binding may be included as a vulnerable site with the greatest importance in the oxidative modification of 5'-nucleotidase.

5'-Nucleotidase↗
PubMed1998

Selenium-dependent GSH-Px in erythrocytes of patients with hypertension treated with ACE inhibitors.

This study is aimed at examining whether essential arterial hypertension (HTN) or ACE inhibitors have any effect on erythrocyte selenium (Se)-dependent and Se-non-dependent glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity. Eleven patients with HTN (2 men and 9 women) and 9 healthy volunteers were included in this study after clinical examination and laboratory investigation. The activities of all three enzymes were determined and then the patients were assigned to receive ACE inhibitor therapy consisting of captopril, 25 to 50 mg daily, or enalapril, 10 to 40 mg daily. After 1 year, the determination of antioxidant enzymes was repeated. Our results showed that the initial values of Se-dependent GSH-Px in patients treated with ACE inhibitors were significantly lower (19.60 +/- 3.50 microM NADPH/min(-1)/mgHb(-1)) compared with the controls (28.64 +/- 4.93 microM NADPH/min(-1)/mgHb(-1); p < 0.001), whereas the activity of Se-non-dependent GSH-Px was significantly enhanced (13.55 +/- 1.46 microM NADPH/min(-1)/mgHb(-1); p < 0.001) compared with the control group (9.44 +/- 0.81 microM NADPH/min(-1)/mgHb(-1); p < 0.001). ACE inhibitors did not significantly change the activity of Se-dependent GSH-Px or Se-non-dependent GSH-Px. No significant alteration was observed in SOD activity.

Adult↗
PubMed1997

Changes of lipid peroxides and antioxidative factors levels in blood of patients treated with ACE inhibitors.

In 14 patients (4 males and 10 females) with systemic hypertension plasma and erythrocyte lipid peroxides, plasma and erythrocyte catalase activity, plasma glutathione S-transferase (GST) activity, blood reduced glutathione (GSH) content and erythrocyte oxidant stress were investigated. All parameters were performed after clinical examination and then the patients were assigned to receive ACE inhibitor therapy, captopril (25-50 mg given twice per day) or enalapril (10-40 mg given twice per day). After six months the determination of lipid peroxides and antioxidative factors was repeated. At the beginning of the study both treated groups showed significantly higher plasma lipid peroxides compared to the control group. Both used ACE inhibitors produced significant decrease of plasma lipid peroxides after six months. Blood GSH content was also significantly higher in both patient groups before the treatment compared to the controls. Neither captopril nor enalapril produced any significant effect on GSH. Initial values of plasma GST activity in the patients were similar to the control group and did not significantly change after six month treatment. The patients assigned to receive enalapril showed significantly enhanced initial plasma catalase activity according to the controls. After six months treatment both ACE inhibitors significantly decreased plasma catalase activity. Erythrocyte lipid peroxides, erythrocyte catalase activity and oxidant stress of erythrocytes in both groups studied neither differ significantly at initial time of investigation according to the control group nor during or after six month treatment.

Adult↗
PubMed1992

[Dental pulp in carious teeth].

Various etiologic causes lead to dental pulp changes ranging from inflammation to necrosis. The most frequent changes, however, are caused by bacterial activity and toxins from carious process. According to the opinion of various authors and on the basis of our investigations the conclusion can be made that all the forms of dental pulp changes can be developed as the sequela of the disease of supporting apparatus. Pathohistologic examination of dental pulp of cariously damaged teeth showed that the occurred changes are mostly the sequela of inflammation and regressive and progressive changes are found as well.

Adult↗