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O Ulicná

Publications and source records attributed to O Ulicná.

At least 19 recordsLinked to original sources
PubMed2005

Rooibos tea (Aspalathus linearis) partially prevents oxidative stress in streptozotocin-induced diabetic rats.

The aim of this study was to investigate the effects of rooibos tea as a natural source of a wide scale of antioxidants on the prevention and treatment of oxidative stress in streptozotocin-induced diabetic rats. Expected significant changes of biochemical parameters characteristic for experimental diabetic state were found in plasma and tissues eight weeks after single dose streptozotocin application. Administration of aqueous and alkaline extracts of rooibos tea (or N-acetyl-L-cysteine for comparison) to diabetic rats did not affect markers of the diabetic status (glucose, glycated hemoglobin and fructosamine). Besides the parameters characterizing hepatotoxic effect of streptozotocin, rooibos tea significantly lowered advanced glycation end-products (AGEs) and malondialdehyde (MDA) in the plasma and in different tissues of diabetic rats, particularly MDA concentration in the lens. From these results we can conclude that antioxidant compounds in rooibos tea partially prevent oxidative stress and they are effective in both hydrophobic and hydrophilic biological systems. Therefore, rooibos tea as a commonly used beverage can be recommended as an excellent adjuvant support for the prevention and therapy of diabetic vascular complications, particularly for protecting ocular membrane systems against their peroxidation by reactive oxygen species.

Acetylcysteine↗
PubMed2004

Regeneration of coenzyme Q9 redox state and inhibition of oxidative stress by Rooibos tea (Aspalathus linearis) administration in carbon tetrachloride liver damage.

The effect of rooibos tea (Aspalathus linearis) on liver antioxidant status and oxidative stress was investigated in rat model of carbon tetrachloride-induced liver damage. Synthetic antioxidant N-acetyl-L-cysteine (NAC) was used for comparison. Administration of carbon tetrachloride (CCl4) for 10 weeks decreased liver concentrations of reduced and oxidized forms of coenzyme Q9 (CoQ9H2 and CoQ9), reduced -tocopherol content and simultaneously increased the formation of malondialdehyde (MDA) as indicator of lipid peroxidation. Rooibos tea and NAC administered to CCl4-damaged rats restored liver concentrations of CoQ9H2 and alpha-tocopherol and inhibited the formation of MDA, all to the values comparable with healthy animals. Rooibos tea did not counteract the decrease in CoQ9, whereas NAC was able to do it. Improved regeneration of coenzyme Q9 redox state and inhibition of oxidative stress in CCl4-damaged livers may explain the beneficial effect of antioxidant therapy. Therefore, the consumption of rooibos tea as a rich source of natural antioxidants could be recommended as a market available, safe and effective hepatoprotector in patients with liver diseases.

Acetylcysteine↗
PubMed2003

Hepatoprotective effect of rooibos tea (Aspalathus linearis) on CCl4-induced liver damage in rats.

Hepatoprotective properties of rooibos tea (Aspalathus linearis) were investigated in a rat model of liver injury induced by carbon tetrachloride (CCl(4)). Rooibos tea, like N-acetyl-L-cysteine which was used for the comparison, showed histological regression of steatosis and cirrhosis in the liver tissue with a significant inhibition of the increase of liver tissue concentrations of malondialdehyde, triacylglycerols and cholesterol. Simultaneously, rooibos tea significantly suppressed mainly the increase in plasma activities of aminotransferases (ALT, AST), alkaline phosphatase and billirubin concentrations, which are considered as markers of liver functional state. The antifibrotic effect in the experimental model of hepatic cirrhosis of rats suggests the use of rooibos tea as a plant hepatoprotector in the diet of patients with hepatopathies.

Acetylcysteine↗
PubMed2003

Influence of 2,5-dihydroxybenzylidene aminoguanidine on lipid oxidative damage and on antioxidant levels in model diabetes mellitus.

2,5-Dihydroxybenzylidene aminoguanidine (BAG) is a structural analogue of the antidiabetic compound aminoguanidine, and is an example of a substance protecting diabetic rats from lipoprotein oxidation arising in oxidative stress conditions characteristic of diabetes mellitus. We found that administration of BAG to diabetic rats decreases their susceptibility to lipoprotein oxidation, decreases formation of conjugated dienes and 4-hydroxy-2-nonenal, and increases antioxidant potential of plasma. On the other hand, our results show that BAG has a negative influence on lipoprotein oxidation in control rats. Increased formation of 4-hydroxy-2-nonenal and conjugated dienes and a decrease in plasma antioxidant potential was observed when BAG was administered to control rats. It is therefore necessary to search for other structural modifications of this substance that would combine higher antidiabetic activity with less toxicity in healthy individuals.

Aldehydes↗
PubMed2002

Influence of beta-resorcylidene aminoguanidine on selected metabolic parameters and antioxidant status of rats with diabetes mellitus.

We studied the effects of administration of beta-resorcylidene aminoguanidine (RAG) to Wistar strain rats with experimental diabetes mellitus (DM) induced by streptozotocin. The effects studied included antioxidant levels in plasma and the liver, oxidative damage of lipids represented by the formation of substances reacting with thiobarbituric acid (TBARP) and selected biochemical indicators. The administration of RAG did not significantly affect antioxidant status of diabetic rats or hemoglobin glycation and plasma concentration of fructosamine. In diabetic rats, application of RAG decreased formation of TBARP in plasma but not in the liver. Moderate steatosis of liver and increased plasma levels of triacylglycerols in diabetic rats were significantly improved by application of RAG.

Animals↗
PubMed2002

Effects of aminoguanidine Schiff's base on biomarkers of the oxidative stress, 4-hydroxy-2-nonenal and conjugated dienes, in the model diabetes mellitus.

Diabetes mellitus evoked by streptozotocine in rats is associated with the oxidative stress. We examined the effect of Schiff's base 2,5-dihydroxybenzaldehyde with a well-known antidiabetic drug aminoguanidine, 2,5-dihydroxybenzilideneaminoguanidine (BAG) on the production of markers of oxidative stress such as 4-hydroxy-2-nonenal (4HNE) and conjugated dienes in diabetic rats. BAG administration did not affect glucose level in diabetic rats but significantly decreased the production of 4HNE and conjugated dienes. On the other hand, BAG caused the elevation of conjugated dienes and an insignificant increase of 4HNE levels in the control animals.

Aldehydes↗
PubMed2001

[Effect of losartan on antioxidant status in rats with diabetes mellitus].

The aim of this study was to monitor the effect of the administration of antihypertensive drug losartan on: (1) the antioxidant status of rats with experimental insulin-dependent diabetes mellitus; (2) oxidative damage which is represented by the production of compounds which can react with thiobarbituric acid (TBARP), and (3) some metabolic parameters. Losartan administration did not significantly influence the concentration of glucose, cholesterol, triacylglycerol, and uric acid in the plasma of control and diabetic animals. In the liver tissue, the concentration of triacylglycerols decreased after losartan administration, but the concentration of cholesterol did not change. The present authors have found that losartan administration increased the levels of water solubile antioxidants in the plasma of diabetic rats, which can result in a decrease of the TBARP levels in the plasma of diabetic rats.

Animals↗
PubMed2000

A rapid, simple, and cost-effective method for screening liver preservation solutions in the rat.

BACKGROUND: Rat liver transplantation models or isolated liver perfusion models are currently used for assessing efficacy of liver preservation methods. We tested the hypothesis that hepatocellular enzymes released into the washout solution after preservation may predict hepatic function during reperfusion and could thus be alternatively used for evaluating efficiency of liver preservation solutions. Furthermore, we applied this approach for assessing the role of Kupffer cells (KC) in preservation-induced liver damage. METHODS: After preservation in University of Wisconsin (UW) or Euro-Collins (EC) solution, rat livers were washed with Ringer-lactate solution. Correlations between enzymes released into the washout solution and hepatocyte functional parameters determined during reperfusion on using a blood-free perfusion model were investigated. RESULTS: In UW-preserved livers, acid phosphatase (ACP) activity correlated negatively with bile flow (R = -0.904), taurocholate intrinsic clearance (R = -0.841), and bromosulfophthalein excretion (R = -0.831). Both alanine transaminase and aspartate transaminase activities correlated with the functional parameters investigated. In EC-stored livers, correlation was also found between ACP activity and bile flow (R = -0.666). Livers stored in UW solution exhibited approximately 3 times lower washout activities of enzymes studied than livers stored in EC solution. Mitochondria isolated from UW-stored livers exhibited significantly better function than those isolated from EC-stored livers. Blockade of KC did not influence enzyme release into the washout solution. CONCLUSIONS: Determination of ACP, alanine transaminase, and aspartate transaminase activities in the washout solution can be used as a rapid, simple, and cost-effective way for screening liver preservation solutions. The results also suggest that KC were not involved in preservation-induced liver damage.

Acid Phosphatase↗
PubMed2000

Impaired erythrocyte transmembrane potential in diabetes mellitus and its possible improvement by resorcylidene aminoguanidine.

Erythrocytes of diabetic patients have abnormal membrane properties. We examined in vitro transmembrane potential and the possible effect of resorcylidene aminoguanidine (RAG) on its modulation in erythrocytes of diabetic subjects. The transmembrane potential was assessed in RAG-treated and untreated erythrocytes, respectively, using a fluorescent dye (3,3'-dipropylthiadicarbocyanine iodide [DiSC3(5)]). We confirmed earlier findings that the transmembrane potential of diabetic erythrocytes is significantly increased compared with control (P < 0.01). The membrane hyperpolarization found in diabetic cells seems to be a result of oxidative stress present in diabetes mellitus. On one hand, the RAG treatment induced decrease in abnormal transmembrane potential values in diabetic erythrocytes (P < 0.01), presumably via its antioxidant and antiglycation activity. On the other hand, RAG moderately hyperpolarized the control erythrocytes (P < 0.05). We suggest that the drug-induced transient membrane expansion leads to an intracellular potassium loss and a subsequent change of the transmembrane potential. However, if controlled by an appropriate dosage, RAG can eliminate certain types of erythrocyte membrane damage induced by diabetes mellitus.

Benzothiazoles↗
PubMed2000

Deficit of coenzyme Q in heart and liver mitochondria of rats with streptozotocin-induced diabetes.

Mitochondrial dysfunction and oxidative stress participate in the development of diabetic complications, however, the mechanisms of their origin are not entirely clear. Coenzyme Q has an important function in mitochondrial bioenergetics and is also a powerful antioxidant. Coenzyme Q (CoQ) regenerates alpha-tocopherol to its active form and prevents atherogenesis by protecting low-density lipoproteins against oxidation. The aim of this study was to ascertain whether the experimentally induced diabetes mellitus is associated with changes in the content of endogenous antioxidants (alpha-tocopherol, coenzymes Q9 and Q10) and in the intensity of lipoperoxidation. These biochemical parameters were investigated in the blood and in the isolated heart and liver mitochondria. Diabetes was induced in male Wistar rats by a single intravenous injection of streptozotocin (45 mg x kg(-1)), insulin was administered once a day for 8 weeks (6 U x kg(-1)). The concentrations of glucose, cholesterol, alpha-tocopherol and CoQ homologues in the blood of the diabetic rats were increased. The CoQ9/cholesterol ratio was reduced. In heart and liver mitochondria of the diabetic rats we found an increased concentration of alpha-tocopherol, however, the concentrations of CoQ9 and CoQ10 were decreased. The formation of malondialdehyde was enhanced in the plasma and heart mitochondria. The results have demonstrated that experimental diabetes is associated with increased lipoperoxidation, in spite of the increased blood concentrations of antioxidants alpha-tocopherol and CoQ. These changes may be associated with disturbances of lipid metabolism in diabetic rats. An important finding is that heart and liver mitochondria from the diabetic rats contain less CoQ9 and CoQ10 in comparison with the controls. We suppose that the deficit of coenzyme Q can participate in disturbances of mitochondrial energy metabolism of diabetic animals.

Animals↗
PubMed2000

Susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic rat heart.

Diabetic heart is suggested to exhibit either increased or decreased resistance to ischemic injury. Ischemic preconditioning suppresses arrhythmias in the normal heart, whereas relatively little is known about its effects in the diseased myocardium. Our objective was to investigate whether development of diabetes mellitus modifies the susceptibility to ischemia-induced arrhythmias and affects preconditioning in the rat heart. Following 1 and 9 weeks of streptozotocin-induced (45 mg/kg, i.v.) diabetes, the hearts were Langendorff-perfused at constant pressure of 70 mm Hg and subjected to test ischemia induced by 30 min occlusion of the left anterior descending (LAD) coronary artery. Preconditioning consisted of one cycle of 5 min ischemia and 10 min reperfusion, prior to test ischemia. Susceptibility to ischemia-induced arrhythmias was lower in 1-week diabetics: only 42 % of diabetic hearts exhibited ventricular tachycardia (VT) and 16 % had short episodes of ventricular fibrillation (VF) as compared to VT 100 % and VF 70 % (including sustained VF 36 %) in the non-diabetics (P<0.05). Development of the disease was associated with an increased incidence of VT (VT 92 %, not significantly different from non-diabetics) and longer total duration of VT and VF at 9-weeks, as compared to 1-week diabetics. Preconditioning effectively suppressed arrhythmias in the normal hearts (VT 33 %, VF 0 %). However, it did not provide any additional antiarrhythmic protection in the acute diabetes. On the other hand, in the preconditioned 9-weeks diabetic hearts, the incidence of arrhythmias tended to decrease (VT 50 %, transient VF 10 %) and their severity was reduced. Diabetic rat hearts are thus less susceptible to ischemia-induced arrhythmias in the acute phase of the disease. Development of diabetes attenuates increased ischemic tolerance, however, diabetic hearts in the chronic phase can benefit more from ischemic preconditioning, due to its persisting influence.

Animals↗
PubMed1999

[The effect of streptozotocin-induced diabetes in the neonatal period on hepatic mitochondrial bioenergetics in adult rats].

BACKGROUND: Previous experimental studies focused on the liver mitochondrial bioenergetic changes in diabetes mellitus type I induced in adult animals. Information about the effects of persisting neonataly induced diabetes mellitus type I on the mitochondrial bioenergetics are missing. AIM: The aim of the study was to assess the degree of diabetes mellitus compensation and parameters of oxidative phosphorylation in rats aged 3 months with DM persisting from neonatal period. METHODS: DM was induced in male Wistar rats by repeated intraperitoneal administration of streptozotocine 45 mg/kg on 2nd and 9th day after birth. The concentrations of glucose, glycosylated haemoglobin, fructosamine were detected in the blood and the concentration of cholesterol and triacylglycerols in the blood and liver tissue, respectively. After mitochondria isolation from the liver we measured parameters of oxidative phosphorylation by polarography using Clark oxygen electrode. RESULTS: In the group of neonataly induced DM the concentration of glucose (23.10 +/- 1.55 vs 8.3 +/- 0.56 mmol/l), glycosylated haemoglobin (6.04 +/- 1.17 vs 3.99 +/- 0.44%) and blood cholesterol concentration (2.15 +/- 0.11 vs 1.83 +/- 0.09 mmol/l) increased significantly (p < 0.001 and p < 0.005 for cholesterol) comparing to a group of healthy rats. No statistically significant differences were found in the remaining parameters when comparing these two groups. The parameters of oxidative phosphorylation were significantly (p < 0.001) decreased in the group with DM comparing to control group of healthy animals--the index of respiratory control (4.87 +/- 0.25 vs 9.57 +/- 0.34), the rate of oxygen consumption in the stage 3 in ADP presence (88.61 +/- 4.62 vs 165.08 +/- 4.5 natO.mg/protein/min) and phosphorylation rate (203.54 +/- 7.26 vs 332.87 +/- 7.39 nmolATP.mg/protein/min) with NAD substrate glutamate. Similar trend was also seen with FAD substrate succinate. The index of oxidative phosphorylation ADP:0 was not changed in both groups. CONCLUSIONS: In 3 months old rats with neonataly induced DM the development of steatosis was not observed and uncoupling of oxidative processes from phosphorylation did not appear. Energy production was sufficient enough for normal functions of the liver and to ensure all needs of the organism. (Tab. 4, Ref. 51.)

Aging↗
PubMed1997

[Bioenergetics of liver mitochondria after administration of ramipril in experimental diabetes mellitus].

BACKGROUND: Diabetes mellitus represents an intense metabolic strain for the liver. Inhibitors of angiotensin-converting enzymes (ACEI) are drugs of choice in the therapy of hypertension in coincidence with diabetes mellitus. The effect of ACEI is complex. The attention is drawn to the study of metabolic effects of ACEI. OBJECTIVES: The aim of the study was to investigate whether the administration of ramipril affects the levels of glycated hemoglobin and fructoseamine in the blood of rats with insulin-dependent diabetes mellitus (IDDM), and whether bioenergetics of mitochondria in the liver undergo changes. METHODS: In our experiments, we used rats of the Wistar strain. The control group was composed of healthy animals. The experimental groups were formed by rats with IDDM evoked by streptozotocine (45 mg/kg) and rats with IDDM + ramipril (10 mg/KG). Both, insulin MONO-ID in the doses of 6 U/kg administered subcutaneously, and water solution of ramipril administered by gastric probe were applied for the period of 8 weeks. We have assessed blood levels of glucose, glycated hemoglobin, fructoseamine and the concentration of cholesterol and triacylglycerols have been assessed also in the liver. Oxidative phosphorylation in mitochondria of the liver were measured polarographically. RESULTS: In the group with IDDM + ramipril, the glycated haemoglobin (M 6.85 CI 5.7-7.0%) and fructoseamine (M 1.45 CI 1.2-1.6 mmol/l) have significantly dropped in comparison with the group with IDDM glycated haemoglobin (M 8.8 7.7-10.7%) and fructoseamine (M 2.04 CI 1.69-2.4 mmol/l). Ramipril did not affect the concentration of cholesterol and triacylglycerols in the blood and liver in rats with IDDM. Ramipril has positively affected oxidative phosphorylation in mitochondria of the liver in coincidence with IDDM. The group with IDDM + ramipril has yielded an increase in the velocity of oxygen consumption in coincidence with stimulated breathing with ADP, the state 3 (M 107.97 CI 96.78-134.51 n AtO/mg of proteins/min.) and phosphorylation velocity (M 232.67 CI 209.38-284.97 nmolATP/protein/min) in contrast to the group with IDDM: the state 3 (M 76.71 CI 66.81-85.99 nAtO/mg of proteins/min and the velocity of phosphorylation (M 161.84 CI 143.55-189.99 nmol ATP/mg of proteins/min) in coincidence with substrate glutamate. A similar trend is present also in coincidence with FAD succinate substrate. CONCLUSIONS: After the administration of ramipril to rats with IDDM, the indicators have improved, and they express the rate of compensation of diabetes mellitus. An increased capacity of the respiratory chain and an increased origin of energy in mitochondria in the livers of rats with IDDM after administration of ramipril indicates an improvement in the metabolic capacity of the liver. (Tab. 4. Ref. 47.)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[Bioenergetics of liver mitochondria in rats in experimental insulin-dependent diabetes].

Oxidative stress in the course of diabetes mellitus can cause disturbance of lipid membranes of cellular organelles. The study is aimed at the determination of oxidative phosphorylation in mitochondria in rats with experimentally induced acute and chronic insulin-dependent diabetes mellitus (IDDM). IDDM was induced by single dose of streptozotocin (45 mg per kg-1). Insulin Interdep (6 U per kg-1) was administered once a day subcutaneously. The authors investigated glycaemia, cholesterol and triacylglycerol concentrations in the blood and liver. Isolation of mitochondria was succeeded by measurement of oxidative phosphorylation indicators after 8 days (acute IDDM) or after 8 weeks (chronic IDDM) from streptozotocin administration. The authors found out that both acute and chronic IDDM were concommited by hyperglycaemia. The group with acute IDDM yielded an increase in cholesterol and triacyglycerols concentrations in the blood, as well as that of cholesterol in the liver. The group with chronic IDDM yields an increase in cholesterol in the blood. Trialcylglycerols in the liver increased in none of the investigated groups. Liver steatosis did not occur. Indicators of oxidative phosphorylation in the liver mitochondria of rats with acute and with chronic IDDM decreased in contrast to healthy controls from NAD substrates glutamate and pyruvate and also form FAD substrate of succinate. Significant decrease in consumption of oxygen in the 3 state occurred, while in acute IDDM the decrease was more significant than in chronic IDDM. Phosphorylation rate significantly decreased in contrast to controls, but there was no difference between IDDM groups. The investigation results imply that in both acute and chronic IDDM there are decreased effectivity of energetic metabolism in liver mitochondria. (Tab. 5, Ref. 29.).

Animals↗
PubMed1994

[Oxidative phosphorylation in liver mitochondria after injury with carbon tetrachloride and during regeneration].

The study investigates the effect of a singular dose of CCl4 (2.5 ml/kg) on the concentration of triacylglycerols in the liver and oxidative phosphorylation in hepatic mitochondria after 24, 72 hours, 2 and 4 weeks since CCl4 application. It was discovered that 24 and 72 hours after CCl4 application the concentration of triacylglycerols increased significantly and steatosis of the liver supervened. After 2 and 4 weeks the triacylglycerol concentration values reached the level of those of control. The hepatic steatosis disappeared. The indices of oxidative phosphorylation index of respiration control, oxygen consumption during stimulated respiration (state 3), oxygen consumption during basal respiration (state 4), and phosphorylation velocity decreased significantly after 24 and 72 hours after CCl4 application in all observed substrates--glutamate, pyruvate and jantarane. After 2 to 4 weeks the observed indices reached the level of values characteristic for healthy controls. The results have indicated that after the CCl4 toxic impairment the energy metabolism in hepatic mitochondria has been significantly impaired. This impairment, in spite of its severeness, was irreversible and hepatocytes were able to compensate it (Tab. 4, Ref. 33).

Animals↗
PubMed1994

[Biochemical and functional study of the liver during treatment of familial hyperlipoproteinemia with Mevacor (lovastatin) and Vasosan S (cholestyramine)].

The aim of our study was the biochemical and functional examination of the liver during the therapy of familiar hyperlipoproteinemia by means of MevacorR (lovostatine) in comparison with the treatment by Vasosan S (cholestyramine). We examined 20 patients treated with a daily dose of MevacorR being 20-40 mg and, 18 patients treated with a daily dose of Vasosan S being 16-32 g for the period of 12 weeks. During the therapy the total cholesterol, LDL-cholesterol, HDL-cholesterol, triacylglycerols, hepatic enzymes (AST, ALT, ALP) activity, functional test of the liver, biological half-time of antipyrine (t 1/2 antipyrine) were investigated at the onset and at the end of the study. We discovered that at the end of the treatments by MevacorR and Vasosan S the hypolipidemic effect increased (cholesterol p < 0.001, LDL cholesterol p < 0.001), and there was difference in the effect on HDL-cholesterol and in that on triacylglycerols. During the treatment we discovered that due to both medicaments the liver enzymes activity increased to a different extent. At the beginning of the study the antipyrine biological half-time statistically increased in both investigated groups, namely in comparison with the control group. At the end of the treatments in both groups the antipyrine half-time was prolonged, however not significantly. Prior to long-term therapy by hypolipidemics the authors recommend biochemical and functional examination of the liver. (Tab. 4, Fig. 8, Ref. 7.)

Cholestyramine Resin↗
PubMed1994

[The effect of beta-escin on metabolism in experimental liver steatosis in rats].

The aim of the study was to investigate the effect of beta-aescin on the selected indices of sugar and lipid metabolisms in blood and hepatic tissue. The study was performed under the conditions of toxic impairment of the liver caused by carbon tetrachloride or hydrazinsulphate which were used in order to evoke experimentally the steatosis of the liver. The study investigated whether beta-aescin can cause deterioration of hepatic steatosis. Carbon tetrachloride was administered to rats by stomach probe in dosis of 2.5 ml per kg of body weight, or hydrazinsulphate in dosis of 2 mmol per kg of body weight, i.m.. Twenty-four hours after administration of these two substances beta-aescin water solution was administered in dosis of 10 mg per kg of body weight by means of stomach probe. The analysis of blood and liver tissue samples discovered that beta-aescin did not affect the metabolic indices, steatosis of the liver did not become more profound. (Tab. 2, Fig. 11, Ref. 23.)

Animals↗