PubMed Health⌕ Search

Biomedical subjects

R Farbiszewski

Publications and source records attributed to R Farbiszewski.

At least 37 records · Page 2Linked to original sources

Endogenic non-enzymatic antioxidative system of polyester grafts during their healing.

OBJECTIVE: Non-enzymatic low-molecular antioxidants are one of the important mechanisms which protect cells against the toxic effect of oxygen. The aim of the present study was to determine the content of glutathione, glutathione reductase, and ascorbic acid in the principal layers of polyester grafts. INTERVENTIONS AND MEASURES: The experiments were carried out on 24 mongrel dogs, in which polyester double velour DALLON grafts were implanted. Seven days, 1, 4, and 12 months after the operation the grafts were excised. The following were determined: glutathione content by use of a GSH-400 system, glutathione reductase activity by the method of Langdon and Mize, and ascorbic acid content by the Kyaw method. RESULTS: It was found that the glutathione content in the graft neointima was 33% lower, in the graft neomedia higher during the first 4 months, in the neoadventitia 50% lower after 4 months than in the corresponding layers of the aorta (p < 0.01). The activity of glutathione reductase was significantly higher in all the graft layers during 12 months' observation than in the normal aorta layers. The ascorbic acid content of the graft layers was lowest 7 days after the implantation, and then in time increased so that 12 months after the operation it reaches its highest values. CONCLUSIONS: Our study shows that low non-enzymatic antioxidative potential is not capable of proteoting the newly forming graft layers, particularly the neointima, against oxygen toxicity. Thus, it would be beneficial to administer antioxidants (vitamin C, vitamin E, and N-acetylcysteine).

Animals↗

Spermine partially normalizes in vivo antioxidant defense potential in certain brain regions in transiently hypoperfused rat brain.

Activities of the antioxidant enzymes such as superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) as well as the level of reduced glutathione and the concentration of thiobarbituric acid-reactive substance (TBARS) in brain regions in transiently hypoperfused rat brain with or without intravenous infusion of spermine were evaluated. Cerebral hypoperfusion was induced by temporary occlusion of common carotid arteries for 30 min and subsequently, by reperfusion for 60 min. Infusion of spermine reversed the decrease in SOD activity in the cerebral cortex, striatum, hippocampus, hypothalamus and midbrain, and amounted to 50.1 U, 61.5 U, 50.3 U, 30.0 U, 38.0 U, respectively, while GSH-Px restored to normal values only in the cerebral cortex and striatum and amounted to 100 U and 110 U, respectively. During hypoperfusion/reperfusion and after use of spermine no changes in GSSG-R were seen in the hypothalamus and midbrain. The activity of GSSG-R was in accordance with the control for the striatum and amounted to 39.0 IU after using spermine. GSH content returned to normal values in the striatum and midbrain after i.v. use of spermine and amounted to 210 and 240 nmol/g of wet tissue, respectively. In addition, the production of TBARS dropped markedly (P < 0.05) in the hippocampus and midbrain and amounted to 100 and 105 mumol/g of wet tissue, respectively. Partially beneficial effect of spermine could result from the inhibition of free radical generation and capability of chelate formation with iron ions.

Animals↗

Diminished antioxidant defense potential of liver, erythrocytes and serum from rats with subacute methanol intoxication.

The activities of superoxide dismutase (SOD), catalase glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) and the concentration of ascorbate, alpha-tocopherol, non-protein and protein-bound sulfhydryl compounds, and thiobarbituric acid-reactive substances (TBA-rs) in liver, erythrocytes and serum of rats dosed with 1.5 g methanol/kg bw were measured after 6, 12 and 24 h and 2, 5 and 7 d. Hematological erythrocyte parameters were also determined. Liver GSH-Px and GSSG-R activities, SH-groups and ascorbate were significantly diminished at 12 and 24 h, while TBA-rs increased. Blood SOD, GSH-Px and GSSG-R activities and sulfhydryl-group concentrations were reduced while TBA-rs were elevated. Methanol given to rats impaired liver, erythrocyte and blood serum antioxidant mechanisms.

Animals↗

[Adaptation mechanisms of cells and removal of damage due to oxidative stress].

This review describe the role of adaptative mechanisms of the cell against oxidative damage induced by free radicals. Adaptative response refers the ability of cells to better resist the damaging effects of toxic agent when first preexposed to a lover dose. Extensive studies have revealed that oxidized proteins are recognized by proteases and completely degraded to amino acids. In this way damaged proteins are removed.

Adaptation, Physiological↗

Spermine protects in vivo the antioxidant enzymes in transiently hypoperfused rat brain.

The antioxidant enzymatic system in brain hypoperfusion/reperfusion model in rats after spermine administration was evaluated. Incomplete cerebral ischemia/reperfusion induced by temporal occlusion of common carotid arteries caused a decrease in the activities of superoxide dismutase and glutathione reductase as well as total and free sulfhydryl groups, while thiobarbituric acid-reactive substances became elevated. Administration of spermine after the reperfusion led to restoring all above parameters to normal values. Protective effect of spermine in transiently hypoperfused and subsequently reperfused rat brain is briefly discussed.

Animals↗

Increase in the peritoneal antioxidative potential in experimental hemorrhagic shock.

Production of the oxygen-derived free radicals in peritoneal lavage after one-hour hemorrhagic shock were investigated on a rat model. A statistically significant increased activity of superoxide dismutase (SOD), and an insignificant enhancement of concentration of -SH groups, comparing to the control animals was shown. There was no difference in the level of malondialdehyde (MDA) in the peritoneal fluid from the bled animals and the control group. The results indicate an increased antioxidative potential of the peritoneal content in the early phase of hemorrhagic shock.

Analysis of Variance↗

[Interaction of free radicals with proteins].

This review describe the generation of free radicals in the cells under the influence of exogenously and endogenously acting factors. The interactions of free radicals with proteins and amino acids and the consequences of these effects are also presented.

Amino Acids↗

The role of free oxygen radicals in children with chronic viral hepatitis B.

Lipid peroxidation of polyunsaturated fatty acids, being important components of cellular membranes, caused by free oxygen radicals is considered to be one of the main causes of hepatocyte injury. The aim of this study is to estimate the malondialdehyde (MDA) level in the red blood cells of children with chronic viral hepatitis B. The decrease of MDA concentration along with the clinical and serological improvement in children with chronic hepatitis B was observed. We also noticed a correlation of MDA with HBeAg-anti HBe seroconversion and obliteration of HBV DNA polimerase activity.

Child↗

Ethanol ingestion decreases superoxide dismutase activity and diminishes -SH compounds in the liver and red blood cells in rats.

SOD activity and -SH compounds in the liver and RBCs, and some hematological parameters were investigated in control rats and in those submitted to chronic (3 months) intoxication with ethanol. We found significantly lower SOD activity and a decrease in -SH groups in the liver and RBCs of ethanol-treated rats in comparison with the control group. The hemoglobin content and mean corpuscular hemoglobin concentration were reduced, while mean corpuscular volume of RBCs was increased when compared with the control group.

Alcoholic Intoxication↗

The 21-aminosteroid U-74389G protects the antioxidant enzymes in the ischemia/reperfusion-induced rat brain damage.

The antioxidant enzymatic system in the ischemia/reperfusion induced brain injury in rats after U-74389G administration was evaluated. Ischemia/reperfusion caused a decrease in the activities of superoxide dismutase and glutathione reductase, as well as of total and free sulfhydryl groups, while thiobarbituric acid-reactive substances became elevated. Administration of U-74389G lead to restoring to normal values of all above parameters. Protective effect of the drug in ischemia/reperfusion induced brain injury has been suggested.

Animals↗

Inhibition of non-enzymatic lipid peroxidation by 'Essentiale' a drug enriched in phosphatidylcholine in ethanol-induced liver injury.

The effect of 'Essentiale'--a drug, now clinically listed in European countries in the treatment of liver diseases was examined in ethanol-induced liver injury in rats (free access to a 20% ethanol solution for 3 months). The antioxidant enzymes, SOD (superoxide dismutase), CAT (catalase), GSH-R (glutathione reductase), non-protein and total SH groups as well as TBA-rs contents were investigated. Following treatment, we found beneficial effects in SOD and CAT activities. The above enzyme activities were restored after a 3-month drug administration. Furthermore, 'Essentiale' treatment normalized TBA-rs levels in the liver. These effects have been briefly discussed.

Animals↗

The diminution of liver glutathione content and changes in activities of antioxidant enzymes in long-term acetaldehyde poisoning.

The effect of acetaldehyde administration for 4 weeks on antioxidant protection systems was investigated in liver of rats. Liver SOD activity was decreased from control value 542.4 U/g of tissue to 411.2 U/g of tissue in experimental group (24% decrease). GSH-Px activity was practically unchanged and liver CAT activity was significantly decreased (35%). Sulfhydryl compounds in liver non-proteins following ACH treatment were decreased from 4.22 mumol/g of tissue in control group to 2.86 mumol/g of tissue (23%). Furthermore acetaldehyde treatment caused significant increase in MDA level in liver (78% increase).

Acetaldehyde↗

The decrease of superoxide dismutase activity and depletion of sulfhydryl compounds in ethanol-induced liver injury.

There appears to be increasing evidence that ethanol toxicity may be associated with an increased production of reactive oxygen intermediates. In rats we studied the effect of 4 weeks of ethanol ingestion on the liver cytosolic defense system against active oxygen species. Compared with the control rats, the ethanol-fed animals had a significantly higher liver malondialdehyde content and significantly lower reduced glutathione level. Moreover, ethanol feeding resulted in a decrease of superoxide dismutase and catalase activities while glutathione peroxidase activity was only slightly diminished. Thus, prolonged ethanol administration profoundly modified the hepatic status of the enzymatic defense system leading to lipid peroxidation that may disrupt vital functions of liver cells.

Animals↗

The effect of Heparegen and D-penicillamine on the activity of some ammonia metabolizing enzymes in liver and brain of rats intoxicated with ethanol.

This paper reports data on the effect of two drugs: Heparegen (thiazalidine-4-carboxylic acid) and D-penicillamine on the blood ammonia concentration and on some ammonia metabolizing enzymes in liver and brain of rats intoxicated with ethanol. It seems, that both drugs decrease ammonia concentration and simultaneously elevate liver and brain glutamine synthetase activity. The effect of D-penicillamine on the nitrogen metabolism in the damaged liver appears to be more favorable than that of Heparegen.

Alcoholic Intoxication↗

[Morphological studies of the effects of protein-free diet and branched-chain amino acids (aminosteril-hepa (Frasenius)) on experimental thioacetamide-induced liver damage].

The studies were performed in two groups of rats in which experimental hepatic encephalopathy was induced with tioacetamide++. One group of rats on protein-free diet was given intraperitoneally a mixture of amino-acids (Aminosteril-Hepa), the other one was given proteins in the diet in a dose 1 g per kg of body weight. Histological and histochemical studies revealed that free-protein diet with a mixture of aliphatic polybranched amino-acids (Aminosteril-Hepa) inhibited hepatotoxic thioacetamide+ action on the rat liver.

Amino Acids↗

Ethanol decreases the level of sulfhydryl compounds in red blood cells and changes their hematological pattern in rats.

The level of sulfhydryl compounds in red blood cells (RBCs) and plasma and some haematological parameters were investigated in rats treated with ethanol for 4 weeks (daily dose of 6g/kg, 30% w/v, p.o.). After ethanol ingestion, the significant decrease of non-protein - SH groups were observed in RBCs and plasma. In treated rats, the mean corpuscular haemoglobin concentration (MCHC) was decreased and the mean corpuscular volume (MCV) was increased. There is a positive correlation between these two parameters and decreased content of sulfohydryl groups in RBCs.

Animals↗

Branched-chain amino acid enriched diet given simultaneously with ethanol partially prevents morphological and biochemical changes in the liver.

Morphological examination of the liver and biochemical studies of the serum were carried out on rats fed: a) ethanol p.o. in the daily dose of 6 g/kg for 4 weeks and maintained on standard diet (Et-OH) and b) ethanol in the same doses but fed the BCAA enriched diet (to amount of 1.174 mM/day/rat) were carried out. It can be concluded that BCAA enriched diet given simultaneously with ethanol prevent in part the morphological and ultrastructural changes in liver and improve positive body weight gain of experimental animals.

Amino Acids, Branched-Chain↗