Biomedical subjects

R Farbiszewski

Publications and source records attributed to R Farbiszewski.

At least 19 recordsLinked to original sources

PubMed2002

Protective effect of green tea against lipid peroxidation in the rat liver, blood serum and the brain.

This paper reports data on the effect of green tea on the lipid peroxidation products formation and parameters of antioxidative system of the liver, blood serum and central nervous tissue of healthy young rats drinking green tea for five weeks. The rats were permitted free access to solubilized extract of green tea. Bioactive ingredients of green tea extract caused in the liver an increase in the activity of glutathione peroxidase and glutathione reductase and in the content of reduced glutathione as well as marked decrease in lipid hydroperoxides (LOOH), 4-hydroksynonenal (4-HNE) and malondialdehyde (MDA). The concentration of vitamin A increased by about 40%. Minor changes in the measured parameters were observed in the blood serum. GSH content increased slightly, whereas the index of the total antioxidant status increased significantly. In contrast, the lipid peroxidation products, particularly MDA was significantly diminished. In the central nervous tissue the activity of superoxide dismutase and glutathione peroxidase decreased while the activity od glutathione reductase and catalase increased after drinking green tea. Moreover the level of LOOH, 4-HNE and MDA significantly decreased. The use of green tea extract appeared to be beneficial to rats in reducing lipid peroxidation products. These results support and substantiate traditional consumption of green tea as protection against lipid peroxidation in the liver, blood serum, and central nervous tissue.

Animals↗

PubMed2002

Green tea as a potent antioxidant in alcohol intoxication.

Ethanol oxidation to acetaldehyde and next to acetate is accompanied by free radical generation. Free radicals can affect cell integrity when antioxidant mechanisms are no longer able to cope with the free radical generation observed in ethanol intoxication. Natural antioxidants are particularly useful in such a situation. The present study was designed to investigate the efficacy of green tea as a source of water-soluble antioxidants (catechins) on the liver and blood serum antioxidative potential of rats chronically (28 days) intoxicated with ethanol. Alcohol caused a decrease in liver superoxide dismutase, glutathione peroxidase and catalase activities and an increase in activity of glutathione reductase. Moreover, a decrease in the level of reduced glutathione, ascorbic acid, vitamins A and E and beta-carotene were observed. The activity of serum glutathione peroxidase decreased while glutathione reductase activity increased. The level of serum non-enzymatic antioxidants was also decreased in the liver. Alcohol administration caused an increase in the liver and serum lipid peroxidation products, measured as thiobarbituric acid-reactive substances. However, green tea prevents the changes observed after ethanol intoxication. Green tea also protects membrane phospholipids from enhanced peroxidation. These results indicate a beneficial effect of green tea in alcohol intoxication.

Alcoholic Intoxication↗

PubMed2001

[Activity of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) and superoxide dismutase in the brain tumors].

The aim of the study was to estimate the activity of glutathione peroxydase, glutathione reductase and superoxide dysmutase in the brain tumours. The activity of GSH-Px was evaluated with the use of spectrophotometry, GSSG-R was evaluated based on the Mize and Langdon method, and SOD-1 with Sykes et al. method. The 55 specimens (45 specimens of neoplasm and 10 specimens of healthy brain tissue) were studied. The statistical analysis revealed significant increase of enzymes within the brain tumours in comparison to the healthy brain tissue.

Brain Neoplasms↗

PubMed2001

[Concentration of glutathione (GSH), ascorbic acid (Vit. C), and thiobarbiturate acid reacting components (MDA) in brain neoplasms].

The aim of the study was to evaluate the concentration of glutathione (GSH), ascorbic acid (Vit C), and thiobarbiturate acid reacting components (MDA) in brain neoplasms in specimens from normal brain tissue. The group of 72 individuals treated surgically for brain neoplasm in Department of Neurosurgery Medical Academy of Białystok (Poland) in the period from 1996 to 1999 was included into the study. The GSH concentration was estimated with GSH-400 method, ascorbic acid by the use of Kyaw method, and MDA by Salaris and Babs method. The statistical analysis revealed diminished concentration of GSH and Vit. C (p < 0.001), and analogous increase of MDA concentration (p < 0.001) in the investigated specimens compared to the mentioned above substances concentration in the specimens obtained from normal brain tissue.

Adult↗

PubMed2000

N-acetylcysteine or trolox derivative mitigate the toxic effects of methanol on the antioxidant system of rat brain.

The effect of two compounds: N-acetylcysteine (NAC) and trolox derivative (U-83836E) on the methanol induced impairment of the antioxidant system of the rat brain was studied in male Wistar rats (approx. 250 g body weight). The animals were divided into six main groups: control group (0.5 ml of physiological saline intragastrically), NAC group (150 mg/kg intraperitoneally-i.p), U-83836E group (10 mg/kg i.p.), methanol group (3 g/kg intragastrically), NAC+methanol and U-83836E+methanol groups. In these particular groups the changes in antioxidant parameters were observed for 6,12,24,48 h and 5 and 7 days. The results proved that the use of methanol and N-acetylcysteine increased the activities of Cu,Zn-superoxide dismutase, glutathione peroxidase and glutathione reductase by about 15,15 and 41%, respectively, in comparison to the group of rats receiving methanol alone. Similarly, the level of GSH increased by about 17%, the concentration of ascorbate by 20%, while the thiobarbituric acid-reactive substances (TBA-rs) diminished to the values as in control group. The use of new antioxidant U8383E and methanol showed less beneficial effect in the measured parameters however, it serves as a better protector for the methanol induced decrease in GSH-content. These data suggest that NAC and U-83836E mitigate the toxic effects of methanol on the antioxidant system of the rat brain.

Acetylcysteine↗

PubMed1999

Protective effect of N-acetylcysteine on reduced glutathione, reduced glutathione-related enzymes and lipid peroxidation in methanol intoxication.

The primary metabolic appropriation of methanol is oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of N-acetylcysteine (NAC) on reduced glutathione (GSH) and on activity of some GSH-metabolising enzymes in the liver, erythrocytes and serum of rats intoxicated with methanol (3 g/kg b.w.) during 7 days after intoxication. Methanol administration, increasing concentration of the lipid peroxidation products, decreased the liver glutathione-peroxidase and glutathione reductase (GSSG-R) activities, GSH concentration and total antioxidant status (TAS). The use of NAC after methanol ingestion apparently diminished lipid peroxidation, elevated the GSH level in the liver and erythrocytes, and increased activity of GSH-related enzymes in the serum, erythrocytes and in the liver. These results suggest that NAC exerts its protective effect by acting as a precursor for glutathione, the main low molecular antioxidant and as a free radical scavenger.

Acetylcysteine↗

PubMed1999

Activity of cathepsin G, elastase, and their inhibitors in plasma during methanol intoxication.

Methanol oxidation in the liver is accompanied by formation of formaldehyde and free radicals. These compounds can react with biologically active proteins, including proteolytic enzymes and their inhibitors. The activity of cathepsin G and elastase and their inhibitors such as alpha-1-antitrypsin and alpha-2-macroglobulin in plasma of rats given methanol orally in doses of 1.5, 3, and 6 g/kg was investigated for 7 days. The activity of cathepsin G and elastase was increased from 12 h to 5 d, proportionally to methanol dose. At the same time, activity of their inhibitors was reduced. Methanol ingestion in humans caused changes in activities of proteases and their inhibitors with similar direction as in rats. These changes in activity of proteases and their inhibitors produce significant disturbances in proteolytic-antiproteolytic balance after methanol administration.

Adult↗

PubMed1999

BN52021 stabilizes the oxidant-antioxidant equilibrium in peritoneal lavage fluid in experimental hemorrhagic shock.

The overproduction of highly reactive oxygen metabolites initiates and contributes to the damage to abdominal organs in hemorrhagic shock (HS). Peritoneal environment including free cells located in peritoneal cavity may interact with the inflammatory processes occurring in abdominal organs during HS. Peritoneal lavage was carried out in 48 rats divided into following groups: (1) control, (2) untreated HS for 75 minutes, (3) HS + restoration of blood volume with polyelectrolyte solution (PES) 60 minutes after blood withdrawal, and (4) HS + platelet activating factor (PAF) receptor antagonist BN52021 directly after bleeding + PES after 60 minutes of HS. Peritoneal lavage fluid (PLF) was examined for Cu-, Zn-superoxide dismutase (SOD) activity, sulfhydryl compound (-SH) concentration, and malondialdehyde (MDA) level measured as thiobarbituric acid reactive substances (TBARS). The untreated shock (group 2) as well as HS + PES (group 3), resulted in significant increase in cell numbers in PLF. In groups 2 and 3, the SOD activities were not detected while -SH group levels were significantly higher, than those in the control. The group of shocked rats after blood volume restoration with PES was the only group where the MDA in PLF was found. The highest -SH group concentrations and detectable SOD activities were recorded in shocked rats treated with BN52021 and PES. Systemic hemorrhage may cause significant alterations in the oxidant-antioxidant (O-A) balance in peritoneal cavity, accompanied by significant elevation of number of cells lavaged from peritoneal cavity. There is an escalation of disturbances in O-A balance in peritoneal lavage fluid due to restoration of blood volume. BN52021 may exert beneficial effects stabilizing peritoneal antioxidant system in the hemorrhagic shock.

Animals↗

PubMed1999

Effects of clobazam and vitamin E on the lipid peroxidation in the rat brain after electroconvulsive shock.

The effect of vitamin E and clobazam on lipid peroxides [LP] in the rat brain and the pattern of electroshock-induced seizures were assessed. Significant increase in the concentration of brain LP at the peak of seizures was found. Both vitamin E and clobazam reduced the levels of LP in the rat brain after electroshock. Clobazam combined with vitamin E inhibited markedly formation of LP in the rats with electroshock-induced seizures. Vitamin E augmented anticonvulsant effect of clobazam though itself it had not exhibited any anticonvulsant effect in this model of seizures. The action of two drugs combined resulted in reducing the intensity and the duration of seizures, and only minimal seizures were observed. In our opinion the obtained results possess some interesting clinical aspect They suggest that the combined treatment with clobazam and vitamin E of epileptic patient may decrease the intensity of epileptic seizures due to inhibition of LP formation.

Animals↗

PubMed1998

Lipid peroxidation and antioxidant status in the liver, erythrocytes, and serum of rats after methanol intoxication.

Lipid peroxidation products measured as a malondialdehyde and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), and concentrations of ascorbic acid, alpha-tocopherol, and glutathione (GSH) were measured in the liver, erythrocytes, and serum of rats 6, 14, and 24 h and 2, 5, and 7 d after treatment with 3 g methanol/kg. GSH-Px and GSSG-R activities, GSH level, and ascorbate concentration in the liver, erythrocytes, and blood serum were significantly decreased. In addition, SOD and alpha-tocopherol in erythrocytes were diminished, while malondialdehyde (MDA) in liver, erythrocytes, and serum were elevated. Further, erythrocyte counts, hemoglobin levels, hematocrit, and mean corpuscular volume (MCV) were reduced. These results indicate that methanol intoxication in rats leads to an increase in the lipid peroxidation and impairment in the antioxidant mechanisms in liver, erythrocytes, and blood serum.

Animals↗

PubMed1998

The comparison of the antioxidant defense potential of brain to liver of rats after methanol ingestion.

The antioxidant enzymatic and nonenzymatic potential in the brain of rats given methanol orally was investigated for 7 days consecutively and compared to that one in the liver. Glutathione (GSH) and the activities of superoxide dismutase (Cu, Zn-SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) were reduced in the brain after the first 24 h, whereas in the liver these parameters were diminished after 6 h. The brain catalase (CAT) activity was very low and constant in contrast to high and changeable CAT in the liver. At the beginning of intoxication, the activities of Cu, Zn-SOD and CAT in the liver were increased; after 5 days they were restored to normal values while Cu, Zn-SOD diminished gradually in the brain. An early change that occurred 6 h after intoxication was a decrease of ascorbate in the brain and in the liver. The increase in thiobarbituric acid-reactive substances (TBA-rs) in the liver was preceded by their increase in the brain. Our findings indicate decreased antioxidative potential both in the brain and in the liver of rats after methanol ingestion. The regulatory mechanisms of the antioxidant enzymes in the brain of intoxicated rats differ from those ones in the liver.

Administration, Oral↗

PubMed1998

Cyclophosphamide-induced generation of reactive oxygen species. Comparison with morphological changes in type II alveolar epithelial cells and lung capillaries.

Cyclophosphamide (CP) causes lung toxicity in animals and humans. The mechanisms of pulmonary damage caused by CP are not fully understood. Possibilities include direct toxicity to pulmonary tissue or indirect toxicity through activation of pulmonary inflammatory cells. The aim of the present study was the ultrastructural analysis (in transmission electron microscope) of the changes following CP administration within the structures forming the interalveolar septum of the lungs, particularly type II epithelial cells. An attempt was also made to reveal a correlation between the morphological changes, intensity of lipid peroxidation in lung tissue homogenates and blood serum collected from the left ventricle of the heart and the alterations in the activities of superoxide dismutase (Cu, Zn-SOD) and glutathione reductase (GSSG-R). The experiment used 40 male Wistar rats of 160-180 g body weight (b.w.). The animals were divided into two groups. Group I - (20 animals) were given single intraperitoneal (i.p.) dose of 150 mg CP/1 kg b.w./1 ml PBS. Group II - (20 animals) were given single i.p. dose of 1 ml PBS. All experimental animals were sacrificed after 1 (subgroups I, II-1) and 7 (subgroups I, II-7) days of CP (or PBS) treatment. I.p. administration of CP caused an increase in lipid peroxidation products (MDA-malondialdehyde) in lung tissue homogenates especially in subgroup I-1 (p = 0.00174). No statistical differences, however, were noted in the blood serum MDA levels, although a statistically significant decrease was found in GSSG-R (p = 0.00174) and SOD (p = 0.00174) activities in the serum. The paper discusses a potential link between the findings of biochemical analysis and the morphological changes found within lung tissue. Pulmonary trombopoesis was indicated as a possible mechanism preventing a decrease in blood platelet count following CP administration.

Animals↗

PubMed1998

Formaldehyde-induced modification of hemoglobin in vitro.

Formaldehyde is known to react with proteins. The purpose of our experiments was to analyse in vitro the effect of formaldehyde on the physicochemical and biological properties of hemoglobin molecules. The effect of formaldehyde concentration, reaction time, pH and temperature on hemoglobin free amino groups was estimated. The modified hemoglobin was analysed using electrophoretic, potentiometric and spectrophotometric techniques. Reaction between formaldehyde and hemoglobin was accelerated by increasing concentration of formaldehyde and higher temperature. This reaction was most intensive during the first few hours at pH 7.4 so the amount of free amino groups of hemoglobin was significantly diminished by directly mixing formaldehyde with hemoglobin. The modified protein was characterized by the increase in electrophoretic mobility and the decrease in maximum absorption derived from porphyrin rings. Formaldehyde modified hemoglobin was less susceptible to the action of cathepsin D.

Cathepsin D↗

PubMed1997

Glutathione consumption and inactivation of glutathione-related enzymes in liver, erythrocytes and serum of rats after methanol intoxication.

The primary metabolic fate of methanol is oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and further hydrogen peroxide. Glutathione plays a unique role in the cellular defense system against xenobiotics. The glutathione (GSH) content and glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) activities were measured in liver, erythrocytes and serum of rats. Rats were intoxicated with 3.0 and 6.0 g methanol/kg body wt. and measurements taken after 6, 12 and 24 h and 2, 5 and 7 days of intoxication. The decrease in GSH content and in GSH-related enzyme activity was observed during the whole time-course of the intoxication. The most significant changes were observed in the erythrocytes. The results obtained show that the protection against oxidative damage due to methanol intoxication in rats seems to be less efficient than in control rats.

Animals↗

PubMed1997

Trolox-derivative antioxidant protects against methanol-induced damage.

This paper reports data on the effect of a new antioxidant, U-83836E, on the lipid peroxidation and antioxidant status of liver, red blood cells (RBCs) and blood serum of rats intoxicated with methanol (3.0 g/kg body weight). Methanol administration slightly increased the levels of peroxidation products in the liver, and markedly increased them in RBCs and serum. In contrast, glutathione-peroxidase, glutathione-reductase activity, reduced glutathione concentration and total antioxidant status were decreased. The use of U-83836E, containing a trolox ring, appeared to be beneficial in reducing lipid peroxidation products and in partially in preventing the decrease in glutathione and antioxidant enzymes induced by methanol in liver and serum. These results show that antioxidant U-83836E may partially prevent methanol toxicity.

Animals↗

PubMed1997

Activity and distribution of superoxide dismutase in the layers of polyester grafts.

The aim of the present study was to evaluate superoxide dismutase (Cu, Zn-SOD) activity in the principal layers of polyester grafts implanted into the abdominal aorta of dogs. The grafts were examined 7 days and 1, 4 and 12 months after the operation. It was found that SOD activity occurred in all polyester graft layers during the whole experiment. The neointima activity ws 1.5-fold lower during the 1st month; with the passage of time, it became 2-fold lower than in the normal aorta (p < 0.01). SOD activity in the medial and outer graft layers behaved similarly: it was lowest after 7 days, increased after 1 month and significantly decreased after 4 and 12 months (p < 0.01). Our study shows that the activity of SOD is low in polyester grafts and it can thus be inferred that protection against the superoxide anion is inadequate.

Animals↗

PubMed1997

Decreased antioxidant defense mechanisms in rat liver after methanol intoxication.

The primary metabolic fate of methanol is oxidation to formaldehyde and then to formate by enzymes of the liver. Cytochrome P-450 and a role for the hydroxyl radical have been implicated in this process. The aim of the paper was to study the liver antioxidant defense system in methanol intoxication, in doses of 1.5, 3.0 and 6.0 g/kg b.w., after methanol administration to rats. In liver homogenates, the activities of Cu,Zn-superoxide dismutase and catalase were significantly increased after 6 h following methanol ingestion in doses of 3.0 and 6.0 g/kg b.w. and persisted up to 2-5 days, accompanied by significant decrease of glutathione reductase and glutathione peroxidase activities. The content of GSH was significantly decreased during 6 hours to 5 days. The liver ascorbate level was significantly diminished, too, while MDA levels were considerably increased after 1.5, 3.0 and 6.0 g/kg b.w. methanol intoxication. Changes due to methanol ingestion may indicate impaired antioxidant defense mechanisms in the liver tissue.

Animals↗

PubMed1997

Liver and serum antioxidant status after methanol intoxication in rats.

Activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) and concentration of ascorbate, alpha-tocopherol, non-protein and protein-bound sulfhydryl compounds and thiobarbituric acid-reactive substances (TBA-rs) were measured in liver and serum of rats 6, 12 and 24 h and 2, 5 and 7 days after intoxication with 1.5 g or 3.0 g methanol/kg b.w. Liver GSH-Px and GSSG-R activities and SH-groups and ascorbate content were significantly diminished at 6 and 24 h, while TBA-rs were increased. Serum SOD, GSH-Px and GSSG-R activities and SH-groups concentration were reduced while TBA-rs were elevated. The changes were more intensive after application of the higher dose of methanol. It is concluded that methanol impairs the liver and blood serum antioxidant mechanisms in rats.

Alcoholic Intoxication↗