Green tea supplementation in rats of different ages mitigates ethanol-induced changes in brain antioxidant abilities.

Oxidative stress induced by chronic ethanol consumption, particularly in aging subjects, has been implicated in the pathophysiology of many neurodegenerative diseases. Antioxidants with polyphenol structures, such as those contained in green tea, given alone for 5 weeks in liquid Lieber de Carli diet followed by administration with ethanol for 4 weeks with ethanol have been investigated as potential therapeutic antioxidant agents in the brain in rats of three ages (2, 12, and 24 months). Ethanol consumption caused age-dependent decreases in brain superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities.

[Concentration of glutathione (GSH), ascorbic acid (vitamin C) and substances reacting with thiobarbituric acid (TBA-rs) in single human brain metastases].

The aim of the study was to estimate the concentration of glutathione (GSH), ascorbic acid (vitamin C) and thiobarbituric acid (TBA-rs) in single human brain metastases and histologically unchanged nerve tissue. The research was conducted on fragments of neoplasmatic tissue collected from 45 patients undergoing surgery in the Department of Neurosurgery, Medical University of Białystok in years 1996-2002. Concentration of GSH was evaluated using the GSH-400 method, vitamin C using the method of Kyaw and TBA-rs using the method of Salaris and Babs.

Evaluation of antioxidant enzymes activity and concentration of non-enzymatic antioxidants in human brain tumours.

Unlabelled: The purpose of our research was to assess the activity of GSH-Px, GSSG-R, SOD-1 and concentration of GSH, Vit.C and reactive substances with thiobarbituric acid, in brain tumours with Ist, IInd, IIIrd and IVth levels of biological malignancy. The research was conducted in 105 samples obtained from patients undergoing surgery in the Department of Neurosurgery of the Medical University of Białystok between the years 1996-2001.

The decrease in antioxidant potential in human brain tumours.

Unlabelled: The objective of our research was to estimate the activity of superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R), as well as the concentrations of free oxygen radicals "sweepers" (GSH, Vit.C) and the concentrations of the substances reacting with thiobarbituric acid in brain tumours with II, III and IV level of biological malignancy. The research was conducted on 61 samples obtained from the patients operated in the Department of Neurosurgery of the Medical Academy of Białystok between the years 1996 and 2000.

[The role of platelet activating factor (PAF) in physiology and pathology of the central nervous system].

This review describes the role of platelet activating factor (PAF) in the central nervous system injury. Cerebral ischaemia, traumatic injury of central nervous system, metabolic, toxic and degenerative neuropathy, and also the increase in Ca2+ concentration in the cell, are strong stimulators of PAF synthesis and its release from cell membranes. Neurons, glial and microglial cells, monocyte cell populations, macrophages and endothelial cells of blood vessels are the targets of platelet activating factor.

[Decreased antioxidant-defence mechanisms in cerebrospinal fluid (CSF) in patients with tick-borne encephalitis (TBE)].

14 patients with Tick-borne Encephalitis (TBE) aged 21-64 (mean = 42.3) were analysed. The activity of superoxide dismutase (SOD), glutathione reductase (GSSG-R), glutathione peroxidase (GSH-Px), concentrations of malondialdehyde (MDA) and total sulphydryl groups (-SH) were measured in cerebrospinal fluid (CSF).

[Activity of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) and superoxide dismutase (SOD-1) in single brain metastasis].

The aim of the study was to evaluate the activity of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) and superoxide dysmutase (SOD-1) in the single brain metastases. The activity of the GSH-Px was evaluated with the use of spectrophotometry, GSSG-R was evaluated basing on the method of Mize and Langdon and SOD-1 with Sykes et al. method.

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.

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).

[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.

[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.

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.

Effect of methanol intoxication on free-radical induced protein oxidation.

Oxygen free radicals are generated during methanol-induced liver injury, as was shown for ethanol. The effect of methanol intoxication (6 g kg(-1) body wt.) on protein modification in the liver of rats was investigated.

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.

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.

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.

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.

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.

Role of reperfusion with polyelectrolyte solution and BN 52021 in hemorrhagic shock-induced changes in rat lungs.

The aim of this study was to test whether reperfusion with isotonic standard polyelectrolyte solution alone has any influence on the redox balance in the lung during hemorrhagic shock, and whether reperfusion and BN 52021, used together have better protective effect on free radical lung injury. The results showed that reperfusion with electrolyte solution increased solely glutathione reductase activity (GSSG-R), and diminished the activities of Cu,Zn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as the content of SH-groups. Thiobarbituric acid reactive substances (TBA-rs) were much more increased in comparison to hemorrhagic shock.

BN 52021, PAF-receptor antagonist, improves diminished antioxidant defense system of lungs in experimentally induced haemorrhagic shock.

The purpose of our experiments was to determine whether BN 52021, PAF-receptor antagonist, has any influence on the production of reactive oxygen species in the lung induced by haemorrhagic shock. The results showed, that the activities of Cu,Zn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the lung after haemorrhagic shock were decreased in comparison with control and sham groups while the activity of glutathione reductase (GSSG-R) was unchanged. The content of SH-groups was decreased while thiobarbituric acid reacting substances (TBA-rs) after haemorrhagic shock were increased.

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.

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.

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.

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.

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.