Search PubMed⌕ Search

Biomedical subjects

Ryszard Farbiszewski

Publications and source records attributed to Ryszard Farbiszewski.

4 recordsLinked to original sources

[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. The examinations were carried out in 36 specimens (10 specimens of healthy brain tissue, 12 specimens of brain metastases, 14 specimens of glioma multiforme). The statistical analysis revealed significant increase (p < 0.001) of GSH-Px and GSSG-R activity within the single brain metastases in comparison with the healthy brain tissue.

Brain Neoplasms↗

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 obtained values of the above enzyme activities and of the concentrations of the examined substances in brain tumours were compared to the adequate values determined in 10 samples of histopathologically unchanged nerve tissue. THE RESULTS: the increase of all enzymes activities in brain tumours is statistically significant (p < 0.05) as compared to the adequate activity level in normal nerve tissue. The significant decrease (p < 0.05) of the GSH and ascorbate concentration and the significant increase (p < 0.05) of the level of the thiobarbituric acid--reactive substances in the examined brain tumours was found in comparison to the adequate concentration of the above substances in normal nerve tissue.

Antioxidants↗

[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). Control group consisted of 10 patients whose CSF parameters remained in normal range. The CSF examination was performed twice: before and 3 weeks after treatment. The analysed activity of SOD, GSH-Px, GSSG-R, MDA and total sulphydryl groups (-SH) during the acute stage of the disease was significantly lower comparing to the control group. Despite the treatment, GSSG-R activity, MDA concentration and total sulphydryl groups--SH further lowered significantly. Although the SOD activity in CSF was higher in the second examination, it remained significantly lower comparing to the control group. We showed that the GSH-Px and GSSG-R activity in CSF after the acute stage of the TBE remained significantly lower than in the control group. Our examinations prove that during the TBE an increased generation of oxygen-derived free radicals occurs what shows decreased activity of the antioxidant parameters (SOD, GSH-Px, GSSG-R) and decreased concentration of total sulphydryl groups--SH in CSF. Our results suggest that during TBE, molecular structures injury of enzymes and antioxidative reactive cofactors may occur.

Adult↗

[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. The release of PAF leads to ischaemia of nervous tissue, acute traumatic or nontraumatic injuries, degenerative and metabolic nervous system disorders in adults. The use of PAF receptor antagonists prevents partially cell injury in central nervous system and leukocyte adhesion to endothelial cells.

Central Nervous System Diseases↗