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Biomedical subjects

Michał Woźniak

Publications and source records attributed to Michał Woźniak.

18 recordsLinked to original sources
PubMed2005

Reactions of *NO2 with chromium(III) complexes with histamine and pyridoxamine ligands studied by the stopped-flow technique.

This study demonstrated the direct formation of the nitrogen dioxide (*NO2) radical during the decomposition of 3-morpholinosydnonimine (SIN-1) in biological buffer 4-morpholinoethanosulfone acid solution. Consequently, at approximately pH 4, SIN-1 can be used successfully as a source of *NO2. This conclusion is drawn from a comparison of the reactions of cis-[Cr(C2O4)(L- L)(OH2)2]+, where L-L denotes pyridoxamine (Hpm) or histamine (hm), with the gaseous *NO2 radical obtained by two methods: from SIN-1 and from a simple redox reaction. These reactions were investigated using the stopped-flow technique. The measurements were carried out at temperatures ranging from 5 to 25 degrees C over a pH range from 6.52 to 9.11 for cis-[Cr(C2O4)(Hpm) (OH2)2]+ and from 6.03 to 8.15 for cis-[Cr(C2O4)(hm)(OH2)2] +. We also determined the thermodynamic activation parameter (E(a)) and the uptake mechanism for each of the coordination compounds studied.

Chromium↗
PubMed2005

Pivotal participation of nitrogen dioxide in L-arginine induced acute necrotizing pancreatitis: protective role of superoxide scavenger 4-OH-TEMPO.

For the first time, a direct sensitive method of *NO(2) detection and measurement in biological material has been established. It is based on the interaction of this radical with the coordination compound of Cr(III) with aminodeoxysugar as biosensor. Our new method makes it possible to precisely assess *NO(2) level in experimental acute necrotizing pancreatitis induced by L-arginine, where oxidative and nitrosative stresses are supposed to play a key role in the pathomechanism of the disease. As much as 20 nmol of *NO(2)/mg protein was detected which correlated with severe deterioration of pancreatic acinar cell ultrastructure. Protective effect of superoxide radical scavenger 4-OH-TEMPO expressed as *NO(2) level decrease confirmed by preserved acinar cell ultrastructure and decreased pancreatic amylase release to blood serum is demonstrated. This study reveals a possible pathomechanism of L-arginine induced acute pancreatitis.

Amylases↗
PubMed2005

[The antioxidative-prooxidative balance in children with asthma treated with inhaled corticosteroids and long acting beta2-agonists].

UNLABELLED: The aim of study was to analyze the effect of treatment with inhaled corticosteroids and long acting beta2-agonists on antioxidative-prooxidative balance in children with asthma. MATERIALS AND METHODS: Twenty children with newly diagnosed asthma before treatment (group 1), fourteen children with diagnosed asthma treated with inhaled corticosteroids and long acting beta2-agonists and 57 healthy children were ioncluded in the study. In all cases plasma protein carbonyls and activity of erythrocyte SOD was assayed. RESULTS: Plasma protein carbonyls in both group I (1,01 nmol/g of protein, SD=0,30) and group II (0,94; SD=0,15) was significantly higher than in group III (0,85; SD=0,24) (I vs III p<0,033; II vs III p<0,031). The highest SOD activity was found in group II (3156,4 U/gHb; SD=976,1) (II vs I p<0,02; II vs III p<0,0001). SOD activity n group I (2435,8, SD=730,2) was higher than in group III (1533,1, SD=703,8) (p<0,0001). CONCLUSIONS: The increase in SOD activity in children with asthma seems to be a response to intensification of oxidative stress. Treatment of asthma with inhaled corticosteroids and long acting beta2-agonists augments antioxidative defense by increase in superoxide dismutase activity.

Administration, Inhalation↗
PubMed2005

[Systemic mastocytosis].

Mastocytosis is group of rare disorders characterized by abnormal mast cells growth. Pathology of the disease is unknown, mechanisms involved in mast cells delineation and growth are considered to play an important role. Unusual and broad spectrum of symptoms therefore requires cooperation of different specialists. The aim of the study was to assess diagnostic and therapeutic methods used in the Gdansk Mastocytosis Centre. 14 patients were studied (9 adults and 5 children). Bone marrow biopsy was performed in order to assess the stage of disease. Pathological, cytological, cytofotometry and genetic examination (C-KIT mutation) of the bone marrow were performed. Patients suffereing from food allergy and wasp venom anaphylaxis were diagnosed with skin prick tests and sIgE. All subjects suffered from urticaria pigmenthosa and anaphylaxis. Indolent mastocytosis was diagnosed in six subjects. Patients were treated with antihistamines, corticosteroids, cromones and immunotherapy with a marked reduction of symptoms. The experience of Gdansk Mastocytosis Centre indicates that mastocytosis is a rare and difficult to diagnose disease.

Adult↗
PubMed2004

The switch mechanism of the cell death mode from apoptosis to necrosis in menadione-treated human osteosarcoma cell line 143B cells.

Time-dependent changes in the cell death mode from apoptosis to necrosis were studied in cultured 143B cells treated with menadione, an anti-cancerous drug, excluding a possible involvement of "secondary necrosis." The population of apoptotic cells judged by FITC-Annexin V and propidium iodide (PI) double staining reached its maximum at 6 hours after 100 microM menadione treatment followed by an abrupt decrease thereafter, while that of necrotic cells continuously increased reaching 90% at 24 hours. Electron microscopically, cells attached to the culture dish at 6 hours after the treatment consisted of two different types of cells: cells with typical apoptotic features occupying the major population and those with condensed nuclei and swollen cytoplasm. Cells attached to the culture dish at 8 hours after the treatment consisted exclusively of those with condensed nuclei and swollen cytoplasm. Mitochondria in these cells showed various structural changes: those swollen to various degrees with deposition of flocculent densities, or those with highly condensed matrix. Distinct decreases both in intracellular levels of ATP and caspase-3-like activities and remarkable elevations of intracellular levels of superoxide, which were partly suppressed by NAD(P)H oxidase inhibitors, occurred at 6 hours after the treatment. These results may suggest that distinct increases of the intracellular level of superoxide derived from plasma membrane NAD(P)H oxidase besides that from mitochondria have triggered the transition of cell death mode from apoptosis to necrosis. Transition of highly condensed mitochondria to extremely swollen ones may reflect necrotic processes in menadione-treated cells. The present study strongly suggests that time-dependent study is essential using the electron microscopic technique to analyze detailed processes in the changes of the cell death mode.

Acetophenones↗
PubMed2004

The morphology of acinar cells during acute pancreatitis in rats induced by intraductal infusion of peracetate.

Many experimental models have been created to explain the pathophysiology of acute pancreatitis (AP). Investigations have been undertaken in this laboratory into the influence of strong oxidants introduced into the pancreas retrogradely through the bile-pancreatic duct. In these experiments a potentially toxic metabolite of ethanol-peracetic acid was used to induce AP. Wistar rats were treated with 1 mM and 40 mM peracetate and with a solvent as a control for 1 and 3 hours respectively. After a period of observation the samples of pancreata were examined in a light and electron microscope together with the content of sulphydryl groups as a marker of intracellular oxidative stress. The morphological examination showed profound changes in the histology of the pancreas and also in its subcellular structures, especially in groups 3 and 4 (with a higher concentration of peracetate). The changes included parenchymal haemorrhage and widespread acinar cell necrosis. The level of the sulphydryl groups decreased in the rats treated with peracetate. This suggests that the severity of the disease strongly depends on the intensity of the oxidative stress. The results confirmed the axial role of oxygen-derived free radicals in the pathogenesis of AP.

Animals↗
PubMed2004

4-OH-TEMPO prevents the morphological alteration of rat thymocytes primed to apoptosis by oxidative stress inducer ButOOH.

Thymocytes exposed to the pro-oxidant tert-butyl-hydroperoxide (ButOOH) display a number of dramatic changes in morphology similar to those observed in the case of dexamethasone-treated cells. Both reagents induce nuclear chromatin peripheral aggregation below the nuclear membrane. Some nuclei themselves break up producing two or more fragments. ButOOH-treated cells are morphologically characterised by cell shrinkage, extensive surface blebbing and, finally, fragmentation into membrane-bound apoptotic bodies composed of cytoplasm and tightly packed with or without nuclear fragments. An increased level of lipid hydroxyperoxides was detected after exposure of thymocytes to ButOOH. Both oxidative stress markers and morphological damage to cells were prevented by the antioxidant 4-OH-TEMPO.

Animals↗
PubMed2004

A possible involvement of plasma membrane NAD(P)H oxidase in the switch mechanism of the cell death mode from apoptosis to necrosis in menadione-induced cell injury.

The effects of inhibitors of plasma membrane NADPH oxidase on menadione-induced cell injury processes were studied using human osteosarcoma 143B cells. The intracellular level of superoxide in the cells treated with menadione for 6 h reached a maximum followed by an abrupt decrease. The population of apoptotic cells detected by Annexin V and propidium iodide double staining also reached its maximum at 6 h of menadione-treatment while that of necrotic cells increased continuously reaching 90% of the total population at 9 h of the treatment. Pretreatment of the cells with inhibitors of NADPH oxidase, including diphenyliodonium chloride, apocynin, N-vanillylnonanamide and staurosporine was effective in lowering the menadione-induced elevations of superoxide, and also in the suppression of the switch of the cell death mode from apoptosis to necrosis in menadione-treated cells except for the case of staurosporine. These results strongly suggest that superoxide generated by NADPH oxidase, besides that generated by the mitochondria, may contribute to the remarkable increase in the intracellular level of superoxide in the cells treated with menadione for 6 h resulting in the switch from apoptosis to necrosis, although a direct evidence of the presence of active and inactive forms of NADPH oxidase in control and menadione-treated 143B cells is lacking at present.

Apoptosis↗
PubMed2004

Partial characterization of human choriocarcinoma cell line JAR cells in regard to oxidative stress.

Characterization of free radical-induced cell injury processes of placenta cells is of vital importance for clinical medicine for the maintenance of intrauterine fetal life. The present study has analyzed cell injury processes in cells of the choriocarcinoma cell line JAR treated with menadione, an anticancer drug, and H(2)O(2) in comparison to osteosarcoma 143B cells using electron microscopic and flow cytometric techniques. Flow cytometry on JAR cells exposed to 100 muM menadione and double-stained with Annexin V and propidium iodide (PI) detected apoptotic cells reaching the maximum after 4 h of incubation with a rapid decrease thereafter. Viable cells became decreased to 46% of the control after 2 h of incubation, reaching 5% after 4 h. Cells stainable with both Annexin V and PI began to increase distinctly after 2 h of incubation, reaching 55% after 4 h. Electron microscopy showed that cells stainable with both dyes specified above had condensed nuclei and swollen cytoplasm, suggesting that they were undergoing a switch of the cell death mode from apoptosis to necrosis. On the other hand, 90% of 143B cells remained intact after 4 h of menadione treatment although the intracellular levels of superoxide were always higher than those of JAR cells treated with the drug. In contrast, JAR cells were more resistant than 143B cells to H(2)O(2)-induced cytotoxicity. These results may suggest that cytotoxicity of menadione cannot be explained simply by oxygen free radicals generated from the drug. The resistance of JAR cells to oxygen free radical-induced cytotoxicity may be advantageous for intrauterine fetal life.

Apoptosis↗
PubMed2004

Fast perinuclear clustering of mitochondria in oxidatively stressed human choriocarcinoma cells.

Mitochondrial dysfunction plays a crucial role in cell types that exhibit necrosis-like death after activation of their death program. Tumour necrosis factor (TNF) induces abnormal, perinuclear clustering of mitochondria from an evenly spread distribution throughout the cytoplasm. The mitochondria withdraw from the cell periphery and aggregate in a unipolar perinuclear cluster. TNF-induced mitochondrial clustering is caused by impaired kinesin-mediated transportation of mitochondria. In this report, we describe a novel activity of menadione (MEN), namely the induction of an altered spatial distribution of mitochondria in the choriocarcinoma JAR cells. Strikingly, 2 hours of cell exposition to menadione did not disrupt the integrity of the plasma membrane, while the intracellular ATP level significantly decreased. Control (untreated) cells displayed a typically scattered distribution of filamentary mitochondria inside the cell. After 2 hours of MEN treatment the spatial distribution of the mitochondria was markedly altered to an asymmetric perinuclear clustered distribution. Menadione-stressed cells displayed a highly asymmetrical perinuclear clustered distribution of the mitochondria. The exposure of cells to MEN also results in a change in shape of the mitochondria into a population of enlarged granular structures. The results of our study demonstrate that in JAR cells menadione causes mitochondria to translocate from the cell periphery into the perinuclear region several hours before disruption of cell membrane integrity and cell death.

Cell Line, Tumor↗
PubMed2003

The correlation of protein peroxidation with morphological changes in experimental oestradiol-induced carcinogenesis.

Oestradiol-induced male Syrian hamster carcinogenesis is a well-known experimental model of human cancer of the breast, ovary and uterus. The pathomechanism postulated in this model is 4-hydroxylation of oestradiol and further free radical formation. The same process is suspected in human breast cancer. Dynamic changes in protein peroxidation were reported during the tumour induction. In this paper we try to correlate the protein peroxidation markers with the histopathological progression of the changes. The biochemical and histopathological evaluations were performed after 1, 3, 6 and 9 months of the hormone exposition. Significant protein peroxidation was observed as soon as after 1 month and increased further until the 6th month. After 9 months however, it was not significantly different from the control. The discrete histopathological changes after 1 month, progressed into tubular and interstitial hyperplasias after 3 and 6 months. After 9 months several dysplastic areas, sometimes with features of carcinoma in situ, were observed. The severe 9-month histopathological changes did not correlate with the protein peroxidation.

Animals↗
PubMed2002

Aromatic indolinic aminoxyls as antioxidants in cardiac sarcoplasmic reticulum lipid and protein oxidation.

The results presented demonstrate the influence of aromatic indolinic aminoxyls: 1,2-dihydro-2-ethyl-2-phenyl-3H-indole-3-phenylimino-1-oxyl (IA-C2) and 1,2-dihydro-2-octadecyl-2-phenyl-3H-indole-3-phenylimino-1-oxyl (IA-C18) on oxidation of lipids and proteins of cardiac sarcoplasmic reticulum membranes. We have used doxorubicin and t-butyl hydroperoxide as agents inducing oxidative stress in isolated rat cardiac sarcoplasmic reticulum membrane system. Carbonyl groups were measured as the end product of membrane protein oxidation, and thiobarbituric acid reactive substances were assessed as a marker of lipid peroxidation. Inhibition of peroxidation of certain membrane components depends on the length of acyl chain. Aminoxyl IA-C2 inhibits the lipid peroxidation process while IA-C18 is an efficient protector against protein oxidation.

Animals↗
PubMed2002

Dual effect of 2-methoxyestradiol on cell cycle events in human osteosarcoma 143B cells.

We have demonstrated for the first time that the steroid metabolite, 2-methoxyestradiol (2-ME) is a powerful growth inhibitor of human osteosarcoma 143 B cell line by pleiotropic mechanisms involving cell cycle arrest at two different points and apoptosis. The ability of 2-ME to inhibit cell cycle at the respective points has been found concentration dependent. 1 microM 2-ME inhibited cell cycle at G1 phase while 10 microM 2-ME caused G2/M cell cycle arrest. As a natural estrogen metabolite 2-ME is expected to perturb the stability of microtubules (MT) in vivo analogously to Taxol--the MT binding anticancer agent. Contrary to 2-ME, Taxol induced accumulation of osteosarcoma cells in G2/M phase of cell cycle only. The presented data strongly suggest two different mechanisms of cytotoxic action of 2-ME at the level of a single cell.

2-Methoxyestradiol↗
PubMed2002

Co-existence of apoptotic and necrotic features within one single cell as a result of menadione treatment.

In the present study we examined the effects of menadione, a redox cycling agent, on structural changes of human osteosarcoma line 143B cells. It has been previously reported that menadione can cause necrotic or apoptotic cell death in a concentration- depending manner. In our experimental model, cells were treated with 100 microM menadione for 24 hours. Using electron microscopy technique cells carrying three kinds of morphological changes were detected: necrotic cells, apoptotic cells and those demonstrating a co-existence of apoptotic and necrotic features in one single cell.

Antifibrinolytic Agents↗
PubMed2002

Divergent effects of quinolinic aminoxyls on mitochondrial ultrastructure and localisation in osteosarcoma 143 B cells.

In the present study we have shown that quinolinic aromatic aminoxyls are very efficient in protecting lipids of endoplasmic reticulum membranes against hydroperoxide-induced oxidation. The efficacy of these aminoxyls as protectors of lipids was much higher than the water-soluble 4-OH-TEMPO. We have also shown that QAL causes distinct changes of the morphology of mitochondria: from filamentous to granular enlarged structure via the folding of the former. QAL induces also perinuclear clustering of mitochondria. C-QAL as well as 4-OH-TEMPO treated cells revealed filamentous and scattered pattern of mitochondria. Antioxidant activity of QAL as well as morphological changes of mitochondrial raise the possibility that this drug can affect cell physiology via changes of mitochondrial function.

Antioxidants↗
PubMedDate not supplied

[Free radical reactions and activity of antioxidant barrier in children with chronic hepatitis B].

UNLABELLED: Recent research has shown that highly reactive oxygen species may take part in pathogenesis of many diseases, in particular chronic inflammatory processes. It was demonstrated that the activation of the inflammatory process is linked with generation of significant quantities of free radicals. This may lead to uncontrolled free radical reactions, particularly in case of antioxidant barrier insufficiency. THE AIM OF THE STUDY: To assess the biochemical parameters of oxidative stress, activation of glutathione peroxidase (GPX) and superoxide dismutase (SOD1) in erythrocytes of children with chronic hepatitis B (CBH). MATERIALS AND METHODS: Group of 47 children aged from 7 to 18 years with histopathologically confirmed CBH was studied. The content of carbonyl groups in plasma proteins and activity of SOD1 and GPX in the erythrocytes was evaluated. The control group consisted of 61 healthy children aged from 7 to 18 years. RESULTS: Verified statistically with Mann-Whitney U test. Significantly higher content of plasma proteins' carbonyl groups was found in the study group (1.07 +/- 0.33 nmol/mg protein) than in the control group (0.86 +/- 0.2, p < 0,001). The activity of GPX [U/gHb] was lower in group of children with CBH (18.7 +/- 9.7) than in healthy children (26.1 +/- 0.2, p =0.005). A significantly higher activity or SOD1 [U/gHb] was found in children with CBH (2470+/- 714) as compared with healthy controls (1857+/- 782, p =0.006). CONCLUSIONS: In patients with CBH the intensification of free radicals' reactions can be observed, which confirms the role of ROS in its pathogenesis. One of the reasons for this phenomenon may be due to the inappropriate activity of antioxidant barrier enzymes. The elevation of SOD activity seems to be a response to increased oxidative stress.

Adolescent↗
PubMedDate not supplied

[Superoxide dismutase in children with juvenile idiopathic arthritis].

UNLABELLED: The use or antioxidants as drugs that may control the inflammatory process recently has become widely studied in adults. One of the most important components or antioxidant barrier in humans is enzyme superoxide dismutase. Experimental treatment with superoxide dismutase proved to be effective in animals. THE AIM of the present study was to estimate the activity of superoxide dismutase (SOD) in patients with rheumatoid disease of childhood -- juvenile idiopathic arthritis and to analyse it in different clinical aspects of the disease including its activity, course and time of duration. MATERIAL AND METHODS: A group of 70 children with juvenile idiopathic arthritis, age from 3 to 18 years, patients of Rheumatologic Hospital in Sopot was examined in years 1996-2001. Juvenile idiopathic arthritis was diagnosed according to the International League Against Rheumatism classification (Durban 1997). The control group consisted of 29 healthy children age from 3 to 18 years. Superoxide dismutase activity was determined in full, heparinised blood with the use of spectrophotometric method or Randox. The study was accepted by the Local Committee of Ethics. RESULTS: A statistically significant increase in superoxide dismutase activity was found in group of children with juvenile idiopathic arthritis compared to the control group. In the polyarticular form of disease the activity of superoxide dismutase was also significantly higher than in the control group. CONCLUSIONS: In course of juvenile idiopathic arthritis, differently from rheumatoid arthritis of adults, superoxide dismutase activity seems to be stimulated in the majority of cases, so the treatment with exogenous superoxide dismutase may not be effective.

Adolescent↗