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1

Rola białka alfa-klotho w procesach starzenia

100%
Sokolowska E., Milczarek R., Hallmann A., Klimek J.
Postępy Biologii Komórki
|
2013
|
tom 40
|
nr 1
2

Effect of hydroperoxides on aromatase activity in choriocarcinoma cells

100%
Sokolowska E., Milczarek R., Hallmann A., Klimek J.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
3

Mimicking of glutathione peroxidase deficiency by exposition of JAR cells to increased level of synthetic hydroperoxide

76%
Hallmann A., Milczarek R., Szkatula M., Wozniak M., Spodnik J. H., Klimek J.
Folia Morphologica
|
2005
|
tom 64
|
nr 4
304-308
A short chain synthetic analogue of lipid hydroperoxides was used to overload glutathione peroxidase (GPx) in human choriocarcinoma cell line JAR cells. Cells exposed to 100 µM tBuOOH displayed a 40% reduction in ATP level and significantly increased in membrane permeability, visualised by the lactate dehydrogenase (LDH) release into the extracellular medium. The intracellular level of oxygen free radicals measured as an oxidation of the dichlorodihydro-fluorescein diacetate (H₂DCF-DA) significantly increased after 2 hours of cell exposition to 100 µM tBuOOH. Concomitantly MDA, 4-HNE level increased to 2 nmol/mg of cell protein after 2 hours. Mitochondria stained with MitoTracker Red CMXRos displayed a filamentous appearance in control cells but changed into granular less energised organelles after exposition to tBuOOH. Collectively, the above results indicate the importance of the contribution of oxidative stress in the development of pre-eclampsia.
4

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

76%
Niemczyk E., Majczak A., Hallmann A., Kedzior J., Wozniak M., Wakabayashi T.
Acta Biochimica Polonica
|
2004
|
tom 51
|
nr 4
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-vani- llylnonanamide 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.
5

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

64%
Hallmann A., Klimek J., Masaoka M., Kaminski M., Kedzior J., Majczak A., Niemczyk E., Wozniak M., Trzonkowski P., Wakabayashi T.
Acta Biochimica Polonica
|
2004
|
tom 51
|
nr 4
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 H2O2 in comparison to osteosarcoma 143B cells using electron microscopic and flow cytometric tech­niques. Flow cytometry on JAR cells exposed to 100 ^M 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 H2O2-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.
6

Fast perinuclear clustering of mitochondria in oxidatively stressed human choriocarcinoma cells

64%
Hallmann A., Milczarek R., Lipinski M., Kossowska E., Spodnik J. H., Wozniak M., Wakabayashi T., Klimek J.
Folia Morphologica
|
2004
|
tom 63
|
nr 4
Mitochondrial dysfunction plays a crucial role in cell types that exhibit necrosislike 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.
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