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1

Effects of menadione [vit.K3] and gamma radiation on dissolution and dimerization of vitamin E in vitamin concentrates, premixes and foodstuff

100%
Kupczyk B., Gogolewski M.
Food Science and Technology. Scientific Papers of Agricultural University of Poznan
|
2001
|
tom 05
2

Effects of gamma irradiation and menadione [vit.K3] on dissolution and dimerization of homologous tocopherols. Effect of storage time. Part two

100%
Kupczyk B., Gogolewski M.
Food Science and Technology. Scientific Papers of Agricultural University of Poznan
|
1999
|
tom 03
3
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The effect of menadione on sarcoplasmic reticulum Ca2plus and contractions of single guinea-pig cardiomyocytes

84%
Lewartowski B., Zdanowski K., Wolska B. M.
Journal of Physiology and Pharmacology
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1991
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tom 42
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nr 2
We investigated the effect of 2-methyl-1,4-naphtoquinone (Menadione) on sarcoplasmic reticulum (SR) Ca2²⁺ content and electrically stimulated contractions (ESCs) of single isolated myocytes of guinea-pig ventricular myocardium. The contractures initiated by means of microinjections of caffeine into the close vicinity of the cell were used as an indirect index of the SR Ca²⁺ content. Superfusion of the cells for 45 min with Menadione resulted in gradual disappearance of contractile respones to caffeine, prolongation of time to peak amplitude of ESCs by 48±15% and complete inhibition of postrest and postextrasystolic potentiation. These results are consistent with those of Floreani and Caipenedo (7) who found that Menadione strongly inhibits the SR Ca²⁺ ATPase. Despite depletion of the SR Ca²⁺ the amplitude of ESCs did not change which suggests that contractions were initiated in the cells treated with Menadione by Ca²⁺ derived from the sources other than the SR.
4

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

84%
Hallmann A., Klimek J., Masaoka M., Kaminski M., Kedzior J., Majczak A., Niemczyk E., Wozniak M., Trzonkowski P., Wakabayashi T.
Acta Biochimica Polonica
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2004
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tom 51
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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.
5

Fast perinuclear clustering of mitochondria in oxidatively stressed human choriocarcinoma cells

84%
Hallmann A., Milczarek R., Lipinski M., Kossowska E., Spodnik J. H., Wozniak M., Wakabayashi T., Klimek J.
Folia Morphologica
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2004
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tom 63
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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.
6
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Przebieg degradacji natywnych tokoferoli w olejach roslinnych wzbogaconych menadionem [wit.K3] pod wplywem promieniowania gamma

67%
Kupczyk B., Gogolewski M., Nogala-Kalucka M.
Rośliny Oleiste - Oilseed Crops
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2004
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tom 25
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nr 2
549-560
7

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

67%
Niemczyk E., Majczak A., Hallmann A., Kedzior J., Wozniak M., Wakabayashi T.
Acta Biochimica Polonica
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2004
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tom 51
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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.
8

Effects of gamma irradiation and menadione [vit.K3] on dissolution and dimerization of homologous tocopherols. Part one

67%
Kupczyk B., Gogolewski M.
Food Science and Technology. Scientific Papers of Agricultural University of Poznan
|
1998
|
tom 02
9

Wplyw menadionu, metotreksatu, cisplatyny i kwasu okadejowego na komorki bialaczki szpikowej HL-60 in vitro

59%
Rozalski M., Krajewska U.
Bromatologia i Chemia Toksykologiczna
|
1997
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tom 30
|
nr 3
283-284
10

Wplyw lacznego podania menadionu i metotreksatu na aktywnosc fosfataz bialkowych jader komorkowych watrobiaka Kirkmana-Robbins u chomikow obarczonych tym nowotworem

59%
Rozalski M., Krajewska U.
Bromatologia i Chemia Toksykologiczna
|
1997
|
tom 30
|
nr 1
99-106
Podanie menadionu łącznie z małą dawką metotreksatu powodowało znaczne hamowanie rozrostu wątrobiaka Kirkmana-Robbins u chomików. Towarzyszyło temu obniżenie zawartości zredukowanego glutationu (GSH) w tkance wątrobiaka. Zastosowane leki antynowotworowe przyczyniały się do obniżenia aktywności jądrowych fosfataz białkowych wątrobiaka - enzymów odgrywających rolę w regulacji cyklu komórkowego. Spośród indywidualnych jądrowych substratów szczególnie słabo defosforyłowane były 32P-fosfoproteiny o małych masach cząsteczkowych.
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