Wyniki wyszukiwania - Biblioteka Nauki

1

Control mechanisms on the size and distribution of mitochondria in the cell

100%

Wakabayashi T.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

2

Structural changes of mitochondria related to apoptosis: swelling and megamitochondria formation

100%

Wakabayashi T.

Acta Biochimica Polonica

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1999

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tom 46

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nr 2

EN

Recently we have found that the formation of megamitochondria in culture cells of various sources, induced by chemicals capable of generating free radicals, is followed by apoptotic changes of the cell. Detailed analysis on functional and morphological aspects of megamitochondria has enabled us to speculate that the formation of megamitochondria may be a prerequisite for free radical-mediated apoptosis: free radicals modify the mitochondrial membranes resulting in the fusion of adjacent mitochondria (megamitochondria formation). If the intracellular level of free radicals is continuously kept high, the permeability transition pores of the megamitochondria membranes are opened and megamitochondria become swollen. Oxygen consumption and the ability to synthesise ATP by swollen megamitochondria decrease distinctly. At the same time, cytochrome c is released from swollen megamitochondria into the cytoplasm. If lowered rates of the generation of reactive oxygen species from swollen megamitochondria, possibly due to decrease in their oxygen consumption, are effective enough to lower the intracellular level of free radicals, megamitochondria may return to normal. If not, decrease in the membrane potential of megamitochondria membranes causes the release of apoptosis-inducing factor into the cytoplasm. Cytochrome c and apoptosis-inducing factor thus released into the cytoplasm may cause cytoplasmic and nuclear apoptotic changes. Experimental data to support this hypothesis are presented.

3

Structural changes of mitochondria during free radical-induced apoptosis

63%

Wakabayashi T. , Spodnik J. H.

Folia Morphologica

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2000

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tom 59

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nr 2

EN

The initial proposal for apoptosis stressed nuclear change (condensation of chromatin) and the intactness of intracellular organelles, including mitochondria, based on light and electron microscopic observations. However, data have accumulated to demonstrate that the opening of megachannels of mitochondrial membranes, resulting in the swelling of the organelles, notably by Ca²⁺ and free radicals, is the crucial step in the apoptotic processes of the cell. Application of fluorescent dyes to mitochondria, combined with flow cytometry, has made it possible to detect subtle changes in the structure and function of the organelles related to apoptosis. The present article overviews structural aspects of mitochondria related to apoptosis, including the free radical-induced formation of megamitochondria.

4

NADPH oxidase participation in switching from apoptosis to necrosis

51%

Niemczyk E. , Kedziora J. , Wakabayashi T. , Wozniak M.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

5

Human skeletal muscle: participation of different metabolic activities in oxidation of L-lactate

45%

Popinigis J. , Antosiewicz J. , Crimi M. , Lenaz G. , Wakabayashi T.

Acta Biochimica Polonica

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1991

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tom 38

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nr 1

6

Protein oxidation and rapid induction of megamitochondria formation in doxorubicin-treated cardiomyocytes

45%

Kedziora J. , Kulawak-Galaska D. , Spodnik J. , Wozniak M. , Wakabayashi T.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

7

Antioxidant effectiveness of acyl chain derivatives of 4-OH-TEMPO

45%

Cwiklak I. , Budzko D. , Wozniak M. , Nowak J. , Wakabayashi T.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

8

Changes in mitochondrial superoxide ion production in osteosarcoma 143B cells after dihydroorotate dehydrogenase inhibitors treatment

45%

Spodnik J. , Wozniak M. , Karbowski M. , Knap N. , Wakabayashi T.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

9

Dysfunction of the outer mitochondrial membrane seems to be compensated inside the cell by the formation of megamitochondria

45%

Popinigis J. , Antosiewicz J. , Yamashita K. , Adachi K. , Wakabayashi T.

Polish Journal of Environmental Studies

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1998

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tom 07

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nr 6

10

Molten globule-like state of cytochrome c displays high peroxidase activity with synthetic hydroperoxide

38%

Piorkowska P. , Cwiklak I. , Celmer-Wozniak E. , Mickiewicz W. , Wakabayashi T. , Nowak J. , Wozniak M.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

11

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

38%

Golebiewska J. , Rozwadowski P. , Spodnik J. H. , Knap N. , Wakabayashi T. , Wozniak M.

Acta Biochimica Polonica

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2002

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tom 49

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nr 1

EN

We have demonstrated for the first time that the steroid metabolite, 2-methoxy- estradiol (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 uM 2-ME inhibited cell cycle at G1 phase while 10 uM. 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.

12

Altered function of permeability transition in liver mitochondria from three months propanol-treated rat

38%

Popinigis J. , Ziolkowski W. , Kaczor J. J. , Antosiewicz J. , Skrobot W. , Matuszkiewicz A. , Wakabayashi T.

Polish Journal of Environmental Studies

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1999

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tom 08

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nr 5

13

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

38%

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

EN

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.

14

Three dimensional structure of actin-based membrane skeleton as revealed by electron microscopic computed tomograpy of rapidly- frozen, deep-etchen plasma membrane

32%

Morone N. , Kasai R. , Fujiwara T. , Ike H. , Hirata Y. , Yuasa S. , Nishizawa Y. , Wakabayashi T. , Usukura J. , Kusumi A.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

15

NADH-generating substrates reduce peroxyl radical toxicity in RL-34 cells

32%

Antosiewicz J. , Spodnik J. H. , Teranishi M. , Herman-Antosiewicz A. , Kurono C. , Soji T. , Wozniak M. , Borkowska A. , Wakabayashi T.

Folia Morphologica

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2009

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tom 68

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nr 4

247-255

EN

There is general agreement that oxidative stress may induce apoptotic and necrotic cell death. Recently it has been shown that NADH can be considered an important antioxidant as it reacts with peroxyl and alkoxyl radicals under in vitro conditions. Therefore, in the present study we hypothesized that an increase in intracellular NADH using specific substrates will protect RL-34 cells against cytotoxicity of 2’-azobis (2-amidinopropane) dihydrochloride (AAPH), which is a peroxyl radical generating compound. Cells treated for 24 hours with 6.0 mM AAPH were severely damaged: mitochondria were vacuolated, and the level of free radicals significantly increased. Both apoptotic and necrotic cells were detected (11.1% and 11.4%, respectively) even after 5 hours of treatment. Pretreatment of the cells with substrates which increase the intracellular level of NADH, such as lactate, beta-hydroxybutyrate, and ethanol, distinctly inhibited AAPH-induced reactive oxygen species (ROS) formation and cell death. On the other hand, acetoacetate (AcA), which decrease the intracellular level of NADH, had opposite effects. Interestingly, NADH-generating substrates augment, while AcA reduced superoxide radical formation induced by AAPH. These results may suggest that although NADH generating substrates may exert some deleterious effects within a cell by inducing reductive stress, they diminish alkoxyl or peroxyl radical cytotoxicity. The protection is associated with a decrease in ROS formation measured by dichlorofluorescein, but with an increase in superoxide radical formation. (Folia Morphol 2009; 68, 4: 247–255)

16

Capase-3 activation in human osteosarcoma 143B cells proceeds through an early cell membrane fluidity perturbation

32%

Gil A. , Trzmiel A. , Niemczyk E. , Kedziora J. , Spodnik J. , Knap N. , Wakabayashi T. , Swirydowicz S. , Wozniak M.

Acta Biochimica Polonica

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2003

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tom 50

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nr Supplement 1

17

Fast perinuclear clustering of mitochondria in oxidatively stressed human choriocarcinoma cells

32%

Hallmann A. , Milczarek R. , Lipinski M. , Kossowska E. , Spodnik J. H. , Wozniak M. , Wakabayashi T. , Klimek J.

Folia Morphologica

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2004

|

tom 63

|

nr 4

EN

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.

18

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

32%

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

EN

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.

19

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

26%

Kossowska E. , Zauszkiewicz A. , Kubasik-Juraniec J. , Tukaj C. , Spodnik J. H. , Hallman A. , Klimek J. , Syta E. , Figarski A. , Wakabayashi T. , Wozniak M.

Folia Morphologica

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2004

|

tom 63

|

nr 3

EN

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.