Wyniki wyszukiwania

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Mitochondrial hog-renal-cortex respiration system activity as a function of taken-out-organ storage conditions

100%

Ogonski T.

Advances in Agricultural Sciences

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2000

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tom 07

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nr 1

2

Is a mathematical model able to predict the result of a biochemical experiment?

88%

Korzeniewski B.

Acta Biochimica Polonica

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1994

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tom 41

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nr 2

3

Generation of adenosine tri-phosphate in Leishmania donovani amastigote forms

75%

Mondal S., Roy J. J., Bera T.

Acta Parasitologica

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2014

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tom 59

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nr 1

Leishmania, the causative agent of various forms of leishmaniasis, is the significant cause of morbidity and mortality. Regarding energy metabolism, which is an essential factor for the survival, parasites adapt to the environment under low oxygen tension in the host using metabolic systems which are very different from that of the host mammals. We carried out the study of susceptibilities to different inhibitors of mitochondrial electron transport chain and studies on substrate level phosphorylation in wild-type L. donovani. The amastigote forms of L. donovani are independent on oxidative phosphorylation for ATP production. Indeed, its cell growth was not inhibited by excess oligomycin and dicyclohexylcarbodiimide, which are the most specific inhibitors of the mitochondrial Fo/F1-ATP synthase. In contrast, mitochondrial complex I inhibitor rotenone and complex III inhibitor antimycin A inhibited amastigote cell growth, suggesting the role of complex I and complex III in cell survival. Complex II appeared to have no role in cell survival. To further investigate the site of ATP production, we studied the substrate level phosphorylation, which was involved in the synthesis of ATP. Succinate-pyruvate couple showed the highest substrate level phosphorylation in amastigotes whereas NADH-fumarate and NADH-pyruvate couples failed to produce ATP. In contrast, NADPH-fumarate showed the highest rate of ATP formation in promastigotes. Therefore, we can conclude that substrate level phosphorylation is essential for the survival of amastigote forms of Leishmania donovani.

4

Inhibition of mitochondrial bioenergetics: the effects on structure of mitochondria in the cell and on apoptosis

75%

Lyamzaev K. G., Izyumov D. S., Avetisyan A. V., Yang F., Pletjushkina O. Y., Chernyak B. V.

Acta Biochimica Polonica

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2004

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tom 51

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nr 2

The effects of specific inhibitors of respiratory chain, FoF1ATP synthase and uncouplers of oxidative phosphorylation on survival of carcinoma HeLa cells and on the structure of mitochondria in the cells were studied. The inhibitors of respiration (piericidin, antimycin, myxothiazol), the F1-component of ATP synthase (aurovertin) and uncouplers (DNP, FCCP) did not affect viability of HeLa cells, apoptosis induced by TNF or staurosporin and the anti-apoptotic action of Bcl-2. Apoptosis was induced by combined action of respiratory inhibitors and uncouplers indicating possible pro-apoptotic action of reactive oxygen species (ROS) generated by mitochondria. Short-term incubation of HeLa cells with the mitochondrial inhibitors and 2-deoxyglucose followed by 24-48 h recovery resulted in massive apoptosis. Apoptosis correlated to transient (3-4 h) and limited (60-70%) depletion of ATP. More prolonged or more complete transient ATP depletion induced pronounced necrosis. The inhibitors of respiration and uncouplers caused fragmentation of tubular mitochondria and formation of small round bodies followed by swelling. These transitions were not accompanied with release of cytochrome c into the cytosol and were fully reversible. The combined effect of respiratory inhibitors and uncouplers developed more rapidly indicating possible involvement of ROS generated by mitochondria. More prolonged (48–72 h) incubation with this combination of inhibitors caused clustering and degradation of mitochondria.

5

Effects of dietary gamma-cyclodextrin on voluntary activity and muscle strength in mice

63%

Wupper S., Fischer A., Luersen K., Ipharraguerre I. R., Chikamoto K., Furune T., Ishida Y., Terao K., Rimbach G.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 3

6

Training-induced acceleration of oxygen uptake kinetics in skeletal muscle: the underlying mechanisms

63%

Zoladz J. A., Korzeniewski B., Grassi B.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 10

67-84

It is well known that the oxygen uptake kinetics during rest-to-work transition (O2 on-kinetics) in trained subjects is significantly faster than in untrained individuals. It was recently postulated that the main system variable that determines the transition time (t1/2) of the O2 on-kinetics in skeletal muscle, at a given moderate ATP usage/work intensity, and under the assumption that creatine kinase reaction works near thermodynamic equilibrium, is the absolute (in mM) decrease in [PCr] during rest-to-work transition. Therefore we postulate that the training-induced acceleration of the O2 on-kinetics is a marker of an improvement of absolute metabolic stability in skeletal muscles. The most frequently postulated factor responsible for enhancement of muscle metabolic stability is the training-induced increase in mitochondrial proteins. However, the mechanism proposed by Gollnick and Saltin (1982) can improve absolute metabolic stability only if training leads to a decrease in resting [ADPfree]. This effect is not observed in many examples of training causing an acceleration of the O2 on-kinetics, especially in early stages of training. Additionally, this mechanism cannot account for the significant training-induced increase in the relative (expressed in % or as multiples of the resting values) metabolic stability at low work intensities, condition in which oxidative phosphorylation is not saturated with [ADPfree]. Finally, it was reported that in the early stage of training, acceleration in the O2 on-kinetics and enhancement of muscle metabolic stability may precede adaptive responses in mitochondrial enzymes activities or mitochondria content. We postulate that the training-induced acceleration in the O2 on-kinetics and the improvement of the metabolite stability during moderate intensity exercise in the early stage of training is mostly caused by an intensification of the “parallel activation” of ATP consumption and ATP supply pathways. A further acceleration in O2 on-kinetics, resulting from prolonged periods of training, may be caused by a further and more pronounced improvement in the muscles’ absolute metabolic stability, caused by an intensification of the “parallel activation” as well as by an increase in mitochondrial proteins.

7

Locomotory response of Amoeba proteus to Hplus and a protonophore (FCCP)

63%

Dolowy K., Grebecki A.

Acta Protozoologica

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1988

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tom 27

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nr 2

8

Abrogation of mitochondrial transcription in smooth muscle cells impairs smooth muscle contractility and vascular tone

63%

Jawien J., Bian Z., Sheikine Y., Olofsson P. S., Pang Y., Edholm T., Dou Y., Metzger D., Hellstrom P. M., Feil R., Hansson G. K.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 2

Background: Smooth muscle cells (SMC) constitute the major contractile cell population of blood vessels and inner organs. SMC contraction depends on energy provided by adenosine triphosphate (ATP) catabolism, which can be generated through oxidative phosphorylation in mitochondria or by anaerobic glycolysis. Mitochondrial activity may also modulate smooth muscle tone by biotransformation of vasoactive mediators. Here, we study the role of mitochondrial DNA gene expression for vascular function in vivo. Methods: Since loss of functional mitochondria in SMC may not be compatible with normal development, we generated mice with inducible SMC-specific abrogation of the mitochondrial transcription factor A (Tfam). Deletion of this gene leads to dysfunctional mitochondria and prevents aerobic ATP production in affected cells. Results: Invasive blood pressure monitoring in live animals demonstrated that SMC specific Tfam deletion results in lower blood pressure and a defective blood-pressure response to stress, changes that were not compensated by increased heart rate. The contractility to agonists was reduced in arterial and gastric fundus strips from Tfam-deficient mice. Endothelium-dependent relaxation of arterial strips in response to ACh was also blunted. Conclusion: Our data show that mitochondrial function is needed for normal gastric contraction, vascular tone, and maintenance of normal blood pressure.

9

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Human mitochondria in health, disease, ageing and cancer

63%

Bartnik E., Lorenc A., Mroczek K.

Journal of Applied Genetics

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2001

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tom 42

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nr 1

10

The mechanism of ADP phosphorylation by ATP synthase

63%

Weber J.

Cellular and Molecular Biology Letters

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2003

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tom 08

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nr 2A

11

Influence of diazoxide on the function of mitochondria in guinea pig liver under myocardium dystrophy

63%

Kurhalyuk N., Tkachenko G.

Bulletin of the Veterinary Institute in Puławy

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2006

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tom 50

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nr 1

12

The Crabtree effect: a new look at the old problem

63%

Wojtczak L.

Acta Biochimica Polonica

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1996

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tom 43

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nr 2

Inhibition of respiration by glucose, known as the Crabtree effect, has been observed in several tumours and some other highly glycolytic cells and tissues. Among mechanisms proposed to explain this effect were: competition between glycolysis and respiration for ADP or for inorganic phosphate, change of intracellular pH, change in the permeability of mitochondrial membranes, specific regulatory behaviour of glycolytic enzymes, and specific enzyme topography within the cell. None of these proposals alone seems satisfactory. The present article describes the research carried out in the author's laboratory, pointing to the role of Ca2+ in the mechanism of the Crabtree effect This supposition is based on the following observations: (1) in Ehrlich ascites tumour cells glucose elicits a steady increase of the cytoplasmic concentration of free Ca2+; (2) isolated Ehrlich ascites mitochondria and mitochondria within digitonin-permeabilised cells, preloaded with Ca2+, exhibit a depression of State 3 respiration and lowering of the rate of ATP synthesis; (3) ATPase activity of toluene-permeabilised Ehrlich ascites mitochondria becomes substantially inhibited at micromolar concentrations of Ca2+; (4) Ca2+ potentiates the effect of the inhibitory subunit of F1F0-ATPase. These results allow to hypothesize on the following sequence of events: (1) glucose elevates the cytoplasmic concentration of Ca2+; (2) this elicits an increased accumulation of Ca2+ in mitochondria; (3) loading of mitochondria with Ca2+ leads to an increased association of the inhibitory subunit with F1F0 which results in (4) the inhibition of coupled respiration. The importance of these mechanisms for glycolytic and rapidly proliferating cells is discussed.

13

Rebamipide attenuates nonsteroidal anti-inflammatory drugs (NSAID) induced lipid peroxidation by the manganese superoxide dismutase (MnSOD) overexpression in gastrointestinal epithelial cell

51%

Nagano Y., Matsui H., Shimokawa O., Hirayama A., Tamura M., Nakamura Y., Kaneko T., Rai K., Indo H. P., Majima H. J., Hyodo I.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 2

Ograniczanie wyników

Mitochondrial hog-renal-cortex respiration system activity as a function of taken-out-organ storage conditions

Is a mathematical model able to predict the result of a biochemical experiment?

Generation of adenosine tri-phosphate in Leishmania donovani amastigote forms

Inhibition of mitochondrial bioenergetics: the effects on structure of mitochondria in the cell and on apoptosis

Effects of dietary gamma-cyclodextrin on voluntary activity and muscle strength in mice

Training-induced acceleration of oxygen uptake kinetics in skeletal muscle: the underlying mechanisms

Locomotory response of Amoeba proteus to Hplus and a protonophore (FCCP)

Abrogation of mitochondrial transcription in smooth muscle cells impairs smooth muscle contractility and vascular tone

Human mitochondria in health, disease, ageing and cancer

The mechanism of ADP phosphorylation by ATP synthase

Influence of diazoxide on the function of mitochondria in guinea pig liver under myocardium dystrophy

The Crabtree effect: a new look at the old problem

Rebamipide attenuates nonsteroidal anti-inflammatory drugs (NSAID) induced lipid peroxidation by the manganese superoxide dismutase (MnSOD) overexpression in gastrointestinal epithelial cell