Wyniki wyszukiwania

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Ultrastructural studies on diurnal variations in mitochondria in various regions of the hepatic lobule

100%

Cieciura L., Okroj W., Krakowski G., Godlewski W.

Folia Histochemica et Cytobiologica

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1985

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tom 23

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nr 3

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Mitochondrial function of human preadipocytes may be modulated by antioxidants quercetin and beta carotene, and exogenous free fatty acids

100%

Sliwa A., Goralska J., Awsiuk M., Czech U., Gruca A., Kiec-Wilk B., Knapp A., Dembinska-Kiec A.

Polish Journal of Food and Nutrition Sciences

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2011

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tom 61

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nr Suppl.1

3

Physiological suppression of superoxide dismutase deficiency in yeast Saccharomyces cerevisiae

100%

Bilinski T., Litwinska J., Krawiec Z., Achremowicz B.

Acta Microbiologica Polonica

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1993

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tom 42

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nr 1

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The relationship between mitochondria function and circadian clock in peripheral oscillators

84%

Kazmierczak A., Schmitt K., Grimm A., Strosznajder J. B., Eckert A.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Circadian rhythms govern a wide variety of physical, behavioral and metabolic changes that follow a roughly 24-hour cycle, responding primarily to light and darkness in an organism’s environment. These are controlled by the circadian clock mechanism, where rhythm-generating mechanism is encoded by a transcription-translation feedback loop. Numerous studies have pointed to a cyclic relationship wherein the rhythm impacts metabolic activity and metabolism feeds back to impinge upon the rhythm. Mitochondria play a pivotal role in regulating cellular energy and were shown to be strategically positioned at the intersection between circadian rhythm and cell metabolism. Nevertheless little is known about their function in controlling the circadian rhythm. In our study, we investigated the involvement of circadian clock in mitochondrial function as well as mitochondria-dependent regulation of circadian clock. The study was carried out in primary human fibroblasts, an already established model to investigate molecular clock mechanisms in vitro. We have found that mitochondria activity as well as network activities showed rhythmic changes within 24 hours. Circadian pattern was detected for mitochondrial ROS including superoxide anion production. A significant 24-hour oscillation was found for cellular redox state. Furthermore, mitochondrial ATP levels were rhythmic and the maximum of ATP production paralleled the peak of mitochondrial ROS level and the mitochondrial network formation. Circadian rhythm was also detected for calcium ions concentration. Increase of ATP synthesis as well as changes in calcium and ROS level activated AMP-dependent protein kinase (AMPK). We have found that in primary human fibroblasts AMPK protein level and activity fluctuate in an antiphase relationship with rhythmic ATP production. Summarizing, our data provide the evidence for circadian regulation of mitochondrial dynamics and suggest that changes of mitochondrial activity may directly influence cellular clock. Supported by grants from Sciex 10. 258 to A.K. as well as Swiss National foundation (SNF No 310030_122572) and Synapsis Foundation to A.E

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The increase in mitochondrial DNA copy number in the tissues of gamma-irradiated mice

84%

Malakhova L., Bezlepkin V. G., Antipova V., Ushakova T., Fomenko L., Sirota N., Gaziev A. I.

Cellular and Molecular Biology Letters

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2005

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tom 10

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nr 4

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Mitochondrial integrity and function in model systems of CNS diseases

67%

Culmsee C.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

Mitochondria are key regulators of energy metabolism, redox balance, calcium homeostasis, and programmed cell death. In the past, we characterized mitochondria acting as targets of both caspase-dependent and caspase- independent death signalling triggered by increased oxidative stress and as executioners of programmed death signalling in neurons. For example, we identified mitochondrial damage in caspase‑independent neuronal death after cerebral ischemia in vivo, and in oxidative cell death, i.e., ferroptosis in vitro. Protective intervention against oxidative damage further confirmed the conclusion that mitochondria represent the “point of no return” in caspase‑independent paradigms of programmed cell death. Further, we found more recently that mitochondri al-targeted alpha-synuclein caused severe mitochondrial toxicity and caspase-dependent cell death in human dopaminergic neurons, a model system relevant to Parkinson’s disease. In different model systems of neuronal death, neuroprotective interference with mitochondrial pathways of programmed cell death was frequently attributed to metabolic switches, i.e., reduced mitochondrial respiration and increased glycolytic activity. Accordingly, targeting metabolic switches may serve as a general strategy for mitochondrial protection and, thereby, neuroprotection, but may also affect mechanisms of neuroinflammation involving activation of microglia. The understanding of the underlying mechanism of such metabolic protection may reveal novel therapeutic targets in neural diseases featuring mitochondrial impairments and neuroinflammation.

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Effects of heat shock and teprenone on ethanol-induced damage to cultured rabbit gastric mucosal cells

67%

Takahashi S., Yamazaki T., Okabe S.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 3

Ograniczanie wyników

Ultrastructural studies on diurnal variations in mitochondria in various regions of the hepatic lobule

Mitochondrial function of human preadipocytes may be modulated by antioxidants quercetin and beta carotene, and exogenous free fatty acids

Physiological suppression of superoxide dismutase deficiency in yeast Saccharomyces cerevisiae

The relationship between mitochondria function and circadian clock in peripheral oscillators

The increase in mitochondrial DNA copy number in the tissues of gamma-irradiated mice

Mitochondrial integrity and function in model systems of CNS diseases

Effects of heat shock and teprenone on ethanol-induced damage to cultured rabbit gastric mucosal cells