Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 5

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Impairment of cholinergic septal SN56 cells by thiamin deficiency

100%
Bizon-Zygmanska D., Bielarczyk H., Jankowska-Kulawy A., Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Cholinergic dementias are accompanied by inhibition of pyruvate and ketoglutarate dehydrogenase (PDH, KDH) in affected brains. Therefore, we investigated how amprolium-evoked thiamine pyrophosphate defi cits impair acetyl-CoA metabolism as well as function and viability of cholinergic neurons. Two day exposure of differentiated (DC) or nondifferentiated (NC) SN56 cholinergic cells cultured in Minimal Eagles Medium to amprolium caused concentration-dependent inhibition of cell MTT reducing capacity and increased their mortality, that at 5 mM inhibitor concentration reached values 30 and 15% or 43 and 10%, respectively. However, neither PDH nor KDH activities nor cell growth were signifi cantly, inhibited by their culture with amprolium. On the other hand, amprolium decreased acetyl-CoA levels in DC and NC by 39 and 46%, respectively. The inhibitor altered choline acetyltransferase activity neither in NC nor in DC. Acetylcholine content in DC and was suppressed by amprolium for over 40%. On the contrary, in NC it had no effect on the transmitter level. These fi ndings indicate that increased ACh synthesis in DC made them more vulnerable to acetyl-CoA shortages caused by amprolium-evoked inhibition of thiamine uptake. Low rate of ACh synthesis in NC, allowed them to save more acetyl-CoA to support energy metabolism and thereby facilitated their survival under pathologic conditions. Supported by MNiSW projects PO5A 11030, NN401 2333 33 and AMG fund W-144.
2

Zaburzenia metabolizmu energetycznego mózgu w stanie niedoboru tiaminy

88%
Jankowska-Kulawy A., Bielarczyk H., Ronowska A., Bizon-Zygmanska D., Szutowicz A.
Diagnostyka Laboratoryjna
|
2014
|
tom 50
|
nr 4
3

LPS changes energy metabolism in microglial N9 and cholinergic SN56 neuronal cells

76%
Klimaszrwska-Lata J., Gul-Hinc S., Bielarczyk H., Ronowska A., Bizon-Zygmanska D., Dys A., Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Inhibition of brain energy metabolism, accompanied by inflammatory activation of microglial cells is a characteristic feature of several neurodegenerative brain diseases, including Alzheimer’s, aluminum or vascular encephalopathies. Microglial inflammatory response to neurotoxic signals may contribute to neuronal degeneration through excessive production of nitric oxide (NO) and a vast range of pro-inflammatory cytokines. The aim of this work was to investigate whether and how lipopolysaccharide (LPS), and its key mediator NO, may differentially affect energy and acetyl-CoA metabolism of microglial N9 and cholinergic SN56 neuroblastoma cells. METHODS: In experimential model cell cultures were used: N9 murine microglial cells and SN56.B5.G4 cholinergic murine neuroblastoma cells. RESULTS: Exposition of murine microglial N9 cells to LPS caused concentration-dependent several-fold increases of nitrogen oxide synthesis, accompanied by inhibition of pyruvate dehydrogenase complex (PDHC), aconitase and α-ketoglutarate dehydrogenase complex (KDHC) activities, and by depletion of acetyl-CoA, but by small losses in ATP content and cell viability. On the other hands, SN56 cells were insensitivity to LPS, which was probably caused by lower than in N9, expression of TLR4. However, exogenous NO caused inhibition of PDHC and aconitase activities, depletion of acetyl-CoA and loss of SN56 cells viability. Microglial cells appeared to be more resistant than neuronal cells to acetyl-CoA and ATP depletion evoked by these neurodegenerative condition. CONCLUSIONS: These data indicate that preferential susceptibility of cholinergic neurons to neurodegenerative insults may results from competition for acetyl-CoA between mitochondrial energyproducing and cytoplasmic acetylocholine synthesizing pathways. One of the reasons for greater resistance of microglial cells to cytotoxic inputs could be their lower energy demand. Supported by MNSW project MN 01-0067/08 and GUMed fund ST-57.
4

Cytotoxic effects of zinc on cholinergic SN56 neuroblastoma and C6 astrocytoma cells

76%
Dys A., Ronowska A., Gul-Hinc S., Klimaszewska-Lata J., Bizon-Zygmanska D., Szutowicz A., Bielarczyk H.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. METHODS: Exposition of cAMP/RA-differentiated (DC) and nondifferentiated (NC) cells cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent accumulation. The level of Zn was measured by fluorimetric method with TSQ. RESULTS: After 24 h exposition of SN56 cells to 0.15 mM Zn their death rates were equal to 35 and 50% for NC and DC at cation levels equal to 4.0 and 5.5 nmol/mg protein, respectively. In the same conditions, the death rates of astroglial cells were close to 1–2% only, at intracellular Zn levels of 1.6 and 2.1 nmol/mg protein, respectively. Higher, about 0.25 mM Zn levels were required to evoke death rates of astroglial cells, similar to those seen in neuronal cells. In such conditions Zn levels in astroglia were about 6.4 and 27.0 nmol/mg protein, respectively. In thisstudy we examined the effects of accumulation of Zn in cholinergic neurons and adjacent astrocytes on activity of enzymes involved in energy metabolism. It caused inhibition of PDHC, aconitase and IDH activities. The high susceptibility of cholinergic neurons and a relative high resistance of astrocytes induced by cytotoxic concentration of zinc. Higher levels of Zn may cause deeper inhibition of acetyl-CoAsynthesis and the flow rate of the TCAcycle, which leads to a decrease in ATP synthesis and cell damage. CONCLUSIONS: Chronic exposition to Zn apparently induced adaptative mechanisms eliminating excess of the metal from the cells. These changes may directly inhibit intramitochondrial acetyl-CoA synthesis and its transport to cytoplasmic compartment, yielding impairment of cell viability and suppression their transmitter functions. Chronic neurons are more susceptible to increase extracellular concentrations of zinc than astrocytes. Supported by MNiSW projects MN 01-0108/08/248 and MUG fund ST-57.
5

Thiamine pyrophosphate deficiency causes energy disturbances in astroglial C6 and microglial N9 cells

64%
Romowska A., Bizon-Zygmanska D., Gul-Hinc S., Dys A., Klimaszewska-Lata J., Bielarczyk H., Wolska A., Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Inhibition of pyruvate (PDHC) and ketoglutarate (KDHC) dehydrogenase complexes induced by thiamine pyrophosphate deficits is known to cause disturbances of cholinergic transmission in the brain, yielding clinical symptoms of cognitive and motor deficits. However, particular alterations in distribution of acetyl-CoA, in the glial cells of thiamine pyrophosphate-deficient brain remain unknown. Therefore, the aim of our work was to find out how amprolium-induced thiamine pyrophosphate deficits (TD) affect distribution of acetyl-CA in the compartments of glial cells. As an experimental model we used astroglial C6 and microglial N9 cell line cultured in low thiamine medium. In such conditions microglial N9 cells displayed significantly greater loss of viability than the C6 ones. In both groups of the cells the activity of the key enzymes of energy/acetyl-CoA metabolism such as: PDHC, KDHC, aconitase was inhibited by amprolium-induced thiamine deficits. It explains why acetyl-CoA levels in the mitochondrial compartment were decreased in the cells. Supported by the Ministry of Research and Higher Education projects: IP 2011 046071, 01-0100/08 and St 57.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.