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1
Fluorymetryczna metoda oznaczanie wewnątrzkomórkowego cynku z użyciem barwnika TSQ
100%
Dys A. , Szutowicz A. , Bielarczyk H.
|
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nr 1A
2
Modification of acetyl-CoA and ACh metabolism in nerve terminals by dichloroacetate
100%
Szutowicz A. , Bielarczyk H. , Tomaszewicz M.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
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nr 3
3
Content available remote Essentiality and toxicity of vanadium supplements in health and pathology
100%
Gruzewska K. , Michno A. , Pawelczyk T. , Bielarczyk H.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 5
4
Rola cynku w procesach fizjologicznych i patologicznych organizmu
100%
Gapys B. , Raszeja-Specht A. , Bielarczyk H.
Diagnostyka Laboratoryjna
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2014
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tom 50
|
nr 1
5
Paracrine interactions between non-activated N9 microglial cells in co-culture with SN56 cholinergic neuronal cells
100%
Gul-Hinc S. , Ronowska A. , Bielarczyk H. , Szutowicz A.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
EN
Microglial cells, through the proinflammatory mediators play an important role in host defense and tissue repair in CNS. They contribute to pathomechanisms of Alzheimer’s and other neurodegenerative diseases. The aim of this work was to investigate modifying effects of non-activated migroglia on cholinergic neuronal SN56 cells subjected to common neuroprotective and/or neurotoxic signals. Chronic exposure to Zn or SNP caused loss of viability (30%), inhibition of pyruvate dehydrogenase (PDH) (40%), isocitrate dehydrogenase (60 and 50%) and aconitase activities as well as decrease of acetyl-CoA levels. These alterations in enzyme activities displayed strong direct correlation with depletion of acetylCoA (r=0.86, P<0.0001) and inverse correlation with cell viability (r=0.87, P<0.0001). Resveratrol, free radical scavenger, increased viability of Zn/SNP treated cholinergic cells but did not overcome suppresive effects of SNP and Zn on enzymes activities. Under same neurotoxic conditions, N9 microglial cells cultured on isoporated inserts and added to neuronal culture dishes, also overcame neurotoxic effect Zn and SNP maintaining control levels of acetyl-CoA, enzymes activites and high cell viability. These data sugest that in some specific, pathologic conditions, non-activated microglia may protect neuronal cholinergic neurons against neurotoxic insults by paracrine-like mechanism by protecting their energy metabolism. On the other hand resveratrol neuroprotection may depend on entirely different yet undefined mechanism. Supported by GUMed MN-15, MNiSW NN401029937, IP2010035370, GUMed ST-57 projects.
6
Impairment of cholinergic septal SN56 cells by thiamin deficiency
100%
Bizon-Zygmanska D. , Bielarczyk H. , Jankowska-Kulawy A. , Szutowicz A.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
EN
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.
7
Resveratrol and nitric oxide cholinergic neurotoxity
100%
Gul-Hinc S. , Bielarczyk H. , Jankowska-Kulawy A. , Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
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nr 3
EN
Several scavengers of free radicals like resveratrol (RV) are claimed to be useful in complementary therapy of Alzheimer’s dementia (AD) and other cholinergic encephalopathies, through the protection of mitochondrial energy metabolism. NO excess is one of recognized pathogens in AD brains. Therefore, we investigated whether RV might overcome cytotoxic effects of NO excess on septal cholinergic neuroblastoma SN56 cells. Chronic, 16 h exposure of nondifferentiated SN56 cells (NC) to 0.2 mM sodium nitroprusside (SNP) caused 30 and 27% suppression of pyruvate dehydrogenase (PDH) activity and acetyl-CoA level and the increase of nonviable cells fraction to 30%. In cAMP/retinoic acid-differentiated cells (DC), similar 30% inhibition of PDH by SNP caused 50% suppression of acetyl-CoA content and 47% loss of cell viability. RV (0.005 mM) itself affected none of parameters, neither in NC nor in DC. It did not overcome SNP-evoked inhibition of PDH and suppression of acetyl-CoA content in NC and DC. Despite of that RV partially prevented SNP-induced increase of DC and NC mortality to 31 and 14%, respectively. These data demonstrate that greater cytotoxic effects of SNP in DC than in NC correlated with evoked acetyl-CoA defi cits that might be linked with higher level of acetylcholine metabolism in the former. Protective effects of RV in NO-challenged cholinergic neurons were not connected with improvement of their acetyl-CoA metabolism. Supported by MNiSW projects NN401 2333 33, P05A 11030.
8
Synthesis of glutamate and aspartate in rat brain synaptosomes
100%
Bielarczyk H. , Lysiak W. , Szutowicz A.
Acta Biochimica Polonica
|
1986
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tom 33
|
nr 4
9
Competitive interactions between N-acetyl-L-aspartate and acetylcholine for acetyl-CoA in cholinergic neuroblastoma cells?
100%
Romianowski P. , Zygmanska-Bizon D. , Bielarczyk H. , Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2011
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tom 71
|
nr 1
EN
Cholinergic neurons like the other ones may synthesize N-acetylL-aspartate (NAA), which serves as a source for acetyl units for lipid synthesis in oligodendroglial cells. Pyruvate-derived acetylCoA is a substrate for NAA synthesis in aspartoacylase reaction in the mitochondrial and cytoplasmic compartments of neuronal cells. Highly differentiated cholinergic neurons were found to be more susceptible to neurodegenerative signals due to relative shortage of acetyl-CoA in the former ones. It gives rise to hypothesis that in cholinergic neurons, NAA synthesizing pathway might compete for acetyl-CoA with acetylcholine synthesis and energy producing pathways in their cytoplasmic and mitochondrial compartments, respectively. Therefore, the aim of this work was to investigate whether neurotoxic conditions that inhibit acetyl-CoA synthesis alter interactions between acetylcholine and NAA metabolism in neurons of low and high expression of the cholinergic phenotype. The differentiation of SN56 cholinergic neuroblastoma cells with cAMP and retinoic acid caused 30% increase of NAA content and 100% elevation of intracellular acetylcholine content and its synthesis. Simultaneously, the decrease of mitochondrial and increase of cytoplasmic acetyl-CoA levels were observed, respectively. Inhibition of pyruvate dehydrogenase activity by amprolium-evoked thiamine pyrophosphate deficit, brought about concentration-dependent suppression of acetyl-CoA content both in mitochondrial and cytoplasmic compartments along with inhibition of acetylcholine synthesis/ release. However, NAA content was affected by these conditions neither in nondifferentiated nor in differentiated cells. On the other hand, acetylcholine synthesis was stronger inhibited in differentiated than in nondifferentiated cells. Zinc (0.15 mM) and L-aspartate (1.0 mM) increased NAA level but inhibited acetylcholine synthesis and decreased cell viability and their acetyl-CoA content. These alterations were more evident in differentiated than in nondifferentiated cells. These data indicate that NAA metabolism may compete with acetylcholine sythesis for common precursor - acetyl-CoA thereby negatively affecting their chance for survival in different neurodegenerative conditions. Work was supported by MNiSW projects NN401233333, NN401029937 and GUMed St57 fund.
10
Energy metabolism in neurons exposed to hypoxia-inducing chemicals
100%
Gapys B. , Zysk M. , Ronowska A. , Bielarczyk H.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
EN
BACKGROUND AND AIMS: Excess of zinc ions and intermittent hypoxia both cause neurodegeneration by disruption in energy metabolism and oxidative stress, resulting in diminished pyruvate dehydrogenase complex (PDHC) and aconitase activity and consequent shortages in acetyl-CoA. This deficiency may be particularly dangerous for cholinergic neurons as they consume acetyl-CoA in additional pathway of acetylcholine synthesis apart from energy production. Aim of our study was to investigate effect of hypoxia on acetylCoA metabolism in neuronal cells under cytotoxic conditions. METHODS: The SH-SY5Y neuroblastoma cells were recognized as an in vitro model of brain cholinergic neurons after differentiating with all-trans-retinoic acid and cAMP. Hypoxic conditions were induced by 24 h (chronic) exposition of SH-SY5Y cells to cobalt ions (Co). Zinc (Zn) ions were used to evoke cytotoxicity. RESULTS: Chronic exposition of SH-SY5Y NC to 0.2 mM and 0.5 mM Co decreased cells number by 22% and 53%, respectively. The activities of PDHC and aconitase were reduced by 70% (0.2 mM Co) and over 75% (0.5 mM Co). IDH activity, in both concentrations, was decreased by 18%. The level of acetyl-CoA in SH-SY5Y NC was 28.4 pmol/mg of protein and chronic exposition of SH-SY5Y to 0.5 mM Co decreased acetyl-CoA level by about 60%. Chronic exposure of SH-SY5Y DC to 0.2 mM and 0.5 mM Co decreased number of cells by 28 and 60%, respectively, reduced activities of PDHC by 52% (0.2 mM) and 31% (0.5 mM Co). Aconitase activity was decreased by 77 and 90%, respectively. Activity of NADP-IDH and level of acetyl-CoA were also diminished regardless of the cobalt concentration by approximately 28% and 30%, respectively. In both groups addition of 0.1 mM Zn-aggravated cells mortality. CONCLUSION: Presented data indicate that hypoxia enhance cytotoxic effects of Zn in highly differentiated cholinergic cells. Supported by Ministry of Research and Higher Education projects: MN 01-0058/08 and ST-57, IP 2011046071.
11
Relationships between acetyl-CoA level and function of fenotypically modified N9 murine microglial cells
100%
Klimaszewska-Lata J. , Ronowska A. , Bielarczyk H. , Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
EN
Neurodegenerative lesions in cholinergic encephalopathies include an excessive activation of microglia, which may aggravate this process. Infl amatory cytokines were reported to affect viability of cultured cholinergic cells, through the infl uence on their acetyl-CoA metabolism. The aim of this work was to investigate whether phenotypic modifi cations of N9 microglia by common neuron-differentiating stimuli can alter its energy metabolism, viability and biological activity in neurodegenerative conditions. In basal conditions lipopolysaccharide (LPS) slightly decreased PDH activity and acetyl-CoA content and activated NO synthesis (600%). The cyclic AMP alone (0.25 mM), caused 15% increase of nonviable cells at 300% rise in NO synthesis and 50 and 30% decreases in acetyl-CoA and ATP contents, respectively. In such conditions LPS resulted in further increase of NO accumulation and aggravated loss of cell viability and their acetyl-CoA content. In basic conditions retinoic acid (RA) alone did not alter viability and NO synthesizing capacity but increased acetyl-CoA and blunted cytotoxic potencies of cAMP and LPS to N9. RA-evoked restoration of N9 cell viability was accompanied by the increase in their acetyl-CoA content. These data indicate that activation of microglia depletes their acetyl-CoA, making them more vulnerable to cytotoxic insults. On the contrary, rescue of microglia by RA-signaling pathways is connected with restoration their acetylCoA pool. Supported by MNiSW projects P05A 11030 and NN401 2333 33 and AMG fund St-57.
12
The effect of NO on metabolism of acetylcholine in the brain
100%
Szutowicz A. , Tomaszewicz M. , Jankowska A. , Bielarczyk H.
Polish Journal of Environmental Studies
|
1998
|
tom 07
|
nr 6
13
Disturbances of acetyl-CoA, energy and acetylcholine metabolism in some encephalopathies
100%
Szutowicz A. , Tomaszewicz M. , Bielarczyk H.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 1
14
Suppression of ID1 expression in colon cancer cells increases sensitivity to 5-fluorouracil
88%
Przybyla T. , Sakowicz-Burkiewicz M. , Maciejewska I. , Bielarczyk H. , Pawelczyk T.
Acta Biochimica Polonica
|
2017
|
tom 64
|
nr 2
15
Voltage-gated calcium chanels affected acetyl-CoA metabolism in cholinergic neurons exposed on Zn ions
88%
Zysk M. , Gapys B. , Gul-Hinc S. , Szutowicz A. , Bielarczyk H.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
EN
BACKGROUND AND AIMS: Cholinergic neurons produce acetylCoA, which is subsequently used as a fuel for energy production. Furthermore, exclusively those neurons produce acetylcholine from acetyl-CoA. As a results, extra utilization pathway may induce acetyl-CoA shortages and consequently impairment of brain energy metabolism. Disturbances in Ca-signaling could play regulatory role in neurons susceptibility to neurodegenerative conditions. The aim of our study was to investigate whether the Voltage-Gated Calcium Channels (VGCCs) could moderate the cholinergic neurons susceptibility on neurodegeneration. METHODS: Selected blockers of VGCCs (10 µM nifedipine, 0.2 µM ω-conotoxin-MVIIC, 0.5 µM ω-conotoxin-GVIA) were used as a Ca-depletion factors in SN56 neuroblastoma cells. RESULTS: Short-term SN56 cells exposition on 0.15 mM Zn increased the Zn level from 0.6 to 36 nmol/mg protein. However, in the presence of 10 µM nifedipine and ω-conotoxins, the Zn-accumulation were decreased by about 50%. Zn caused in SN56 about 49% increase of nonviable cells fraction. Whereas incubation cells with VGCCs blockers and Zn, led to 25% decline in the number of trypan blue positive cells the acetyl-CoA level in SN56 was 26.9 pmol/mg protein. However, the SN56 cells exposition on 0.15mM Zn decreased its level by 43%. In addition, acetyl-CoA level in VGCCs-blocked SN56 was as high as in control conditions. CONCLUSIONS: Achieved results indicated that VGCCs regulated the Zn-evoked neurotoxic effects on acetyl-CoA metabolism in SN56 cholinergic cells. Moreover, VGCCs might play particular role in neurotoxicity of Zn and show that disturbance of Ca homeostasis in this condition can be one of the factors which moderate acetyl-CoA metabolism in cholinergic neurons. Supported by MN0059/08 and ST-57 GUMed fund.
16
Acute cytotoxicity of zinc on SN56 cholinergic cells
88%
Dys A. , Ronowska A. , Jankowska-Kulawy A. , Szutowicz A. , Bielarczyk H.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
EN
Zinc is a trace element essential for living organisms. However, its excess in the aging human brain is claimed to contribute to patomechanisms Alzheimerís disease. The aim of this work was to fi nd out whether acute effects of Zn on neurons may be caused by alterations in their acetyl-CoA metabolism. Zn quickly accumulated in cholinergic SN56 cells in concentration-dependent fashion. In cell homogenates Zn caused, inhibition of pyruvate dehydrogenase (PDH), aconitase, isocitrate dehydrogenase and ketoglutarate dehydrogenase (KDH) activities, with Ki values equal to 0.058, 0.010, 0.005 and 0.0015 mM, respectively. For choline acetyltransferase [IC 0.5] for Zn was above 0.3 mM. No inhibition of succinate dehydrogenase activity was found. It also decreased cytoplasmic acetyl-CoA and ACh levels ([IC 0.5] 0.15 mM), and inhibited ACh release ([IC 0.5] 0.10 mM). Lipoamide (LA) or EDTA, added before or simultaneously with Zn prevented these inhibitions. When LA or EDTA were added 10 min after Zn, they did not reverse aconitase inhibition, partially restored KDH activity and totally reversed inhibition of PDH. Activities of PDH and KDH but not aconitase suppressed by 24 hour cell culture with Zn, were also restored by post culture additions of LA and EDTA to harvested cell homogenates. It indicates that, Zn could exert its acute effects on cholinergic cells through inhibitory-binding to crucial enzymes of energy metabolism, yielding acute depletion of cytoplasmic acetyl-CoA and suppression of cholinergic transmitter functions. Supported by MNiSW grants NN401 2333 33 and P05A 110 30
17
Acetyl-CoA metabolism in cholinergic neurons and their susceptibility to neurotoxic inputs
88%
Szutowicz A. , Tomaszewicz M. , Jankowska A. , Madziar B. , Bielarczyk H.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
18
Acetyl-CoA-dependent alterations in susceptibility of cholinergic neurons to neurotoxic signals
88%
Szutowicz A. , Gul-Hinc S. , Ronowska A. , Bielarczyk H. , Jankowska-Kulawy A.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
19
Role of acetyl-CoA in cytotoxic and cytoprotective effects in cholinergic SN56 cells
88%
Gul-Hinc S. , Runowska A. , Jankowska-Kulawy A. , Bielarczyk H. , Szutowicz A.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
20
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
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