Acetyl-CoA metabolism in amprolium-evoked thiamine pyrophosphate deficits in cholinergic SN56 neuroblastoma cells

2011 ◽  
Vol 59 (2) ◽  
pp. 208-216 ◽  
Author(s):  
D. Bizon-Zygmańska ◽  
A. Jankowska-Kulawy ◽  
H. Bielarczyk ◽  
T. Pawełczyk ◽  
A. Ronowska ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Thiamine Pyrophosphate ◽  
Acetyl Coa ◽  
Sn56 Neuroblastoma

Short term effects of Zn in cholinergic SN56 neuroblastoma cells

2009 ◽  
Vol 61 (6) ◽  
pp. 1233
Author(s):  
Ronowska Anna ◽  
Dyś Aleksandra ◽  
Gul-Hinc Sylwia ◽  
Jankowska-Kulawy Agnieszka ◽  
Bielarczyk Hanna ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Short Term ◽  
Sn56 Neuroblastoma ◽  
Short Term Effects

Intracellular redistribution of acetyl-CoA, the pivotal point in differential susceptibility of cholinergic neurons and glial cells to neurodegenerative signals

2014 ◽  
Vol 42 (4) ◽  
pp. 1101-1106 ◽  
Author(s):  
Andrzej Szutowicz ◽  
Hanna Bielarczyk ◽  
Anna Ronowska ◽  
Sylwia Gul-Hinc ◽  
Joanna Klimaszewska-Łata ◽  
...  
Keyword(s):  
Cell Viability ◽  
Pyruvate Dehydrogenase Complex ◽  
Neuronal Cells ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Cholinergic Neurons ◽  
Thiamine Pyrophosphate ◽  
Amyloid Β Peptide ◽  
Acetyl Coa ◽  
Dehydrogenase Complex

Intramitochondrial decarboxylation of glucose-derived pyruvate by PDHC (pyruvate dehydrogenase complex) is a principal source of acetyl-CoA, for mitochondrial energy production and cytoplasmic synthetic pathways in all types of brain cells. The inhibition of PDHC, ACO (aconitase) and KDHC (ketoglutarate dehydrogenase complex) activities by neurodegenerative signals such as aluminium, zinc, amyloid β-peptide, excess nitric oxide (NO) or thiamine pyrophosphate deficits resulted in much deeper losses of viability, acetyl-CoA and ATP in differentiated cholinergic neuronal cells than in non-differentiated cholinergic, and cultured microglial or astroglial cell lines. In addition, in cholinergic cells, such conditions caused inhibition of ACh (acetylcholine) synthesis and its quantal release. Furthermore, cholinergic neuronal cells appeared to be resistant to high concentrations of LPS (lipopolysaccharide). In contrast, in microglial cells, low levels of LPS caused severalfold activation of NO, IL-6 (interleukin 6) and TNFα (tumour necrosis factor α) synthesis/release, accompanied by inhibition of PDHC, KDHC and ACO activities, and suppression of acetyl-CoA, but relatively small losses in their ATP contents and viability parameters. Compounds that protected these enzymes against inhibitory effects of neurotoxins alleviated acetyl-CoA and ATP deficits, thereby maintaining neuronal cell viability. These data indicate that preferential susceptibility of cholinergic neurons to neurodegenerative insults may result from competition for acetyl-CoA between mitochondrial energy-producing and cytoplasmic ACh-synthesizing pathways. Such a hypothesis is supported by the existence of highly significant correlations between mitochondrial/cytoplasmic acetyl-CoA levels and cell viability/transmitter functions respectively.

Relationships between cholinergic phenotype and acetyl-CoA level in hybrid murine neuroblastoma cells of septal origin

2003 ◽  
Vol 73 (5) ◽  
pp. 717-721 ◽  
Author(s):  
Hanna Bielarczyk ◽  
Maria Tomaszewicz ◽  
Beata Madziar ◽  
Justyna ?wikowska ◽  
Tadeusz Pawe?czyk ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Acetyl Coa ◽  
Murine Neuroblastoma ◽  
Cholinergic Phenotype

Purification of the Chloroplast Pyruvate Dehydrogenase Complex from Spinach and Maize Mesophyll

1986 ◽  
Vol 41 (11-12) ◽  
pp. 1011-1017 ◽  
Author(s):  
Hans-Jürgen Treede ◽  
Klaus-Peter Heise
Keyword(s):  
Pyruvate Dehydrogenase ◽  
High Speed ◽  
Pyruvate Dehydrogenase Complex ◽  
Thiamine Pyrophosphate ◽  
Partial Purification ◽  
Reaction Products ◽  
Acetyl Coa ◽  
Aggregation State ◽  
Dihydrolipoyl Dehydrogenase ◽  
Dehydrogenase Complex

Abstract This paper deals with the partial purification of the pyruvate dehydrogenase complex (PDC) from chloroplasts of spinach and maize mesophyll which hitherto has been isolated only from pea chloroplasts. Starting with membrane free suspensions of lyophilized chloroplasts, and following a high-speed (140000 Xg) centrifugation of this “stromal extract”, the initial specific PDC-activities were concentrated by a factor 10 in the sediment. While most of the purification procedures described earlier resulted in almost complete loss of enzyme activities, a rate zonal sedimentation on linear glycerol gradients allowed for an additional up to 100-fold enrichment of the labile multienzyme complex, albeit with low yields. In contrast to chloroplast PDC from maize mesophyll, inactivation of the spinach complex during glycerol fractionation was due to the dissociation of its loosely bound dihydrolipoyl dehydrogenase component which collected in a lower density fraction of the gradient. Its recombination with PDC constituents of the bottom layer nearly restored initial activities. The chloroplast complex has been identified as true PDC by its substrate specificity for pyru­vate, NAD+, and coenzyme A and the 1:1:1 stoichiometry of its reaction products NADH, CO2, and acetyl-CoA. The chloroplast PDC of both plant species showed the well known higher pH-and Mg-requirements than the mitochondrial complex. The observed species-specific differences in the stability of this multienzyme system suggest a connection with the aggregation state of its components. Apparently, the individual subcomplexes are able to function either together in acetyl-CoA formation or independently from each other, e.g. in the synthesis of acetolactate via hydroxy-ethyl-thiamine pyrophosphate or dihydrolipoyl dehydrogenase activities.

scholarly journals Protection of Cholinergic Neurons against Zinc Toxicity by Glial Cells in Thiamine-Deficient Media

2021 ◽  
Vol 22 (24) ◽  
pp. 13337
Author(s):  
Sylwia Gul-Hinc ◽  
Anna Michno ◽  
Marlena Zyśk ◽  
Andrzej Szutowicz ◽  
Agnieszka Jankowska-Kulawy ◽  
...  
Keyword(s):  
Glial Cells ◽  
Thiamine Deficiency ◽  
Neuronal Loss ◽  
Cholinergic Neurons ◽  
Competitive Inhibitor ◽  
Thiamine Pyrophosphate ◽  
Zinc Toxicity ◽  
Astroglial Cells ◽  
Acetyl Coa ◽  
Zinc Excess

Brain pathologies evoked by thiamine deficiency can be aggravated by mild zinc excess. Cholinergic neurons are the most susceptible to such cytotoxic signals. Sub-toxic zinc excess aggravates the injury of neuronal SN56 cholinergic cells under mild thiamine deficiency. The excessive cell loss is caused by Zn interference with acetyl-CoA metabolism. The aim of this work was to investigate whether and how astroglial C6 cells alleviated the neurotoxicity of Zn to cultured SN56 cells in thiamine-deficient media. Low Zn concentrations did not affect astroglial C6 and primary glial cell viability in thiamine-deficient conditions. Additionally, parameters of energy metabolism were not significantly changed. Amprolium (a competitive inhibitor of thiamine uptake) augmented thiamine pyrophosphate deficits in cells, while co-treatment with Zn enhanced the toxic effect on acetyl-CoA metabolism. SN56 cholinergic neuronal cells were more susceptible to these combined insults than C6 and primary glial cells, which affected pyruvate dehydrogenase activity and the acetyl-CoA level. A co-culture of SN56 neurons with astroglial cells in thiamine-deficient medium eliminated Zn-evoked neuronal loss. These data indicate that astroglial cells protect neurons against Zn and thiamine deficiency neurotoxicity by preserving the acetyl-CoA level.

Effects of NGF on acetylcholine, acetyl-CoA metabolism, and viability of differentiated and non-differentiated cholinergic neuroblastoma cells

2004 ◽  
Vol 90 (4) ◽  
pp. 952-961 ◽  
Author(s):  
Andrzej Szutowicz ◽  
Beata Madziar ◽  
Tadeusz Pawelczyk ◽  
Maria Tomaszewicz ◽  
Hanna Bielarczyk
Keyword(s):  
Neuroblastoma Cells ◽  
Acetyl Coa

Hydroxyurea induces a senescent, non-malignant, immunogenic state in neuroblastoma cells – a new therapeutic strategy?

2010 ◽  
Vol 222 (03) ◽  
Author(s):  
S Taschner-Mandl ◽  
A Kowalska ◽  
H Binder ◽  
D Rieder ◽  
Z Trajanoski ◽  
...  
Keyword(s):  
Therapeutic Strategy ◽  
Neuroblastoma Cells

The role of rice bran extract on acetyl CoA carboxylase in liver of rats fed a high-fat diet

Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
C Charkhonpunya ◽  
S Sireeratawong ◽  
S Komindr ◽  
N Lerdvuthisopon
Keyword(s):  
Rice Bran ◽  
High Fat Diet ◽  
Acetyl Coa Carboxylase ◽  
High Fat ◽  
Acetyl Coa ◽  
Rice Bran Extract
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