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

Znaleziono wyników: 3

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

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.
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.
2

Rola cynku w procesach fizjologicznych i patologicznych organizmu

100%
Gapys B., Raszeja-Specht A., Bielarczyk H.
Diagnostyka Laboratoryjna
|
2014
|
tom 50
|
nr 1
3

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.
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.
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.