The influence of Methylprednisolone on the energy metabolism of Ehrlich ascites tumour cells

1994 ◽  
Vol 14 (6) ◽  
pp. 283-290 ◽  
Author(s):  
Frank Buttgereit ◽  
Marianne Müller ◽  
Karsten Wolbart ◽  
Bernhard Thiele ◽  
Falk Hiepe
Keyword(s):  
Plasma Membrane ◽  
Oxygen Consumption ◽  
Energy Metabolism ◽  
Membrane Permeability ◽  
Plasma Membrane Permeability ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Cellular Oxygen ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

Using Ehrlich ascites tumour cells, the short-term effects of the therapeutic glucocorticoid Methylprednisolone (MP) on the cellular energy metabolism were studied. ATP-consuming processes involved in the rapid MP effects were identified indirectly from the effects of MP on cellular oxygen consumption related to the inhibition of respiration by selective inhibitors of Ca2+-ATPase and protein synthesis. The effects of MP on plasma membrane permeability for Ca2+ ions and phospholipid turnover were studied directly by using confocal laser scanning microscopy and tracerkinetic measurements, respectively. MP inhibited cellular oxygen consumption, suppressed the inhibitory effect of lanthanum but not that of cycloheximide on oxygen consumption, blocked the [Ca2+]i rise in response to calcium ionophore A 23187, and decreased phospholipid turnover. MP acted instantly in a dose-dependent manner. The observed effects of MP are discussed in relation to the hypothesis that the drug has direct membrane effect affecting plasma membrane permeability and function.

scholarly journals Uptake of Ca2+ and refilling of intracellular Ca2+ stores in Ehrlich-ascites-tumour cells and in rat thymocytes

1990 ◽  
Vol 271 (2) ◽  
pp. 535-540 ◽  
Author(s):  
M Montero ◽  
J Alvarez ◽  
J Garcia-Sancho
Keyword(s):  
Plasma Membrane ◽  
Tumour Cells ◽  
Ehrlich Cell ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Filling Time ◽  
Ehrlich Ascites Tumour ◽  
Order Of Magnitude ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

We have studied the uptake of Ca2+ and its redistribution between the cytoplasm and the intracellular stores in Ehrlich-ascites-tumour cells and rat thymocytes previously depleted of Ca2+ by incubation in Ca2(+)-free medium. Measurements included changes of the cytoplasmic Ca2+ concentration ([Ca2+]i), uptake of 45Ca2+ and uptake of Mn2+, a Ca2+ surrogate for Ca2+ channels. Refilling of the Ca2+ stores in thymocytes was very fast (half-filling time: 4 s at 37 degrees C) and very sensitive to temperature (10 times slower at 20 degrees C). It was always preceded by increase of [Ca2+]i. In the Ehrlich cell, both refilling and increase of [Ca2+]i were about one order of magnitude slower. The increase of [Ca2+]i and the refilling of the intracellular stores were both almost completely blocked by Ni2+ in thymocytes, but only partially in the Ehrlich cell. The rates of 45Ca2+ and Mn2+ uptake varied consistently with temperature and the kind of cell. These results suggest that the intracellular stores are refilled by Ca2+ taken up from the cytoplasm. We also find that filling of the Ca2+ stores decreases by about 90% the rate of Mn2+ uptake in thymocytes. This is direct evidence of modulation of the plasma-membrane Ca2+ entry by the degree of filling of the intracellular stores. This modulation occurs in the absence of agonists, suggesting some kind of signalling between the intracellular stores and the Ca2+ entry pathways of the plasma membrane.

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