Nitric Oxide and Peroxynitrite Anion Modulate Liver Plasma Membrane Fluidity and Na+/K+-ATPase Activity

Nitric Oxide ◽  
2000 ◽  
Vol 4 (4) ◽  
pp. 333-342 ◽  
Author(s):  
Pablo Muriel ◽  
Gabriela Sandoval
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Atpase Activity ◽  
Membrane Fluidity ◽  
Liver Plasma Membrane ◽  
Plasma Membrane Fluidity ◽  
Peroxynitrite Anion

Effects of vitamin A and ethanol on liver plasma membrane fluidity

Hepatology ◽  
1988 ◽  
Vol 8 (4) ◽  
pp. 735-741 ◽  
Author(s):  
Cho-Il Kim ◽  
Maria Anna Leo ◽  
Nancy Lowe ◽  
Charles S. Lieber
Keyword(s):  
Plasma Membrane ◽  
Vitamin A ◽  
Membrane Fluidity ◽  
Liver Plasma Membrane ◽  
Plasma Membrane Fluidity

Chronic ethanol increases liver plasma membrane fluidity

Biochemistry ◽  
1985 ◽  
Vol 24 (13) ◽  
pp. 3114-3120 ◽  
Author(s):  
Mark A. Polokoff ◽  
Thomas J. Simon ◽  
R. Adron Harris ◽  
Francis R. Simin ◽  
Mieko Iwahashi
Keyword(s):  
Plasma Membrane ◽  
Membrane Fluidity ◽  
Chronic Ethanol ◽  
Liver Plasma Membrane ◽  
Plasma Membrane Fluidity

Acyl-CoA: 1-acyl-glycero-3-phosphoethanolamine O-acyltransferase and liver plasma membrane fluidity

Biochimie ◽  
1990 ◽  
Vol 72 (12) ◽  
pp. 863-866 ◽  
Author(s):  
A.B. Momchilova-Pankova ◽  
T.T. Markovska ◽  
K.S. Koumanov
Keyword(s):  
Plasma Membrane ◽  
Membrane Fluidity ◽  
Liver Plasma Membrane ◽  
Plasma Membrane Fluidity

DMSO Modifies Structural and Functional Properties of RPMI-8402 Cells by Promoting Programmed Cell Death

2003 ◽  
Vol 16 (3) ◽  
pp. 253-259 ◽  
Author(s):  
O. Trubiani ◽  
E. Salvolini ◽  
R. Staffolani ◽  
R. Di Primio ◽  
L. Mazzanti
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Plasma Membrane ◽  
Programmed Cell Death ◽  
Membrane Fluidity ◽  
Membrane Damage ◽  
Lymphoid Cells ◽  
Plasma Membrane Fluidity ◽  
Structural And Functional Properties ◽  
Intracellular Ca

Apoptosis in lymphoid cells can be induced in different ways depending on cell type and acquired signal. Biochemical modifications occur at an early phase of cell death while at late times the typical morphological features of apoptosis can be visualized. The aim of this study is to verify by multiparametric analyses the plasma membrane fluidity, the intracellular Ca2+ concentration and the nitric oxide synthase (NOS) activity during cell death progression induced by DMSO treatment. The RPMI-8402 human pre-T lymphoblastoid cell line was induced to cell death by DMSO. Analyses rescued at early times of treatment prove a substantial modification of plasma membrane fluidity associated with an increase of intracellular Ca2+. Moreover, these modifications are associated with an up regulation of NOS activity. Our results are consistent with the hypothesis that programmed cell death can be induced by up regulation of the intracellular Ca2+ associated with an increase of cell membrane fluidity. The apoptotic mechanisms seem to involve not only membrane damage and increased intracellular calcium levels but also production of nitric oxide.

Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction

1986 ◽  
Vol 60 (3) ◽  
pp. 826-835 ◽  
Author(s):  
E. R. Block ◽  
J. M. Patel ◽  
K. J. Angelides ◽  
N. P. Sheridan ◽  
L. C. Garg
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Pulmonary Artery ◽  
Atpase Activity ◽  
Membrane Fluidity ◽  
Atp Content ◽  
Aortic Endothelial Cells ◽  
Plasma Membrane Fluidity ◽  
High O2 ◽  
Aortic Endothelial

To evaluate the relative contributions of three possible mechanisms that can be advanced to explain the observation that hyperoxia decreases serotonin uptake by endothelial cells, we examined the effect of high O2 tensions on Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in cultured endothelial cells. Confluent monolayers of pulmonary artery and aortic endothelial cells were exposed to 95% O2 (hyperoxia) or 20% O2 (controls) in 5% CO2 at 1 ATA for 4–42 h. Exposure to high O2 tensions had no effect on Na+-K+-ATPase activity or ATP content in pulmonary artery or aortic endothelial cells in culture. However, hyperoxia decreased the fluidity of the plasma membrane of pulmonary artery and aortic endothelial cells in culture, and the time course for the decrease in fluidity parallels that of the hyperoxic inhibition of serotonin transport. These results indicate that hyperoxia decreases fluidity in the hydrophobic core of the plasma membranes of cultured endothelial cells. Such decreases in plasma membrane fluidity may be responsible for hyperoxia-induced alterations in membrane function including decreases in transmembrane transport of amines.

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