Using of the EPR Spin Labeling for the Investigation of the Synaptosomal Membrane Fluidity Changes Under Dimebon Injection in vivo

2015 ◽  
pp. 105-116
Keyword(s):  
Membrane Fluidity ◽  
Spin Labeling ◽  
Synaptosomal Membrane

Mechanism of increased erythrocyte membrane fluidity during magnesium deficiency in weanling rats

1989 ◽  
Vol 257 (2) ◽  
pp. C270-C276 ◽  
Author(s):  
S. Tongyai ◽  
Y. Rayssiguier ◽  
C. Motta ◽  
E. Gueux ◽  
P. Maurois ◽  
...  
Keyword(s):  
Membrane Fluidity ◽  
Erythrocyte Membrane ◽  
Magnesium Deficiency ◽  
Osmotic Fragility ◽  
Magnesium Content ◽  
Male Rats ◽  
Surface Irregularities ◽  
Erythrocyte Membrane Fluidity ◽  
And Control

The erythrocyte membrane was investigated in weanling male rats pair fed with magnesium-deficient and control diets for 8 days. Fluorescence polarization studies revealed a 15% increase in the fluidity of membranes from deficient rats. A similar increase in the fluidity of liposomes indicated that protein was not involved. The change was associated with decreased osmotic fragility of intact erythrocytes; the cells lost their biconcavity and had a flattened appearance with surface irregularities. Analysis of the membranes showed decreased amounts of magnesium, cholesterol, and sphingomyelin in the deficient group. The reduced ratios of cholesterol to phospholipid and sphingomyelin to phosphatidylcholine were consistent with the increased fluidity. Addition of physiological amounts of magnesium to the medium rigidified membranes incubated in tris(hydroxymethyl)-aminomethane buffer, and this was prevented by the presence of EDTA. Cross-incubation experiments with erythrocyte ghosts and plasma from the two groups of rats showed that magnesium-deficient plasma increased the fluidity of control ghosts and control plasma rigidified ghosts from magnesium-deficient rats. Addition of sufficient magnesium chloride to raise the magnesium content of deficient plasma to normal had no significant effect. These results show that the increased fluidity of the erythrocyte membrane in magnesium deficiency is due to physicochemical exchange with the plasma. Although magnesium can directly influence membrane fluidity, the change during its deficiency in vivo is mainly mediated indirectly via disturbances in lipid metabolism.

scholarly journals Impact of Deficiencies in Branched-Chain Fatty Acids and Staphyloxanthin inStaphylococcus aureus

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Hannah Braungardt ◽  
Vineet K. Singh
Keyword(s):  
Fatty Acids ◽  
Membrane Fluidity ◽  
Skin Infections ◽  
Deep Tissue ◽  
Environmental Survival ◽  
Branched Chain Fatty Acids ◽  
Superficial Skin ◽  
Branched Chain ◽  
Chain Fatty Acids

Staphylococcus aureusis a well-known human pathogen with the ability to cause mild superficial skin infections to serious deep-tissue infections, such as osteomyelitis, pneumonia, and infective endocarditis. A key toS. aureusinfections and its pathogenicity is its ability to survive in adverse environments, especially at lower temperatures, by regulation of its cell membrane. Branched-chain fatty acids (BCFAs) and staphyloxanthin have been shown to regulate membrane fluidity and staphylococcal virulence. This study was conducted with the hypothesis that the simultaneous lack of BCFAs and staphyloxanthin will have a far greater implication on environmental survival and virulence ofS. aureus. Lack of a functional branched-chainα-keto acid dehydrogenase (BKD) enzyme because of a mutation in thelpdAgene led to a decrease in the production of BCFAs, membrane fluidity, slower growth, and poorin vivosurvival ofS. aureus. A mutation in thecrtMgene eliminated the production of staphyloxanthin but it did not affect membrane BCFA levels, fluidity, growth, orin vivosurvival. AcrtM:lpdAdouble mutant showed much slower growth and attenuation compared to individual mutants. The results of this study suggest that simultaneous targeting of the BCFA and staphyloxanthin biosynthetic pathways can be a strategy to controlS. aureusinfections.

Decreased membrane fluidity and beta-adrenergic responsiveness in atherosclerotic quail

1985 ◽  
Vol 249 (2) ◽  
pp. H380-H385 ◽  
Author(s):  
K. G. Lurie ◽  
J. H. Chin ◽  
B. B. Hoffman
Keyword(s):  
Membrane Fluidity ◽  
Elevated Serum ◽  
Erythrocyte Membranes ◽  
Paramagnetic Resonance ◽  
Beta Adrenergic ◽  
Severe Atherosclerosis ◽  
Phospholipid Ratio ◽  
Erythrocyte Membrane Fluidity ◽  
Elevated Serum Cholesterol

The effects of increased cholesterol on erythrocyte membrane fluidity and beta-adrenergic function were studied in a quail model of atherosclerosis. Birds fed a cholesterol-supplemented diet developed severe atherosclerosis and hypercholesterolemia after 6 wk. This cholesterol-enriched diet led to a markedly elevated serum cholesterol and a 26% increase in the cholesterol-to-phospholipid ratio in erythrocyte membranes. Electron paramagnetic resonance spectra measured with 5- and 12-doxyl-stearic acid spin-label probes were used to estimate the order of quail erythrocyte membranes. Membrane preparations from cholesterol-fed birds were more highly ordered near the membrane leaflet surface, as well as deeper in the membrane interior, compared with controls. beta-Adrenergic receptor stimulation of adenosine 3',5'-cyclic monophosphate accumulation was blunted in erythrocytes from the hypercholesterolemic quail. There was no change in beta-receptor density or affinity in the cholesterol-enriched membranes. These studies demonstrate that cholesterol incorporation into erythrocyte membranes in vivo is associated with decreased membrane fluidity and decreased beta-adrenergic responsiveness. The atherosclerotic quail may serve as a useful model to further probe the sequelae of hypercholesterolemia on the function of integral membrane proteins.

Sign in / Sign up

Export Citation Format

Share Document