scholarly journals Effect of trimethylarsine on osmotic fragility of erythrocyte membrane.

Sangyo Igaku ◽  
1989 ◽  
Vol 31 (6) ◽  
pp. 440-441
Author(s):  
Keiko TAKAHASHI ◽  
Hiroshi YAMAUCHI ◽  
Yukio YAMAMURA ◽  
Yoshiro KUDOU
Keyword(s):  
Erythrocyte Membrane ◽  
Osmotic Fragility

Membrane Alterations Induced by Amphiphiles

1989 ◽  
Vol 16 (3) ◽  
pp. 274-280
Author(s):  
Boris Isomaa ◽  
Henry Hägerstrand ◽  
Gun I.L. Paatero
Keyword(s):  
Ion Transport ◽  
Lipid Bilayer ◽  
Erythrocyte Membrane ◽  
Cell Shape ◽  
Osmotic Fragility ◽  
Molecular Shape ◽  
Specific Interactions ◽  
Amphiphilic Compounds ◽  
Rapid Formation ◽  
Polar Parts

Amphiphilic compounds with distinct apolar and polar parts are readily intercalated into the erythrocyte membrane. When intercalated into the membrane, amphiphiles are probably orientated so that the polar head is at the polar-apolar interface of the lipid bilayer and the hydrophobic part within the apolar core of the bilayer. However, by virtue of their difference in molecular shape from the bulk lipids of the lipid bilayer, it is possible that the intercalated amphiphiles are partly segregated from bulk lipids and accumulate at protein-lipid interfaces in the bilayer, where the packing of the bilayer lipids may be less ordered. Our studies show that amphiphiles, when intercalated into the erythrocyte membrane, trigger alterations in several membrane-connected functions. Some of the alterations induced (decreased osmotic fragility, increased passive potassium fluxes) seem to be due to non-specific interactions of the amphiphiles with the membrane, whereas other functions (ion transport mediated by membrane proteins, regulation of cell shape) seem to be sensitive to particular features of the amphiphiles. Our studies indicate that the intercalation of amphiphiles into the erythrocyte membrane must involve rearrangements within the lipid bilayer. We have suggested that, when intercalated into the lipid bilayer, amphiphiles trigger a rapid formation of non-bilayer phases, which protect the bilayer against a collapse and bring about a trans-bilayer redistribution of intercalated amphiphiles as well as of bilayer lipids. At high sublytic concentrations, this process may also involve a release of microvesicles from the membrane.

Attenuation of erythrocyte membrane oxidative stress bySesbania grandiflorain streptozotocin-induced diabetic rats

2015 ◽  
Vol 93 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Chandrabose Sureka ◽  
Thiyagarajan Ramesh ◽  
Vavamohaideen Hazeena Begum
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Blood Glucose ◽  
Erythrocyte Membrane ◽  
Osmotic Fragility ◽  
Diabetic Rats ◽  
Glycosylated Haemoglobin ◽  
Albino Rats ◽  
Enzymatic Antioxidants ◽  
Protective Effects

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.

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.

Effects of Proteus mirabilis Lipopolysaccharides with Different O-Polysaccharide Structures on the Plasma Membrane of Human Erythrocytes

2008 ◽  
Vol 63 (5-6) ◽  
pp. 460-468 ◽  
Author(s):  
Michał Arabski ◽  
Krzysztof Gwoździński ◽  
Beata Sudak ◽  
Wiesław Kaca
Keyword(s):  
Plasma Membrane ◽  
Membrane Proteins ◽  
Erythrocyte Membrane ◽  
Osmotic Fragility ◽  
Membrane Lipid ◽  
Membrane Properties ◽  
Physical Parameters ◽  
Chemical Structures ◽  
Lipid Fluidity ◽  
Membrane Lipid Fluidity

The effects of O33 and O49 P. mirabilis lipopolysaccharides (LPSs) on human erythrocyte membrane properties were examined. Physical parameters of the plasma membrane, such as membrane lipid fluidity, physical state of membrane proteins, and osmotic fragility, were determined. The fluidity of the lipids was estimated using three spin-labeled stearic acids of doxyl derivatives: 5-doxylstearic acid, 12-doxylstearic acid, and 16-doxylstearic acid. All the applied labels locate to different depths of the lipid layer and provide information on the ordering of phospholipid fatty acyl chain mobility. LPSs O49 increased the membrane lipid fluidity in the polar region of the lipid bilayer as indicated by spin-labeled 5-doxylstearic acid. An increase in fluidity was also observed in the deeper region using 12-doxylstearic acid only for O33 LPSs. The highest concentration of O33 LPSs (1 mg/ml) increased the motion of membrane proteins detected by the spin-label residue of iodoacetamide. These results showed different actions of O33 and O49 LPSs on the plasma membrane due to the different chemical structures of O-polysaccharides. P. mirabilis O33 and O49 LPSs did not induce changes in the membrane cytoskeleton, osmotic fragility and lipid peroxidation of erythrocytes. On the other hand a rise in the content of carbonyl compounds was observed for the highest concentrations of O33 LPS. This result indicated protein oxidation in the erythrocyte membrane. Lipid A, the hydrophobic part of LPS, did not change the membrane lipid fluidity and osmotic fragility of erythrocytes. Smooth and rough forms of P. mirabilis LPSs were tested for their abilities for complement-mediated immunohemolysis of erythrocytes. Only one out of seven LPSs used was a potent agent of complement-mediated hemolysis. It was rough, Ra-type of P. mirabilis R110 LPS. The O-polysaccharide-dependent scheme of reaction is presented.

Alterations in rat erythrocyte membrane due to hexachlorocyclohexane (technical) exposure

1998 ◽  
Vol 17 (11) ◽  
pp. 638-642 ◽  
Author(s):  
Pankaj Bhalla ◽  
Deepa Agrawal
Keyword(s):  
Membrane Fluidity ◽  
Erythrocyte Membrane ◽  
Osmotic Fragility ◽  
Structure And Function ◽  
Membrane Structure And Function ◽  
Hydrophobic Molecule ◽  
Erythrocyte Membrane Fluidity ◽  
Membrane Bound ◽  
And Function ◽  
Membrane Bound Enzymes

1 Hexachlorocyclohexane (HCH), an organochlorine pesticide having hydrophobic molecule is known to act on membranes. HCH mediated alterations in erythrocyte membrane occur through disorganization of the lipid bilayer. Therefore the changes in erythrocyte membrane fluidity, osmotic fragility and certain membrane bound enzymes were studied. Administration of HCH (technical) to rats at 5 mg/kg, orally, 5 days a week for 1, 2 and 3 months caused marked increase in erythrocyte membrane fluidity, osmotic fragility anddecreaseinlevelsofNa+, K+-ATPase, acetylcholinesterase in erythrocytes and glutathione in blood. 2 These changes indicate that HCH adversely affects membrane structure and function.

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