Erythrocyte membranes-effect of increased cholesterol content on permeability

Kroes, J.G.; Ostwald, Rosemarie

doi:10.1016/0005-2736(71)90147-7

Cited by 136 publications

(40 citation statements)

References 7 publications

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“…In in vitro models, cholesterol alters the fluidity of pure phospholipid membranes and enhances the degree of order within membrane lipids (25). A direct relationship between transport and membrane fluidity has been demonstrated in red cells where an increase in the cholesterol/phospholipid ratio decreased permeability to compounds entering by carrier mediated transport or facilitated a diffusion such as erythritol and glycerol (24). Decrease of membrane fluidity induced by cholesterol prevents stimulation of adenyl cyclase activity by sodium fluoride or by prostaglandin El in platelets (37) and adenyl cyclase activity of the rat intestine can be influenced by changes in cell membrane fluidity (38).…”

Section: Discussionmentioning

confidence: 99%

“…It delays the onset of hemorrhagic cholecystitis in the canine gallbladder when solutions of pure bile acids are introduced into this organ (23). Cholesterol also reduces the permeability of erythrocyte membranes (24) and artificial membranes (25) to water and electrolytes. We therefore performed experiments to test whether cholesterol might mitigate the effects of dihydroxy bile acids and fatty acids on jejunal transport processes.…”

Section: Introductionmentioning

confidence: 99%

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Cholesterol reduces the effects of dihydroxy bile acids and fatty acids on water and solute transport in the human jejunum.

Broor¹,

Slota²,

Ammon³

1980

J. Clin. Invest.

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A B S T R A C T Jejunal perfusion studies were performed in 16 healthy volunteers to test the hypothesis that initraluminal cholesterol can mitigate the fluid secretion induced by dihydroxy bile acids and fatty acids. Fluid secretion in the presence of 5 mM taurodeoxycholate was somewhat reduced by 4 mM mono-olein which was used for the solubilization of cholesterol. Addition of 0.8 mM cholesterol reduced fluid secretion further (P < 0.05). Fluid secretion induced by 4 mM oleic acid was changed to net absorption in a linear fashion with increasing cholesterol concentration in the perfusion solutions. 1 mM cholesterol reduced fluid secretion induced by 6 mM oleic acid (P < 0.005), but had no effect on fluiid secretion induced by 6 mM linolenic acid. Glucose absorption was generally affected in a similar manner as water transport. In vitro, 1 mM cholesterol reduced monomer activity of 6 mM oleic acid to 72.3+0.9% of control and that of linolenic acid to 81.1±1.7% ofcontrol. Although statistically significant (P < 0.001), the difference in the effects of cholesterol on monomer activities of the two fatty acids was rather small and it is unlikely that changes in monomer concentration of fatty acids and bile acids account for the protective effect of cholesterol. The in vivo observations point to a new physiological role for biliary cholesterol: the modification ofthe response ofthe small intestine to the effects of dihydroxy bile acids and fatty acids.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cholesterol reduces the effects of dihydroxy bile acids and fatty acids on water and solute transport in the human jejunum.

Broor¹,

Slota²,

Ammon³

1980

J. Clin. Invest.

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“…Characteristics of lipid dispersions. The C/P of dispersions prepared by sonication was similar to the C/P of lipids added before sonication for all mixtures except that obtained by the addition of more than 40 mg of cholesterol to 40 To assess the chemical stability of dispersions, the cholesterol and phospholipid content of sonicated lipids, with and without added serum, was measured at various times during storage at 0C and 370C. Samples were centrifuged immediately before lipid determinations.…”

Section: Methodsmentioning

confidence: 99%

Modification of red cell membrane structure by cholesterol-rich lipid dispersions. A model for the primary spur cell defect.

Cooper¹,

Arner²,

Wiley³

et al. 1975

J. Clin. Invest.

342

138

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A B S T R A C T Cholesterol-rich membranes are the hallmark of "spur" red cells. Spur cells accumulate cholesterol from cholesterol-rich serum lipoproteins. Previous studies suggested that this added cholesterol is responsible for both the altered morphology and the destruction of spur cells. To examine this process in the absence of other serum factors, cholesterol-lecithin dispersions with varying amounts of unesterified cholesterol (C) relative to phospholipid (P) were prepared, and their influence on normal human red cells was studied.Cholesterol-rich lipid dispersions (C/P mole ratio > 1.0) transferred cholesterol to both red cell membranes and serum lipoproteins, and cholesterol-poor dispersions (C/P mole ratio < 1.0) depleted red cells of cholesterol. Changes in membrane cholesterol paralleled changes in membrane surface area, as calculated from osmotic fragility, with a 0.22% variation in surface area per 1.0% variation in cholesterol content. Cold-induced compression of membrane surface area was increased in cholesterol-poor red cells (C/P = 0.4), whereas the surface area of cholesterol-rich membranes (C/P = 1.80) underwent no compression. Although the Na and K permeability of red cells severely depleted of cholesterol was increased, lesser degrees of depletion had no effect, and the permeability of cholesterol-rich cells was normal. However, increasing membrane cholesterol caused a progressive decrease in red cell deformability, as measured by filtration.Cholesterol-poor red cells were spherocytic in appearance and cholesterol-rich cells were broad and flat, indicative of their surface areas. In addition, cholesterol-

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“…It stabilizes membrane structure (Bloom and Mouritsen, 1988), limits membrane permeability (Kroes and Ostwald, 1971) and imparts a suitable working environment for membrane proteins (Yeagle et al, 1988). Despite the physicochemical influences of cholesterol, its distribution in biological membranes is far from homogenous.…”

Section: Introductionmentioning

confidence: 99%

Habitat temperature is an important determinant of cholesterol contents in copepods

Hassett

Crockett

2009

Journal of Experimental Biology

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SUMMARYEffects of habitat and acclimation temperature on cholesterol contents were examined in oceanic and inshore species of copepods. The cholesterol content of five species of thermally acclimated copepods was determined, and nine species (representing six families) were sampled to assess the role of habitat temperature. The species selected have maximum habitat temperatures (and temperature tolerances) that vary at least twofold. Levels of dietary cholesterol required to achieve maximum growth were also studied at different acclimation temperatures in a eurythermal copepod. Both eggs and copepodites of Calanus finmarchicus had higher cholesterol levels at the warm acclimation temperature (16°C) than at the cooler temperature (6°C). Neither Acartia tonsa, Acartia hudsonica, Temora longicornis nor Eurytemora affinis altered cholesterol contents with acclimation temperature. Maximum growth rates were achieved at fourfold higher concentrations of dietary cholesterol in warm-acclimated Eurytemora affinis than in cold-acclimated animals. The most consistent trend is the positive relationship between cholesterol content and habitat temperature. Species residing in warmer habitats (e.g. Centropages typicus, Eurytemora affinis) had approximately twice the cholesterol of species living in colder waters (e.g. Calanus glacialis, Euchaeta norvegica). A similar pattern was observed for comparisons of species within genera (Calanus, Acartia and Centropages), with the species abundant at lower latitudes having more cholesterol than the northern congener. These data indicate that habitat temperature is an important determinant of cholesterol content, and cholesterol endows membranes with the stability required for a range of body temperatures.

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Erythrocyte membranes-effect of increased cholesterol content on permeability

Cited by 136 publications

References 7 publications

Cholesterol reduces the effects of dihydroxy bile acids and fatty acids on water and solute transport in the human jejunum.

Cholesterol reduces the effects of dihydroxy bile acids and fatty acids on water and solute transport in the human jejunum.

Modification of red cell membrane structure by cholesterol-rich lipid dispersions. A model for the primary spur cell defect.

Habitat temperature is an important determinant of cholesterol contents in copepods

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