Literature DB >> 5780200

The selective and conjoint loss of red cell lipids.

R A Cooper, J H Jandl.   

Abstract

The pattern of lipid loss from the membrane of red cells incubated in serum is influenced by the availability of glucose. Under homeostatic conditions with respect to glucose, cholesterol alone is lost. This results from esterification of free cholesterol in serum by the serum enzyme, lecithin:cholesterol acyltransferase, and is associated with a proportional decrease in membrane surface area, reflected by an increased osmotic fragility. This selective loss of membrane cholesterol also occurs in hereditary spherocytosis (HS) red cells, even after incubation for 65 hr in the presence of glucose. The loss of free cholesterol from red cells relative to its loss from serum, under these conditions, is greatest at higher hematocrits, similar to those found in the spleen. Although the selective loss of membrane cholesterol increases the spherodicity of normal red cells, it does not lead to a change in their rate of glucose consumption, and both the loss of cholesterol and the increase in osmotic fragility are reversible in vitro. Moreover, normal red cells made osmotically fragile by cholesterol depletion in vitro rapidly become osmotically normal and survive normally after their reinfusion in vivo.In contrast to this selective loss of membrane cholesterol, red cells incubated in the absence of glucose lose both cholesterol and phospholipid. This occurs more rapidly in HS than normal red cells and is followed by a disruption of cation gradients and then by hemolysis. Cholesterol and phospholipid lost under these conditions is not restored during subsequent incubations in vitro. Selective loss of membrane cholesterol is a physiologic event secondary to an altered state of serum lipids. It is reversible both in vitro and in vivo and neither influences cellular metabolism nor impairs viability. Conjoint loss of phospholipid and cholesterol, however, results from intrinsic injury to the red cell membrane which results from prolonged metabolic depletion.

Entities:  

Mesh:

Substances:

Year:  1969        PMID: 5780200      PMCID: PMC322299          DOI: 10.1172/JCI106049

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  34 in total

1.  Studies on the electron transfer system. LXV. Formation of membranes by purified cytochrome oxidase.

Authors:  D G McConnell; A Tzagoloff; D H MacLennan; D E Green
Journal:  J Biol Chem       Date:  1966-05-25       Impact factor: 5.157

Review 2.  Cholesterol ester metabolism.

Authors:  D S Goodman
Journal:  Physiol Rev       Date:  1965-10       Impact factor: 37.312

Review 3.  Increased splenic pooling and the pathogenesis of hypersplenism.

Authors:  J H Jandl; R H Aster
Journal:  Am J Med Sci       Date:  1967-04       Impact factor: 2.378

Review 4.  Membrane alterations leading to red cell destruction.

Authors:  R I Weed; C F Reed
Journal:  Am J Med       Date:  1966-11       Impact factor: 4.965

5.  The influence of pH and temperature on some physical properties of normal erythrocytes and erythrocytes from patients with hereditary spherocytosis.

Authors:  J R Murphy
Journal:  J Lab Clin Med       Date:  1967-05

6.  Spur-shaped erythrocytes in Laennec's cirrhosis.

Authors:  R Silber; E Amorosi; J Lhowe; H J Kayden
Journal:  N Engl J Med       Date:  1966-09-22       Impact factor: 91.245

7.  Erythrocyte lipid loss in hereditary spherocytosis.

Authors:  C F Reed; S N Swisher
Journal:  J Clin Invest       Date:  1966-05       Impact factor: 14.808

8.  Plasma membranes: phospholipid and sterol content.

Authors:  L A Ashworth; C Green
Journal:  Science       Date:  1966-01-14       Impact factor: 47.728

9.  Turnover of plasma esterified cholesterol in normocholesterolemic and hypercholesterolemic subjects and its relation to body build.

Authors:  P J Nestel; E A Monger
Journal:  J Clin Invest       Date:  1967-06       Impact factor: 14.808

10.  Concomitant alterations of sodium flux and membrane phospholipid metabolism in red blood cells: studies in hereditary spherocytosis.

Authors:  H S Jacob; M L Karnovsky
Journal:  J Clin Invest       Date:  1967-02       Impact factor: 14.808

View more
  5 in total

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

Authors:  R A Cooper; E C Arner; J S Wiley; S J Shattil
Journal:  J Clin Invest       Date:  1975-01       Impact factor: 14.808

2.  Chemical synthesis of dinitrodiphenysulfone derivatives of ethanolamine and serine and its application to the study of neighbor analysis of amino-phospholipids in the erythrocyte membrane.

Authors:  G V Marinetti; R Love
Journal:  J Membr Biol       Date:  1976       Impact factor: 1.843

3.  Hereditary spherocytosis of man. Altered binding of cytoskeletal components to the erythrocyte membrane.

Authors:  J S Hill; W H Sawyer; G J Howlett; J S Wiley
Journal:  Biochem J       Date:  1982-02-01       Impact factor: 3.857

4.  Loss of membrane components in the pathogenesis of antibody-induced spherocytosis.

Authors:  R A Cooper
Journal:  J Clin Invest       Date:  1972-01       Impact factor: 14.808

5.  An analysis of lipoproteins, bile acids, and red cell membranes associated with target cells and spur cells in patients with liver disease.

Authors:  R A Cooper; M Diloy Puray; P Lando; M S Greenverg
Journal:  J Clin Invest       Date:  1972-12       Impact factor: 14.808

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.