scholarly journals Degradation of Membrane Phospholipids and Thiols in Peroxide Hemolysis: Studies in Vitamin E Deficiency

Blood ◽  
1968 ◽  
Vol 32 (4) ◽  
pp. 549-568 ◽  
Author(s):  
HARRY S. JACOB ◽  
SAMUEL E. LUX
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Hemolytic Anemia ◽  
Phosphatidyl Ethanolamine ◽  
Red Cells ◽  
Membrane Phospholipids ◽  
Vitamin E Deficiency ◽  
Red Cell Membrane ◽  
Inhibition Of Metabolism

Abstract To understand more clearly the hemolytic anemia associated with administration of certain oxidant drugs, the mechanism by which H2O2 causes hemolysis in rat red cells, deficient in vitamin E was investigated. It was demonstrated that the locus of attack by H2O2 was the red cell membrane, in which one phospholipid, i.e., phosphatidyl ethanolamine, was specifically destroyed prior to the onset of hemolysis. No perturbation of intracellular components or metabolism was noted during peroxidative hemolysis. E-deficient red cells incorporated 14C-labelled fatty acids into this phosphatide at nearly twice the rate that in E-supplemented cells, reflecting the continual tendency of phosphatidyl ethanolamine to be destroyed. Young red cells were especially active in this regard and concomitantly were less vulnerable to damage by H2O2 both in vitro and when circulating in rats exposed to hyperbaric oxygenation. If, however, replacement of fatty acids in phosphatidyl ethanolamine was prevented by inhibition of metabolism or if fatty acids were enzymatically removed by a phospholipase-A, H2O2 hemolysis was potentiated. Hemolysis was also associated with, and potentiated by, loss of membrane sulfhydryl activity. It is suggested that hemolytic anemia may occur in patients with vitamin E deficiency (i.e., with steatorrhea) if oxidant drugs capable of generating H2O2 and oxidizing membrane thiols are administered. Two such cases are under investigation.

scholarly journals The relationship between in vivo generated hemoglobin skeletal protein complex and increased red cell membrane rigidity

Blood ◽  
1988 ◽  
Vol 71 (5) ◽  
pp. 1427-1431 ◽  
Author(s):  
N Fortier ◽  
LM Snyder ◽  
F Garver ◽  
C Kiefer ◽  
J McKenney ◽  
...  
Keyword(s):  
Protein Complex ◽  
Sodium Dodecyl ◽  
Red Cells ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Cellular Dehydration ◽  
Thalassemia Minor ◽  
Membrane Rigidity

Abstract In vitro induced oxidative damage to normal human RBCs has previously been shown to result in increased membrane rigidity as a consequence of the generation of a protein complex between hemoglobin and spectrin. In order to determine if in vivo generated hemoglobin-spectrin complexes may play a role in increased membrane rigidity of certain pathologic red cells, we measured both these parameters in membranes prepared from hereditary xerocytosis (Hx), sickle cell disease (Sc), and red cells from thalassemia minor (beta thal). Membranes were prepared from density-fractionated red cells, and membrane deformability was measured using an ektacytometer. Hemoglobin-spectrin complex was determined by sodium dodecyl sulfate (SDS)-polyacrylamide gel analysis, as well as by Western blot analysis using a monoclonal antibody against the beta- subunit of hemoglobin. For these three types of pathologic red cells, progressive cellular dehydration was associated with increased membrane rigidity and increased content of hemoglobin-spectrin complex. Moreover, the increase in membrane rigidity appeared to be directly related to the quantity of hemoglobin-spectrin complex associated with the membrane. Our findings imply that hemoglobin-spectrin complex is generated in vivo, and this in turn results in increased membrane rigidity of certain pathologic red cells. The data further suggest that oxidative crosslinking may play an important role in the pathophysiology of certain red cell disorders.

scholarly journals In Vitro Erythrophagocytosis in Acquired Hemolytic Anemia

Blood ◽  
1952 ◽  
Vol 7 (6) ◽  
pp. 592-601 ◽  
Author(s):  
WILLIAM H. ZINKHAM ◽  
LOUIS K. DIAMOND
Keyword(s):  
Hemolytic Anemia ◽  
Red Cells ◽  
In Vitro Method

Abstract It has been found that marked erythrophagocytosis occurred when the buffy coats of 3 patients with idiopathic acquired hemolytic anemia were incubated at 37 C. for one hour. It is suggested that this technic may be used as another in vitro method of demonstrating abnormalities of the red cells in patients with acquired hemolytic anemia, as well as other conditions in which there is damage or alteration of the red cells.

scholarly journals Antisickling effect of tellurite: a potent membrane-acting agent in vitro

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 305-307 ◽  
Author(s):  
T Asakura ◽  
Y Shibutani ◽  
MP Reilly ◽  
RH DeMeio
Keyword(s):  
Hemoglobin Concentration ◽  
Inhibitory Effect ◽  
Red Cells ◽  
Cell Swelling ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Potassium Tellurite ◽  
New Type ◽  
Acting Agent

Abstract Potassium tellurite (K2TeO3) was found to be a potent antisickling agent that inhibited red cell sickling at concentrations less than 10 mumol/L. The inhibitory effect depended on the incubation time, with the effect increasing with longer incubation periods. Because tellurite causes swelling of red cells, and because the antisickling effect of tellurite correlated with the degree of red cell swelling, the antisickling effect of tellurite is assumed to be due to the decreased mean cell hemoglobin concentration. Swelling of red cells by tellurite was accelerated by the addition of reduced glutathione. Tellurite appears to be a new type of antisickling agent that interacts with the red cell membrane.

scholarly journals THE IN VITRO PREPARATION AND HISTOCHEMICAL PROPERTIES OF SUBSTANCES RESEMBLING CEROID

1951 ◽  
Vol 94 (6) ◽  
pp. 549-562 ◽  
Author(s):  
W. G. Bruce Casselman
Keyword(s):  
Fatty Acids ◽  
Blood Cells ◽  
Periodic Acid ◽  
Vitamin E Deficiency ◽  
Silver Carbonate ◽  
Relative Lack ◽  
Unsaturated Lipids ◽  
Lipofuscin Pigment ◽  
Ceroid Pigment

Substances possessing the same histochemical properties as the ceroid in cirrhotic livers of rats fed choline-deficient diets have been prepared from various unsaturated fats, fatty acids and their esters by autoxidation but could not be obtained from hydrocarbons or saturated fats or fatty acids. The formation of ceroid-like substances occurred first on surfaces or at interfaces in the reaction mixtures. It was inhibited by antioxidants and was accelerated by the addition of tissues, blood cells, erythrocytic stroma, or hemoglobin, by emulsification, by increasing the surface exposed to the air, and by increasing the temperature. Histochemical studies provided much evidence that the following properties of ceroid might be attributed to the products of the autoxidation of unsaturated lipids: insolubility in organic solvents, sudanophilia, yellowing by concentrated nitric acid, positive periodic acid-Schiff's reaction, basophilia, acid fastness, positive hernofuscin reaction, and reduction of diammine silver carbonate and alkaline potassium permanganate. The normal reactivity of cells or tissues embedded in ceroid was effectively masked by the pigment, apparently, initially at least, by preventing the reagents' gaining access to them. It is suggested that the iron sometimes demonstrated in ceroid may be that of blood cells or tissue fragments incompletely masked by the ceroid. It is concluded that whenever conditions are such that unsaturated fats accumulate in tissues to such an extent that a relative lack of biological anti-oxidants results, autoxidation of the fats and their conversion to ceroid pigment are favored, and that ceroid and the lipofuscin pigment of vitamin E deficiency may be fundamentally similar.

scholarly journals The effects of vitamin E deficiency on the total fatty acids and the phospholipid fatty acids of rat tissues

1969 ◽  
Vol 23 (2) ◽  
pp. 289-295 ◽  
Author(s):  
D. J. W. Lee ◽  
M. McC. Barnes
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Total Phospholipid ◽  
Rat Tissues ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Acid Deficiency ◽  
Total Fatty Acids ◽  
Fatty Acid Deficiency ◽  
Kidney Liver

1. A vitamin E-low diet containing 7% stripped lard was given to hooded rats for periods up to 14 months. Control rats were given the same diet with a vitamin E supplement (I i.u./rat per day).2. No consistent pattern of changes was found in the total fatty acids of testis, lung, spleen, pancreas, heart, kidney, liver, brain, skeletal muscle and small intestine from rats given the deficient diet for 5, 6 or 7 months when compared with control rats.3. The fatty acids of the total phospholipid from the same tissues were examined after 4, 5, 8 or 14 months. In the rats deficient in vitamin E the polyunsaturated fatty acids of the linoleic series (ω6) decreased, except for 20:4ω6, which in some tissues tended to increase. After 14 months there were considerable decreases in the percentages of all the ω6 series including 20:4ω6 with increases in the percentages of 18:1ω9 and 20:3ω9 the pattern was similar to that found in essential fatty acid deficiency.

Severe Hemolytic Anemia Associated With Vitamin E Deficiency in Infants With Cystic Fibrosis

1994 ◽  
Vol 33 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Benjamin S. Wilfond ◽  
Philip M. Farrell ◽  
Anita Laxova ◽  
Elaine Mischler
Keyword(s):  
Cystic Fibrosis ◽  
Vitamin E ◽  
Hemolytic Anemia ◽  
Vitamin E Deficiency

scholarly journals Altered plasma membrane phospholipid organization in Plasmodium falciparum-infected human erythrocytes

Blood ◽  
1987 ◽  
Vol 69 (2) ◽  
pp. 401-407
Author(s):  
RS Schwartz ◽  
JA Olson ◽  
C Raventos-Suarez ◽  
M Yee ◽  
RH Heath ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Membrane ◽  
Early Stage ◽  
Red Cells ◽  
Membrane Phospholipid ◽  
Cell Membrane Permeability ◽  
Parasite Development ◽  
Red Cell ◽  
Membrane Phospholipids ◽  
Red Cell Membrane

The intraerythrocytic development of the malaria parasite is accompanied by distinct morphological and biochemical changes in the host cell membrane, yet little is known about development-related alterations in the transbilayer organization of membrane phospholipids in parasitized cells. This question was examined in human red cells infected with Plasmodium falciparum. Normal red cells were infected with strain FCR3 or with clonal derivatives that either produce (K+) or do not produce (K-) knobby protuberances on the infected red cells. Parasitized cells were harvested at various stages of parasite development, and the bilayer orientation of red cell membrane phospholipids was determined chemically using 2,4,6-trinitrobenzene sulphonic acid (TNBS) or enzymatically using bee venom phospholipase A2 (PLA2) and sphingomyelinase C (SMC). We found that parasite development was accompanied by distinct alterations in the red cell membrane transbilayer distribution of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS). Increases in the exoplasmic membrane leaflet exposure of PE and PS were larger in the late-stage parasitized cells than in the early-stage parasitized cells. Similar results were obtained for PE membrane distribution using either chemical (TNBS) or enzymatic (PLA2 plus SMC) methods, although changes in PS distribution were observed only with TNBS. Uninfected cohort cells derived from mixed populations of infected and uninfected cells exhibited normal patterns of membrane phospholipid organization. The observed alterations in P falciparum-infected red cell membrane phospholipid distribution, which is independent of the presence or absence of knobby protuberances, might be associated with the drastic changes in cell membrane permeability and susceptibility to early hemolysis observed in the late stages of parasite development.

scholarly journals Hyperhaemolytic Syndrome in Sickle cell disease: clearing the cobwebs

2020 ◽  
Author(s):  
Anazoeze Jude Madu ◽  
Angela Ogechukwu Ugwu ◽  
Chilota Efobi
Keyword(s):  
Blood Transfusion ◽  
Cell Membrane ◽  
Sickle Cell ◽  
Rare Condition ◽  
Red Cells ◽  
Acute Chest Syndrome ◽  
Membrane Phospholipids ◽  
Dynamic Background ◽  
Red Cell Membrane ◽  
Additional Strain

Sickle cell anaemia presents with a dynamic background haemolysis and deepening anaemia. This increases the demand for transfusion if any additional strain on haemopoiesis is encountered due to any other physiological or pathological. Patients with cerebrovascular accident are placed on chronic blood transfusion; those with acute sequestration and acute chest syndrome are likewise managed with blood transfusion. These patients are prone to develop blood transfusion complications including alloimmunization and hyperhaemolytic syndrome (HHS). This term is used to describe haemolysis of both transfused and ‘own’ red cells occurring during or post-transfusion in sickle cell patients. Hyperhaemolysis results in worsening post-transfusion haemoglobin due attendant haemolysis of both transfused and autologous red cells. The mechanism underlying this rare and usually fatal complication of sickle cell has been thought to be secondary to changes in the red cell membrane with associated immunological reactions against exposed cell membrane phospholipids. The predisposition to HHS in sickle cell is also varied and the search for a prediction pattern or value has been evasive. This review to discusses the pathogenesis, risk factors and treatment of hyperhaemolytic syndrome, elaborating what is known of this rare condition.

scholarly journals Lipid analyses and fluidity studies by electron spin resonance of red cell membranes in hereditary high red cell membrane phosphatidylcholine hemolytic anemia

Blood ◽  
1984 ◽  
Vol 64 (5) ◽  
pp. 1129-1134 ◽  
Author(s):  
Y Yawata ◽  
T Sugihara ◽  
M Mori ◽  
S Nakashima ◽  
Y Nozawa
Keyword(s):  
Electron Spin Resonance ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Hemolytic Anemia ◽  
Electron Spin ◽  
Order Parameter ◽  
Red Cells ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Spin Resonance

Abstract Membrane lipid analyses and electron spin resonance (ESR) studies of membrane fluidity were carried out on the red cells of a Japanese patient with hereditary high red cell membrane phosphatidylcholine hemolytic anemia (HPCHA). Increased amounts of phosphatidylcholine (PC) and cholesterol were found in the membrane lipids of the affected patient, despite normal plasma lipids. The order parameter of cholesterol-free pure phospholipid liposomes prepared from this patient's red cells was decreased, apparently because of the increased PC. In contrast, the order parameter of the total red cell lipid liposomes (containing free cholesterol) was essentially normal. The overall fluidity of the intact red cells was determined by ESR with a spin probe, 5-SAL. Again, the order parameters were normal in the intact red cells of the patient with HPCHA. This suggests that the concomitant increase of membrane cholesterol and phosphatidylcholine serves to maintain normal membrane fluidity in the HPCHA red cells.

Sign in / Sign up

Export Citation Format

Share Document