scholarly journals Decreased life span and membrane damage of carbamylated erythrocytes in vitro

Blood ◽  
1976 ◽  
Vol 47 (6) ◽  
pp. 909-917
Author(s):  
TA Lane ◽  
ER Burka
Keyword(s):  
Cell Membrane ◽  
Life Span ◽  
Membrane Damage ◽  
Membrane Lipid ◽  
Red Cell ◽  
Significant Modification ◽  
Red Cell Membrane ◽  
Cell Membrane Damage ◽  
Sickle Erythrocytes

Red blood cells exposed to cyanate (CNO) in vitro have a concentration- dependent decreased cell survival time associated with an inhibition of the ability of the cell membrane to synthesize lipids. The t1/2 of rabbit erythrocytes exposed to 30 mM or 50 mM cyanate for 1 hr at 37 degrees C is reduced from the normal 24 days to 15 and 9 days, respectively. The cyanate-induced defect in membrane lipid metabolism is irreversible. Carbamylation of membrane proteins and damage to metabolism are minimized by limiting exposure in vitro to 15 mM cyanate at 4 degrees C for 30 min. Cells carbamylated under these conditions do not have a shortened life span. Levels of globin carbamylation of 0.5 moles CNO/mole hemoglobin, shown to be clinically effective in prolonging the life span of sickle erythrocytes, are obtained under these conditions and reach maximal levels after only 30 min of incubation. Carbamylation of blood in CPD anticoagulant is inferior to either ACD or heparin. The findings indicate that adequate carbamylation of sickle erythrocytes with minimal red cell membrane damage can be achieved without significant modification of the standard plasmapheresis procedure utilized by the working blood bank.

scholarly journals Decreased life span and membrane damage of carbamylated erythrocytes in vitro

Blood ◽  
1976 ◽  
Vol 47 (6) ◽  
pp. 909-917 ◽  
Author(s):  
TA Lane ◽  
ER Burka
Keyword(s):  
Cell Membrane ◽  
Life Span ◽  
Membrane Damage ◽  
Membrane Lipid ◽  
Red Cell ◽  
Significant Modification ◽  
Red Cell Membrane ◽  
Cell Membrane Damage ◽  
Sickle Erythrocytes

Abstract Red blood cells exposed to cyanate (CNO) in vitro have a concentration- dependent decreased cell survival time associated with an inhibition of the ability of the cell membrane to synthesize lipids. The t1/2 of rabbit erythrocytes exposed to 30 mM or 50 mM cyanate for 1 hr at 37 degrees C is reduced from the normal 24 days to 15 and 9 days, respectively. The cyanate-induced defect in membrane lipid metabolism is irreversible. Carbamylation of membrane proteins and damage to metabolism are minimized by limiting exposure in vitro to 15 mM cyanate at 4 degrees C for 30 min. Cells carbamylated under these conditions do not have a shortened life span. Levels of globin carbamylation of 0.5 moles CNO/mole hemoglobin, shown to be clinically effective in prolonging the life span of sickle erythrocytes, are obtained under these conditions and reach maximal levels after only 30 min of incubation. Carbamylation of blood in CPD anticoagulant is inferior to either ACD or heparin. The findings indicate that adequate carbamylation of sickle erythrocytes with minimal red cell membrane damage can be achieved without significant modification of the standard plasmapheresis procedure utilized by the working blood bank.

Acquired haemolytic anaemia

2020 ◽  
pp. 5479-5489
Author(s):  
Amy Powers ◽  
Leslie Silberstein
Keyword(s):  
Cell Membrane ◽  
Haemolytic Anaemia ◽  
Membrane Damage ◽  
Autoimmune Haemolytic Anaemia ◽  
Red Cell ◽  
Drug Induced ◽  
Red Cell Membrane ◽  
Cell Membrane Damage ◽  
Drug Dependent ◽  
Transfusion Reactions

Premature destruction of red cells occurs through two primary mechanisms: (1) decreased erythrocyte deformability that leads to red cell sequestration and extravascular haemolysis in the spleen and other components of the reticuloendothelial system—may be caused by membrane defects, metabolic abnormalities, exogenous oxidizing agents, or pathological antibodies; and (2) red cell membrane damage and intravascular haemolysis—may be caused by exposure to pathological antibodies, activated complement, mechanical forces, chemicals, and infectious agents. Congenital haemolytic anaemias—congenital disorders resulting in a haemolytic anaemia include (1) disorders of the red cell membrane such as hereditary spherocytosis and hereditary elliptocytosis; (2) disorders of red cell enzymes such as glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency; and (3) disorders of globin structure. Acquired immune haemolytic anaemias—immune haemolysis may occur when IgG, IgM, or IgA antibodies and/or complement bind to the erythrocyte surface. Autoimmune haemolytic anaemias—these are best classified according to the temperature at which the antibody optimally binds to the erythrocyte: warm autoimmune haemolytic anaemia, cold agglutinin-mediated autoimmune haemolytic anaemia, paroxysmal cold haemoglobinuria, and mixed type autoimmune haemolytic anaemia. Drug-induced haemolytic anaemia—haemolysis can be caused by drugs that induce a positive DAT. Drug-induced antibodies may be drug dependent or drug independent depending on whether the presence of the drug is required for their detection. Alloimmune haemolytic anaemias—these include acute haemolytic transfusion reactions and other conditions such as delayed haemolytic transfusion reactions, passenger lymphocyte haemolysis, and haemolytic disease of the newborn. Acquired nonimmune haemolytic anaemias and microangiopathic haemolytic anaemia are also discussed in this chapter.

Haemolytic anaemia—congenital and acquired

2010 ◽  
pp. 4450-4460
Author(s):  
Amy Powers ◽  
Leslie Silberstein ◽  
Frank J. Strobl
Keyword(s):  
Cell Membrane ◽  
Membrane Damage ◽  
Reticuloendothelial System ◽  
Erythrocyte Deformability ◽  
Red Cells ◽  
Red Cell ◽  
Metabolic Abnormalities ◽  
Red Cell Membrane ◽  
Cell Membrane Damage ◽  
Membrane Defects

Premature destruction of red cells occurs through two primary mechanisms: (1) decreased erythrocyte deformability that leads to red-cell sequestration and extravascular haemolysis in the spleen and other components of the reticuloendothelial system—may be caused by membrane defects, metabolic abnormalities, exogenous oxidizing agents, or pathological antibodies; (2) red-cell membrane damage and intravascular haemolysis—may be caused by exposure to pathological antibodies, activated complement, mechanical forces, chemicals, and infectious agents....

scholarly journals Biosynthetic insulin effect on red cell membrane lipid peroxidation in patients with insulin-dependent diabetes

1994 ◽  
Vol 40 (3) ◽  
pp. 12-15 ◽  
Author(s):  
T. S. Balashova ◽  
Ye. N. Golega ◽  
I. A. Rudko ◽  
M. I. Balabolkin ◽  
A. A. Kubatiev
Keyword(s):  
Cell Membrane ◽  
Human Insulin ◽  
Antioxidant Defense ◽  
Vascular Complications ◽  
Membrane Lipid ◽  
Defense Enzymes ◽  
Red Cell ◽  
Membrane Lipid Peroxidation ◽  
Red Cell Membrane ◽  
Antioxidant Defense Enzymes

The aim of our research was elucidation of a relationship between red cell membrane lipid peroxidation (LPO) and antioxidant' defense enzymes, on the one hand and the age disease duration and presence of vascular complications in patients with type I diabetes mellitus on the other. The possibility of correcting red cell peroxide status with human insulin preparations was investigated. Red cell membrane LPO was found increased more than twofold and antioxidant defense enzymes activities virtually unchanged vs. controls in 16 patients with diabetes aged 20 to 43. These characteristics of red cell peroxidation status do not depend on patients age disease standing or presence of vascular complications. A twelve-week therapy with biosynthetic insulin resulted in complete normalization of LPO processes in patients with angiopathies aged under 35 and with disease standing of less than 10 years. In diabetics with angiopathies aged over 35 and disease standing of more than 10 years red cell MDA level reduced under the effect of therapy with human insulin preparations but was still increased vs. that in healthy donors by 1.5 times. Red cell GP and SOD activities reduced in the course of insulin therapy in all the examined groups of diabetics. Catalase activity increased by approximately 50% in patients with angiopathies those aged over 35 and a disease standing of more than 10 years under the effect of insulin. In the rest groups of patients catalase activity did not differ from its initial level. Our results permit us recommending besides human insulin preparations antioxidant therapy for patients with vascular complications those aged over 35 and a disease standing of more than 10 years.

Disorders of the red cell membrane

2020 ◽  
pp. 5456-5463
Author(s):  
Patrick G. Gallagher
Keyword(s):  
Cell Membrane ◽  
Clinical Features ◽  
Parvovirus B19 ◽  
Clinical Manifestations ◽  
Peripheral Blood Smear ◽  
Membrane Lipid ◽  
Red Cell ◽  
Red Cell Membrane ◽  
Membrane Lipid Bilayer ◽  
Parvovirus B19 Infection

The integrity of the red cell membrane depends on molecular interactions between proteins and the phospholipid membrane: vertical interactions stabilize the membrane lipid bilayer; horizontal interactions provide resistance against shear stress. Hereditary spherocytosis—affects 1 in 25 000 individuals of northern European descent. There is typically a dominant family history, but the condition is genetically heterogeneous: combined spectrin and ankyrin deficiency is the most common defect observed, followed by band 3 deficiency, isolated spectrin deficiency, and protein 4.2 deficiency. These affect vertical membrane interactions with loss of surface area relative to red cell volume. Clinical features—the key clinical manifestations are anaemia and signs of persistent haemolysis, with jaundice and a marked propensity to gallstones. Complications and treatment—parvovirus B19 infection of erythropoietic precursors may cause acute aplastic crises. Megaloblastic anaemia due to folate deficiency occurs in response to increased requirements during growth and pregnancy, but is preventable with supplementation. Splenectomy can alleviate the anaemia in many patients and reduces the risk of gallstones. Hereditary elliptocytosis—occurs with a frequency of 1 in 2000 to 1 in 4000 worldwide, and is more frequent in parts of Africa. The inheritance is usually dominant, with defects in red cell proteins such as α‎- and β‎-spectrin causing disturbances in horizontal interactions in the erythrocyte membrane. Clinical features, diagnosis, and treatment—most patients are asymptomatic and are typically diagnosed incidentally during testing for unrelated conditions, but about 10% experience haemolysis, anaemia, splenomegaly, and intermittent jaundice. Diagnosis is based on the presence of elliptocytes on a peripheral blood smear. Treatment is rarely required. Other conditions include hereditary pyropoikilocytosis, South-East Asian (or Melanesian) ovalocytosis, stomatocytosis, and acanthocytosis.

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