Disease relevance of Osmotic Fragility

• The human erythrocyte (RBC) is a target organ for parathyroid hormone (PTH) and the hormone increases RBC osmotic fragility and induces their hemolysis [1].
• In a second study with isolated rabbit cardiomyocytes, the effect of fostriecin pretreatment was assessed by measuring changes in cell osmotic fragility during simulated ischemia [2].
• With these normal ranges as a reference, the diagnosis of hereditary spherocytosis was definitely possible in five newborn infants by demonstration of increased osmotic fragility of fresh and incubated red blood cells, moderately increased autohemolysis, and partial reduction of autohemolysis by the addition of glucose [3].
• To study the effects of diphenylhydantoin (Dilantin, DPH) on membrane function, DPH was incubated with erythrocytes from normal individuals and from patients with congenital spherocytic hemolytic anemia and osmotic fragility measured [4].
• The clinical and hematologic picture of aplastic anemia resulting from benzene exposure is not different from classical aplastic anemia; in some cases, mild bilirubinemia, changes in osmotic fragility, increase in lactic dehydrogenase and fecal urobilinogen, and occasionally some neurological abnormalities are found [5].

High impact information on Osmotic Fragility

• This result may be due to the effect of hexane on the cell membrane because this treatment also affected the osmotic fragility of the cells [6].
• Effect of parathyroid hormone on osmotic fragility of human erythrocytes [7].
• Changes in membrane cholesterol paralleled changes in membrane surface area, as calculated from osmotic fragility, with a 0.22 percent variation in surface area per 1.0 percent variation in cholesterol content [8].
• The graphic recording of time to 50% haemolysis in a glycerine-saline solution is a simple, reproducible method of determining erythrocyte osmotic fragility [9].
• Pooled RCC was aliquoted into PL146 (PVC), PL732 (polyolefin), and PL732 (with added DEHP) bags with samples removed weekly for analysis of osmotic fragility, deformability, and DEHP concentration [10].

Chemical compound and disease context of Osmotic Fragility

• Treatment groups receiving ClO2, ClO2- or ClO3- showed alterations in erythrocyte morphology and osmotic fragility; at higher dosages mild hemolytic anemia occurred [11].
• These results indicate that AQP4 can alter the osmotic fragility of astrocytes and that testosterone can influence brain edema through AQP4 regulation, whereas 17beta-estradiol and dexamethasone cannot [12].
• Effects of lactic acid in red blood cells on osmotic fragility and water content of erythrocytes after hyperthermia were investigated [13].
• The osmotic fragility of nystatin-treated red cells decreased and the deformability increased as dehydration of red cells progressed and alternatively, hydrated cells showed increased osmotic fragility and reduced deformability [14].
• Acidosis caused by CO2 inhalation and lactic and hydrochloric acid infusion raised osmotic fragility and hematocrit; these effects were completely reversed in the animal when we restored normal acid-base status [15].

Biological context of Osmotic Fragility

• A significant positive correlation was observed between the extent of glucose-induced membrane lipid peroxidation and the osmotic fragility of treated RBC [16].
• The present study was initiated to determine if mepacrine also delays cell death and development of osmotic fragility of both metabolically inhibited and ischemic adult rat cardiomyocytes [17].
• The BHT-mediated alterations in osmotic fragility correlated with changes in membrane fluidity, determined by fluorescence polarization of the hydrophobic probe 1,6-diphenyl-1,3,5-hexatriene [18].
• The administration of I.V. O2 releaser and bronchodilator helped in efficiently restoring the altered values of blood pH, haemoglobin, packed cell volume, erythrocyte sedimentation rate and osmotic fragility of erythrocytes to near normal levels [19].
• Colony-forming units-erythroid (CFU-E) development was inhibited in the TAl-1 group, but the median osmotic fragility (MOF) and hematocrit (Ht) values were similar to those of the C1 group [20].

Anatomical context of Osmotic Fragility

• The patient's cells, during incubation with normal plasma, acquired morphologic features of spiculated spherocytes with an increase in osmotic fragility and a 21% decrease in cholesterol content [21].
• The loss of spectrin from purified sarcolemma of autolysed rabbit heart, and both isolated membrane vesicles and Triton solubilized membrane fractions of ischemic cardiomyocytes correlated linearly with the onset of osmotic fragility as assessed by membrane rupture, subsequent to a hypotonic challenge [22].
• Both the increase in osmotic fragility and the lysis of red cells by monocytes were enhanced by cytochalasin B and were inhibited by hydrocortisone [23].
• (2) Membrane alterations: Osmotic fragility was not affected and the activity of acetylcholine esterase in the ghost membranes of the exposed group increased [24].
• Release of tumor cytolytic/cytostatic factor(s) by in vitro cisplatin treated macrophages: enhanced tumoricidal activity by increase in osmotic fragility of target cells [25].

Associations of Osmotic Fragility with chemical compounds

• Incubated osmotic fragility was normal; autohemolysis was increased and corrected with glucose and ATP [26].
• Oxygen equilibria, osmotic fragility, reduced glutathione content, and glutathione reductase activity are totally unaffected, while pyruvic kinase activity is decreased only by butylurea by about 20%, and glucose-6-phosphate dehydrogenase activity is decreased progressively to a maximum of 30% in direct proportion to the length of the alkyl chain [27].
• The increase in osmotic fragility during storage was greater when RCC was stored without DEHP [10].
• In contrast, mepacrine had no effect on the development of osmotic fragility [17].
• Consistent with these studies, a low Ca(2+) Ringer solution increased osmotic fragility, whereas volume recovery following hypotonic shock (measured with a Coulter counter) was potentiated with A23187 (0.5 microM) [28].

Gene context of Osmotic Fragility

• Finally, we show that increased HDL cholesterol levels due to SR-BI deficiency induce erythrocyte cholesterol:phospholipid ratios, resulting in decreased deformability and increased osmotic fragility, thereby providing an explanation for the observed reduced lifespan [29].
• The genetic basis for the osmotic fragility and elevated pyr enzyme synthesis was the result of mutations affecting pyrH, encoding the enzyme uridine 5'-monophosphate kinase [30].
• The genetic basis for erythrocyte osmotic fragility differences between mouse strains C57BL/6 and DBA/2 was examined through analyses of their serial backcross progeny, recombinant inbred (ri) strains (BXD), and congenic C57BL/6 strains with allelic differences at Hbb or Fv-2 [31].
• The addition of exogenous glutathione (50 mg 100 ml-1) or glutathione reductase and NADPH to rat blood in the presence of Alcide returned erythrocyte osmotic fragility to control values [32].
• Red cells incubated with plasma had decreased membrane cholesterol and increased osmotic fragility, but the change was prevented by the inactivation of lecithin cholesterol acyltransferase (LCAT) in the plasma [33].

Analytical, diagnostic and therapeutic context of Osmotic Fragility

• PRBC integrity was assessed by light microscopy, scanning electron microscopy, osmotic fragility, and determination of oximetric p50 [34].
• Supplementation with alpha-tocopherol acetate reduced the elevated osmotic fragility of erythrocytes from atherogenic diet fed rats to that of control levels [35].
• The relationship between serum carnitine levels and erythrocyte osmotic fragility was investigated in 26 chronic hemodialysis patients (10 males and 16 females, mean age: 57.3 +/- 13.5 years) [36].
• Malonyldialdehyde (MDA) levels, osmotic fragility ratios, and methemoglobin and sulfhemoglobin values were significantly higher in the SO2-treated group compared with the control group (P < 0.05), and marked decreases in MDA levels and osmotic fragility ratios were determined in the group treated with SO2 + antioxidant vitamins (P < 0.05) [37].
• A modified osmotic fragility test, based on measurement of hemolysis in four hypotonic NaCl solutions and logarithmic linearization of osmotic fragility curve is, like the "Pink test," a specific and sensitive test for the laboratory diagnosis of hereditary spherocytosis [38].

References