SEARCH · PubMed Health

Results for “ERYTHROCYTES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources

PubMed1979

Comparative effects of CO2 on the affinity for O2 of fetal and adult erythrocytes.

1. Oxygen-linked carbamino formation in fetal erythrocytes was compared to that measured in adult erythrocytes. 2. Whole oxygen binding curves were recorded on washed intact erythrocytes either fresh or D-glycerate-2,3-P depleted with a continuous recording technique. Erythrocytes were resuspended in buffer media of different pH and PCO2 varying from 0-10.7 kPa (80 torr) at physiological ionic strength. Oxygen linked carbamates were estimated as deltalog PO2/delta log PCO2 at constant pH and constant saturation levels from 10-90% oxygen saturation. 3. The overall CO2 effect (deltalog P50/deltalog PCO2) was consistently lower in fetal erythrocytes than in the adult. The deltalog PO2/deltalog PCO2 ratio was markedly dependent on oxygen saturation in both types of erythrocytes and highest at the early part of the oxygen binding curve. This was more so in fetal erythrocytes. 4. Carbamino formation was lower in fetal erythrocytes than in adult erythrocytes at any pH value, indicating a higher apparent pK of the alpha amino groups involved in CO2 binding in fetal erythrocytes. This may be related to the different primary structures of the non alpha chains of HbFII and HbAI. 5. The large effect of low PCO2 on both fetal and adult erythrocytes was related to the higher affinity for CO2 of deoxyhemoglobin compared to oxyhemoglobin and a model for CO2 binding analogous to that described by de Bruin et al. [6] for anion binding is proposed. 6. It is concluded that the lower CO2 binding to fetal erythrocytes is in keeping with the lower allosteric effect of other major effectors of hemoglobin within the cells. This leads to a higher affinity for O2 of fetal erythrocytes well suited for O2 transport in utero.

Adult↗

PubMed2006

Asymmetric dimethylarginine reduced erythrocyte deformability in streptozotocin-induced diabetic rats.

To investigate the effect of asymmetric dimethylarginine on erythrocyte deformability in streptozotocin-induced diabetic rats, a single intraperitoneal injection of streptozotocin (STZ, 65 mg/kg) in male Sprague-Dawley rats was carried out to induce diabetes and normal erythrocytes were incubated with asymmetric dimethylarginine or aortic rings from diabetic rats in the presence of L-arginine or vitamin E. We found that erythrocyte deformability was significantly decreased in diabetic rats. The levels of asymmetric dimethylarginine in plasma and erythrocytes of diabetic rats were elevated significantly from 2-week diabetic duration to 8-week diabetic duration. Nitric oxide in erythrocytes was decreased at 8-week diabetic duration while plasma nitric oxide remained unchanged all along. The content of malondialdehyde in erythrocytes of diabetic rats was increased. After incubation of erythrocytes with asymmetric dimethylarginine (10(-6) M) for 30 min, erythrocyte deformability and nitric oxide level in erythrocytes were decreased markedly. Reactive oxygen species and malondialdehyde production in erythrocytes were promoted by asymmetric dimethylarginine. Both L-arginine and vitamin E reversed the effects of asymmetric dimethylarginine. After incubation of erythrocytes with aortic rings from diabetic rats, erythrocyte deformability was decreased, which was attenuated by L-arginine. These results indicated that reduction of erythrocyte deformability in diabetic rats was associated with promoted oxidant stress as well as impaired nitric oxide synthesis by elevation of asymmetric dimethylarginine.

Animals↗

PubMed1987

Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum.

Plasmodium falciparum malaria merozoites require erythrocyte sialic acid for optimal invasion of human erythrocytes. Since mouse erythrocytes have the form of sialic acid found on human erythrocytes (N-acetyl neuraminic acid), mouse erythrocytes were tested for invasion in vitro. The Camp and 7G8 strains of P. falciparum invaded mouse erythrocytes at 17-45% of the invasion rate of human erythrocytes. Newly invaded mouse erythrocytes morphologically resembled parasitized human erythrocytes as shown on Giemsa-stained blood films and by electron microscopy. The rim of parasitized mouse erythrocytes contained the P. falciparum 155-kD protein, which is on the rim of ring-infected human erythrocytes. Camp but not 7G8 invaded rat erythrocytes, indicating receptor heterogeneity. These data suggest that it may be possible to adapt the asexual erythrocytic stage of P. falciparum to rodents. The development of a rodent model of P. falciparum malaria could facilitate vaccine development.

Animals↗

PubMed2006

Modulation of malaria virulence by determinants of Plasmodium falciparum erythrocyte membrane protein-1 display.

PURPOSE OF REVIEW: Plasmodium falciparum malaria parasites carry approximately 60 var genes that encode variable adhesins termed P. falciparum erythrocyte membrane protein-1. Clonal expression of a single P. falciparum erythrocyte membrane protein-1 variant on the surface of the parasitized host erythrocyte promotes binding of the cell to blood elements (including noninfected erythrocytes, leukocytes) and walls of microvessels. These binding events enable parasitized erythrocytes to sequester and avoid clearance by the spleen, and they also contribute to disease by causing microvascular inflammation and obstruction. RECENT FINDINGS: Steps by which P. falciparum erythrocyte membrane protein-1 is exported to the parasitized erythrocyte surface have recently been elucidated. The ability of parasites to cytoadhere and cause disease depends on the variant of P. falciparum erythrocyte membrane protein-1 as well as its amount and distribution at the erythrocyte surface. An example of a host polymorphism that affects P. falciparum erythrocyte membrane protein-1 display is hemoglobin C, which may protect against malaria by impairing the parasite's ability to adhere to microvessels and induce inflammation. Interference with P. falciparum erythrocyte membrane protein-1-mediated phenomena appears to diminish cytoadherence in vivo and to protect against disease in animal models. SUMMARY: Plasmodium falciparum erythrocyte membrane protein-1-mediated sequestration of parasitized erythrocytes plays a central role in malaria pathogenesis. Clinical interventions aimed at reducing cytoadherence and microvascular inflammation may improve disease outcome.

Animals↗

PubMedDate not supplied

Post-transfusion survival of 50Cr-labeled erythrocytes in neonatal foals.

Erythrocytes transfused allogeneically into mature horses have a short survival (less than 4 days) compared with an expected erythrocyte life span of 140-150 days. Yet, foals undergo transfusions for neonatal isoerythrolysis successfully. The authors have determined the survival of transfused erythrocytes in neonatal foals, using the stable isotope, 50Cr, to label the erythrocytes. Normal foals underwent transfusions with labeled erythrocytes from three sources: their own erythrocytes (autologous), the erythrocytes of their dam, and the erythrocytes of an unrelated castrated male. After transfusion, samples were taken at 15 minutes and then daily for a week and every 2 or 3 days for 20 days. A stable isotope of iron (57Fe) and 50Cr were determined on diluted-packed erythrocytes by inductively coupled argon-coupled mass spectrometry techniques. 57Fe was used as measure of the sample hemoglobin concentration. The ratio of 50Cr to 57Fe decreased exponentially in all foals. Half-time (T1/2) was 11.7 days (standard error = 2.2) for four foals that underwent autologous transfusions, 5.5 +/- 1.0 days for five foals that underwent transfusions with the erythrocytes of their dams, and 5.2 +/- 1.1 days for five foals that had transfusions with erythrocytes from an unrelated gelding. The authors conclude that erythrocytes that are transfused allogenically into neonatal foals will survive longer than those transfused into mature horses and that 50Cr labeling can be used to measure survival of transfused erythrocytes.

Animals↗

PubMed2000

Increased rate of adenine incorporation into adenine nucleotide pool in erythrocytes of patients with chronic renal failure.

BACKGROUND: Elevated purine nucleotide pool (mainly ATP) in erythrocytes of patients with chronic renal failure (CRF) is a known phenomenon, however the mechanism responsible for this abnormality is far from being clear. We hypothesize that the increased rate of adenine incorporation into adenine nucleotide pool is responsible for the elevated level of ATP in uremic erythrocytes. METHODS: In chronically uremic patients we evaluated using HPLC technique: (a) plasma adenine concentration; (b) the rate of adenine incorporation into adenine nucleotide pool in uremic erythrocytes. Additionally, the effect of higher than physiological phosphate concentration (2.4 mM) and lower than physiological pH (7.1) on adenine incorporation into erythrocytes adenine nucleotide pool was investigated. Healthy volunteers with normal renal function served as control. RESULTS: The concentration of adenine in plasma of CRF patients was found to be significantly higher than in plasma of healthy subjects. In contrast, adenosine concentration was similar both in healthy humans and in CRF patients. In isolated erythrocytes of uremic patients (incubated in the medium pH 7.4, containing 1.2 mM inorganic phosphate) adenine was incorporated into adenine nucleotide pool at a rate approximately 2-fold higher than in erythrocytes from healthy subjects. The rate of adenosine incorporation into adenine nucleotide pool was similar in erythrocytes of both studied groups. Incubation of erythrocytes obtained from healthy subjects in the medium pH 7.4, containing 2.4 mM inorganic phosphate, caused the increase of adenine incorporation into adenine nucleotide pool by about 60%. Incubation of the cells in the pH 7.1 buffer containing 2. 4 mM inorganic phosphate increased the rate of adenine incorporation into adenylate approximately 2-fold as compared to erythrocytes incubated in the medium pH 7.4 containing 1.2 mM inorganic phosphate. Erythrocytes obtained from uremic patients and incubated in the pH 7.1 medium containing 2.4 mM phosphate incorporated adenine into adenine nucleotide pool at a rate similar to erythrocytes incubated in the medium pH 7.4 containing 1.2 mM phosphate. Erythrocytes obtained from either healthy subjects or from patients with CRF and incubated in the presence of higher than physiological concentration of inorganic phosphate (2.4 mM) and lower than physiological pH (7. 1) did not exhibit any increase in the rate of adenisine incorporation into adenine nucleotide pool. CONCLUSION: These results suggest that the increased rate of adenine incorporation into adenine nucleotide pool could be partially responsible for the increased concentration of ATP in uremic erythrocytes.

Adenine↗

PubMed2002

Lipid peroxidation and erythrocyte antioxidant enzymes in patients with Behçet's disease.

In spite of unknown etiology, it is now accepted that reactive oxygen species (ROS) produced by neutrophils may be related to the pathogenesis of Behçet's Disease (BD). The objective was to investigate whether increased production of ROS may affect erythrocyte oxidant/antioxidant system in patients with BD. The levels of malondialdehyde (MDA), one of the end products of lipid peroxidation, in plasma and erythrocyte, and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), antioxidant enzymes, in erythrocyte, also C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured in 22 patients in active stage of the disease and also in 30 healthy controls. Increased CRP, ESR, and MDA levels in plasma and erythrocyte and increased SOD but decreased GSH-Px activities in erythrocytes were observed in the patients, when compared to the controls. In addition, significantly positive correlations between plasma and erythrocyte MDA levels, and erythrocyte MDA-CRP, MDA-ESR, MDA-SOD, SOD-ESR and SOD-CRP levels, but negative correlation between plasma MDA and erythrocyte GSH-Px, were found in BD patients. It may be suggested that increased production of ROS in BD, as reflected by higher plasma and erythrocyte MDA levels, may impair erythrocyte membrane integrity and also may lead to the alterations in the erythrocyte antioxidant defense system, as reflected by higher SOD and lower GSH-Px activities in erythrocytes.

Adult↗

PubMed1993

Thrombospondin from activated platelets promotes sickle erythrocyte adherence to human microvascular endothelium under physiologic flow: a potential role for platelet activation in sickle cell vaso-occlusion.

Adherence of erythrocytes to vascular endothelium likely contributes to the pathophysiology of episodic vascular occlusion in patients with sickle cell disease (SCD). In addition, coagulation activation has been reported in sickle patients during complications such as pain episodes. To test the hypothesis that platelet activation contributes to sickle erythrocyte binding, we investigated whether factors released from activated sickle platelets promote adherence of sickle erythrocytes to human microvascular endothelial cells (MEC) under flow conditions. Activated sickle platelet supernatant (ASPS) promoted high levels of sickle erythrocyte adherence to MEC (55.4 +/- 3.9 erythrocytes/mm2) but only moderate adherence of normal erythrocytes to MEC (14.1 +/- 0.7 erythrocytes/mm2). When MEC were incubated with an antibody (OKM5) against CD36 (a thrombospondin [TSP] receptor), platelet supernatant mediated sickle erythrocyte adherence was inhibited 86%, suggesting that TSP participated in the adherence. To further define the role of TSP in adherence, additional studies using purified TSP were performed. At a concentration of 0.2 micrograms/mL TSP in serum-free media (SFM), sickle erythrocyte adherence to MEC was 33.9 +/- 2.7 erythrocytes/mm2 and sixfold greater than either sickle erythrocyte adherence in the absence of TSP or normal erythrocyte adherence in the presence of TSP. Doubling the concentration of TSP to 0.4 micrograms/mL proportionally increased adherence of sickle erythrocytes. Incubation of MEC with OKM5 or anti-alpha v monoclonal antibodies inhibited TSP-mediated sickle erythrocyte adherence more than 95%. These data suggest that activated platelet release factors, including alpha-granule TSP, which promote receptor-mediated sickle erythrocyte adherence to microvascular endothelium. Such factors released during in vivo platelet activation could contribute to vaso-occlusive complications by promoting erythrocyte adherence and microvascular occlusion.

Anemia, Sickle Cell↗

PubMed1981

Invasion of erythrocytes by malaria merozoites: evidence for specific receptors involved in attachment and entry.

Invasion of erythrocytes by malaria merozoites involves attachment of the merozoite membrane at the point of collision with the erythrocytes, then reorientation of the merozoite such that its apex is opposed to the erythrocyte membrane, followed by invaginatin of the erythrocyte membrane and interiorization of the parasite. Specific recognition of erythrocyte surface components by the merozoite has been shown by studies on the specificity of merozoites of different malaria species for a limited range of host-species erythrocytes, for erythrocytes of particular maturity, and for erythrocytes possessing particular blood-group determinants. Different malaria species capable of invading erythrocytes of the same host also exhibit differences in specificity for components on enzyme-treated erythrocytes. The attachment phase of merozoite invasion has been isolated from subsequent steps by treatment of merozoites with cytochalasin B -- they then attach to but do not invade susceptible erythrocytes. There is now evidence for other differences between initial attachment steps and subsequent invasion steps form studies on merozoite treatments in vitro which affect invasion but not attachment. It has also been shown that addition of N-acetyl-D-glucosamine to cultures of Plasmodium falciparum inhibits merozoite invasion. Elucidation of the sequence and nature of molecular interactions of merozoite and erythrocyte membrane molecules during invasion will be based on the fundamental ultrastructural observations and on the specificity of attachment and invasion steps already described.

Acetylglucosamine↗

PubMed1992

Lipid peroxidation in Plasmodium falciparum-parasitized human erythrocytes.

cis-Parinaric acid (PnA) was used as a fluorescent probe to study lipid peroxidation in nonparasitized and Plasmodium falciparum-parasitized erythrocytes, upon challenge by cumene hydroperoxide and tert-butyl hydroperoxide. Parasitized erythrocytes were less susceptible toward lipid peroxidation than nonparasitized erythrocytes with which they had been cultured. Furthermore, nonparasitized erythrocytes cultured together with parasitized cells, and thereafter isolated on a Percoll gradient, were less susceptible toward lipid peroxidation than erythrocytes kept under the same experimental conditions but in the absence of parasitized cells. We concluded, therefore, that the intracellular development of the parasite leads to an increase in the resistance against oxidative stress, not only of the host cell membrane of the parasitized erythrocyte, but also in the plasma membrane of the neighboring cells. The erythrocyte cytosol of parasitized cells and/or the intraerythrocytic parasite was required for the increased protection of the host cell membrane, since ghosts prepared from parasitized erythrocytes were more susceptible to lipid peroxidation than those prepared from nonparasitized ones. Vitamin E content of parasitized erythrocytes was lower than that of nonparasitized cells. However, parasitized erythrocytes promoted extracellular reduction of ferricyanide at higher rates, which might be indicative of a larger cytosolic reductive capacity. It is suggested that the improved response of intact erythrocytes is due to an increased reduction potential of the host-erythrocyte cytosol. The role of vitamin C as a mediator of this process is discussed.

Animals↗

PubMed1980

Interaction of dilauroylglycerophosphocholine with erythrocytes: pre-hemolytic events and hemolysis.

The process of interaction of dilauroylglycerophosphocholine with erythrocytes that eventually results in hemolysis was examined. 1. The rate of uptake of dilauroylglycerophosphocholine by human erythrocytes was rather slow, but increased with increasing temperature. 2. The first observable change of human erythrocytes induced by dilauroylglycerophosphocholine was a morphological change from discocytes to spheroechinocytes. This change preceded K+ leakage. 3. Adsorption of dilauroylglycerophosphocholine to human erythrocytes caused K+ leakage. The rate of K+ leakage was also temperature-dependent. The temperature-dependence was due to the temperature-dependence of lipid uptake, because in order to cause K+ leakage a given amount of dilauroylglycerophosphocholine must be bound to the erythrocytes, irrespective of the temperature. 4. The temperature-dependence of hemolysis of human erythrocytes was different from that of pre-hemolytic events (morphological change, adsorption of lipids and K+ leakage). Hemolysis was rapid below 10 and above 37 degrees C, but slow at about 25 degrees C. The hemolysis observed below 10 degrees C seemed to be a 'colloid osmotic lysis', since it occurred immediately after K+ leakage, but the hemolysis above 37 degrees C may not be a colloid osmotic lysis. Above 37 degrees C, additional binding of dilauroylglycerophosphocholine to the erythrocyte membrane may cause hemolysis by a different mechanism from that working below 10 degrees C. 5. Above 25 degrees C, most human erythrocytes are resistant to colloid osmotic lysis induced by dilauroylglycerophosphocholine. It can be concluded that human erythrocytes are composed of two types of population, one resistant, and one sensitive to colloid osmotic lysis. The mechanism of the resistance was sensitive to temperature, pH and various sulfhydryl agents. 6. Pig erythrocytes were hemolysed immediately after K+ leakage even above 25 degrees C, indicating that they were sensitive to a colloid osmotic mechanism over the whole temperature range tested. Pig erythrocytes may lack the 'mechanism' giving resistance to colloid osmotic lysis. The process of hemolysis of erythrocytes by dilauroylglycerophosphocholine is shown schematically.

Absorption↗

PubMed1986

Ribonuclease from cytosolic fraction of human erythrocytes.

Ribonuclease (RNase) activity is detectable in only one third of specimens of human erythrocyte haemolysates. On the other hand, treatment of erythrocytic cytosoles with sulphosalicylic acid reveals an inhibitor-bound RNase activity which is present in all erythrocyte specimens studied. The level of the erythrocyte inhibitor-bound RNase activity is comparable to that in human lymphocytes. Isolated RNase from the cytosolic fraction of human erythrocytes is poly-C avid RNase with maximum activity at pH 6.5. The enzyme is resistant to treatment with strong acids and heating up to 95 degrees C. Molecular filtration of the erythrocyte RNase shows that it is composed of two fractions differing in molecular mass, 19 000 and 15 000. No difference in enzymic properties between these fractions was found. The general properties of erythrocyte cytosolic RNase are much like those of acid RNases of human granulocytes and lymphocytes. As the erythrocytes do not metabolize RNA no function for the inhibitor-bound RNase can be suggested. Assuming that the observed erythrocyte RNase is the residual enzyme, persisting in the cell since it was functioning in the nucleated erythrocyte precursors, one may surmise that levels of free and inhibitor-bound erythrocyte RNase activity may be related to the normality or abnormality of erythrocyte maturation.

Adolescent↗

PubMed1981

Freeze-fracture study on the erythrocyte membrane during malarial parasite invasion.

Invasion of erythrocytes by malarial merozoites requires the formation of a junction between the merozoite and the erythrocyte. Migration of the junction parallel to the long axis of the merozoite occurs during the entry of the merozoite into an invagination of the erythrocyte. Freeze-fracture shows a narrow circumferential band of rhomboidally arrayed particles on the P face of the erythrocyte membrane at the neck of the erythrocyte invagination and matching rhomboidally arrayed pits on the E face. The band corresponds to the junction between the erythrocyte and merozoite membranes observed in thin sections and may represent the anchorage sites of the contractile proteins within the erythrocyte. Intramembrane particles (IMP) on the P face of the erythrocyte membrane disappear beyond this junction. When the erythrocytes and cytochalasin B-treated merozoites are incubated together, the merozoite attaches to the erythrocyte membrane and a junction is formed between the two, but the invasion process does not advance further and no movement of the junction occurs. Although there is no entry of the parasite, the erythrocyte membrane still invaginates. Freeze-fracture shows that the P face of the invaginated erythrocyte membrane is almost devoid of the IMP that are found elsewhere on the membrane, suggesting that the attachment process in and of itself is sufficient to create a relatively IMP-free bilayer.

Animals↗

PubMed1978

Laboratory studies of erythrocytic pyruvate kinase deficiency. Pathogenesis of the hemolysis.

Genetic polymorphism exists in erythrocytic pyruvate kinase (PK)-deficient hemolytic anemia, as briefly described. Destruction of erythrocytes varied in extent, but its mechanisms in different PK-deficient polymorphic persons investigated were similar. A paradoxical post-splenectomy reticulocytosis regularly occurred. Qualitative enzymatic differences, the biochemistry, and measurements of erythrocytic destruction were made in several PK variants. 51Cr autologous and cross-transfusions of PK-deficient erythrocytes into volunteers showed multimodel regression lines of several erythrocytic cohorts. 59Felabeled PK-deficient reticulocytes donated by PK-deficient splenectomized subjects were transfused 20 hours before splenectomy into two PK-deficient infants with hemolysis, and into two adult volunteers with autoimmune thrombocytopenia. The highest reticulocyte concentration in any organ initially was within the spleen. Radioiron-labeled erythrocytes and cytologic data showed large splenic reticulocyte pools. Splenic macrophages ingesting reticulocytes and erythrocytes were seen by both light and electron microscopy of the splenic pulp. After cyanide additives inhibiting reticulocyte oxidative phosphorylation, a bizarre erythrocytic cytologic configuration was found by scanning electron microscopy. These studies of PK-mutant subjects with PK-deficient erythrocytic hemolysis showed age dependent destruction of erythrocytes. Bimodal Cr survival data suggested reticuloendothelial removal of short-lived erythrocytes and reticulocytes. The transfusions of radioironlabeled PK reticulocytes and the data obtained by scanning electron microscopy suggested that the spleen was the initial hostile organ destroying a cohort of susceptible erythrocytes, prinicpally reticulocytes.

Anemia, Hemolytic↗

PubMed1994

Increased proportion of docosahexanoic acid and high lipid peroxidation capacity in erythrocytes of stroke patients.

BACKGROUND AND PURPOSE: Intracellular accumulation of lipid peroxides that derive from the autoxidation of membrane polyunsaturated fatty acids reduces the deformability of erythrocytes contributing to the hemorheological disturbances observed in acute cerebral ischemia. The present study deals with the biochemical background of increased lipid peroxidation capacity in the erythrocytes of stroke patients. METHODS: A complete clinical and laboratory assessment was made of 24 men and 18 women (aged 50 to 78 years; 64.5 +/- 13.9 years, mean +/- SD) who had an ischemic hemispheric lesion of the brain. Lipid peroxide content, lipid peroxidation capacity, superoxide dismutase activity, and fatty acid composition of erythrocytes were compared in stroke patients and 22 healthy subjects matched for age. The lipid peroxide content of the erythrocytes was estimated before and after the autoxidative test; the results were expressed as nanomoles of malondialdehyde per gram of hemoglobin. The increase of the lipid peroxide content in the erythrocytes during the autoxidative test measures the lipid peroxidation capacity. RESULTS: In comparison with healthy subjects (1.45 +/- 0.30 nmol MDA/g Hb per 24 hours), the lipid peroxidation capacity was found to be significantly higher (4.18 +/- 0.41 nmol MDA/g Hb per 24 hours) (P < .01) in the erythrocytes of stroke patients. The stroke patients could be divided into two groups on the basis of lipid peroxidation capacity of their erythrocytes. Twenty patients had erythrocytes with high lipid peroxidation (< 4 nmol MDA/g Hb per 24 hours), and 22 patients had very high lipid peroxidation capacity (> 4 nmol MDA/g Hb per 24 hours). There was no significant difference in superoxide dismutase activity in the erythrocytes of patients compared with healthy subjects. Before the autoxidative test was conducted, the fatty acid composition in the erythrocytes of stroke patients with very high lipid peroxidation capacity was measured and found to be generally normal; only the proportion of docosahexanoic acid (22:6 n-3) was markedly (P < .01) increased. CONCLUSIONS: The results suggest that the erythrocytes of ischemic stroke patients with very high lipid peroxidation capacity displaying an abnormal fatty acid composition are much more vulnerable to lipid peroxidation. The increased proportion of docosahexanoic acid and the high lipid peroxidation capacity of erythrocytes play a pathogenetic role and explain the hemorheological disturbances observed in the microcirculation of stroke patients.

Aged↗

PubMed1993

Impaired erythrocyte deformability and membrane fluidity in alcoholic liver disease: participation in disturbed hepatic microcirculation.

The erythrocyte deformability, membrane fluidity, mean corpuscular volume (MCV), and lipid compositions of erythrocyte membrane were investigated to evaluate the possible role in disturbed hepatic microcirculation in alcoholic liver disease. Erythrocyte deformability was assessed in 37 alcoholic patients and 20 normal subjects. Erythrocyte deformability determined by the filtration method was found to be decreased significantly in alcoholic patients. Erythrocyte membrane fluidity in alcoholic liver disease analysed by fluorescence recovery time after photobleaching was decreased significantly. The decrease of erythrocyte membrane fluidity in alcoholic patients correlated significantly with a decrease of erythrocyte deformability (r = -0.65, P < 0.02). The increased MCV in alcoholic liver disease also correlated with a decrease of erythrocyte deformability significantly (r = 0.652, P < 0.02). The lipid compositions of erythrocyte membrane were abnormal in alcoholic liver disease; the phosphatidylcholine:sphingomyelin ratio was increased (P < 0.001) and unsaturated:saturated fatty acid ratio was decreased (P < 0.01). We conclude that, in alcoholic liver disease, the decreased erythrocyte deformability was closely associated with changes of membrane fluidity and MCV. It was also associated with abnormalities of membrane lipid compositions. It is speculated that these abnormalities of erythrocytes result in further reduction of sinusoidal blood flow in alcoholic liver disease, and consequently disturb metabolic functions of the liver.

Analysis of Variance↗

PubMed2002

Alterations in erythrocyte membrane lipid and its fragility in a patient with familial lecithin:cholesterol acyltrasferase (LCAT) deficiency.

Lecithin:cholesterol acyltrasferase (LCAT) plays a key role in the cholesterol metabolism-mediated esterification of free cholesterol into the cholesterol ester in normal plasma. Familial LCAT deficiency is frequently associated with anemia. Using biochemical and physiological techniques, the erythrocytes of this patient were investigated to gain an insight into the relationship between the abnormalities of lipid metabolism and erythrocyte membrane fragility. Abnormal erythrocytes, so-called Target cells and/or Knizocytes, were observed at 20% in our patient's erythrocytes. Moreover, the mean corpuscular volume of the patient's cells was 7% greater than that of a normal individual. In the membrane lipids of the patient's erythrocytes, cholesterol and phosphatidylcholine increased, and phosphatidylethanolamine decreased. The electron spin resonance technique with a fatty acid spin probe showed that the membrane fluidity was more elevated than that of normal cells in spite of the increase in cholesterol content and the cholesterol/phospholipid ratio of the membrane of patient's erythrocytes. The patient's abnormally shaped erythrocytes were less deformed than those of the normal individual under high shear stress. The partial depletion of membrane cholesterol from the patient's erythrocytes was demonstrated by incubation with normal plasma with LCAT activity. The increment of transformed erythrocytes during the incubation could be prevented by cholesterol depletion from the patient's erythrocyte membrane. These findings indicate that normochromic anemia of the patient might be caused by erythrocyte fragility resulting from decreased deformity and/or abnormal shape of the cells due to abnormal lipid composition in the membrane.

Adult↗

PubMed1996

Reproducibility of erythrocyte polyamine measurements and correlation with plasma micronutrients in an antioxidant vitamin intervention study.

Erythrocyte polyamine measurements have been previously investigated as candidate biomarkers for hyperproliferation and recently as a potential intermediate endpoint in clinical chemoprevention trials with difluoromethylornithine, an inhibitor of polyamine biosynthesis. This study was performed to determine the reproducibility of erythrocyte polyamine measurements and their possible correlation with plasma micronutrients in seven healthy adults in an antioxidant vitamin intervention study. As part of this cross-over intervention study, three subjects took beta-carotene (31.4 mg/day) plus D-alpha-tocopherol acetate (720 IU/day) supplements during the first 3 months and four subjects took the supplements during the second 3 months. Heparinized blood samples were collected at baseline and every month over total 6 months for simultaneous determination of erythrocyte polyamines and plasma micronutrients by the high-performance liquid chromatographic method. For all the measures of erythrocyte polyamines the intraindividual variation was smaller than that between subjects, and three or four measurements required to accurately characterize long-term erythrocyte polyamines for an individual. The intra-class correlations were moderately high for all erythrocyte polyamine measurements, indicating a good reproducibility for intra-individual erythrocyte polyamine measurements. Based on monthly values, significant inverse correlations were found between erythrocyte spermidine and the plasma levels of retinol (r = -0.50) and lutein (r = -0.52). There were also significant inverse associations between erythrocyte spermine and plasma levels of alpha-tocopherol (r = -0.29), lutein (r = -0.44), lycopene (r = -0.29), beta-cryptoxanthin (r = -0.30), and total carotenoids (r = -0.29). The effects of supplementation upon the associations between erythrocyte polyamines and plasma nutrient levels were additionally addressed. The results indicate an acceptable longitudinal reproducibility of erythrocyte polyamine measurements, support the hypothesis that erythrocyte polyamine measurements may be correlated with plasma levels of certain nutrients, and suggest a further biomarker application in cancer prevention trials involving dietary modifications or specific relevant micronutrients.

Adult↗