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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Red blood cell plasma membranes contain a number of enzymes: ATPases, anion transport protein, glyceraldehyde 3-phosphate dehydrogenase, protein kinases, adenylate cyclase, acetylcholinesterase. Most of them are tightly bound to the membrane and are present in small amounts. As a result, structural characterization of erythrocyte membrane enzymes has not yet been successful. Functional studies have, however, yielded a great deal of information. ATPases allow active transport of cations (calcium, sodium, potassium). Anion transport protein controls movements of chloride and phosphate ions, and of glucose and water. Among glycolytic enzymes: glyceraldehyde 3-phosphate dehydrogenase is partially bound to the membrane. Protein kinases catalyze the phosphorylation of several membrane proteins, one of which (spectrin) is involved in red blood cell mechanical properties. The physiological role of adenylate cyclase is unknown. Acetylcholinesterase is an ectoenzyme. Calcium-dependent ATPase, adenylate cyclase and phosphorylation of erythrocyte membrane proteins have been found abnormal in various conditions: hereditary spherocytosis, sickle-cell anemia, progressive muscular dystrophies, all of these disorders being associated with a decreased deformability of the erythrocyte.
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PMID:The enzymes of the red blood cell plasma membrane. 14 25

The key to symptomatology in uremia is nitrogen retention leading to amidination and transmidination of a variety of substrates. The product of this activity is a series of guanidino acids which are methyl receptors converting S-adenosylmethionine to adenosine and homocysteine. Adenosine is a potent inhibitor of the enzyme ATPase and, in this way, contributes to the anemia, the bleeding diathesis and the CNS symptoms of uremia. Homocysteine is an inhibitor of pyridoxal phosphate-induced reactions and contributes to the angiitis and thromboembolism so unexpectedly encountered in chronic uremia.
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PMID:Alternate reasons for atherogenesis in uremia. 15 May 96

Experimental infection of hamsters with Leishmania donovani caused visceral leishmaniasis in which hematological changes occurred. The infected hamsters were anemic and reticulocyte counts were high. No significant change in the serum erythropoietin level was noted. Red cell membrane Na(+)-K(+)-ATPase and acetylcholinesterase activities increased. Osmotic fragility of the erythrocytes from infected animals increased. The level of 2,3-diphosphoglycerate of the red cells increased with the degree of anemia.
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PMID:Anemia in experimental visceral leishmaniasis in hamsters. 131 Jul 31

The influences of iron deficiency on erythrocyte spanning membrane proteins, band 3 protein and Na(+)-K(+)-ATPase, were studied in the growing rats with iron deficient anemia. The main findings were (1) reduction of band 3 and increment of band 4.1 protein. (2) diminished rate constant of pyruvate-chloride exchange (Kp:Cl.h-1) of the erythrocytes and (3) significant decrease of Na(+)-K(+)-ATPase activity only at the early stage of iron exhaustion. In addition, there was a significant negative correlation between Kp:Cl.h-1 and Na(+)-K(+)-ATPase activity both in iron deficient rats and in the controls. It is suggested that the composition and function of the erythrocyte spanning-membrane proteins for ion exchange could be affected by iron deficiency.
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PMID:Abnormalities of ion-exchange proteins of the red cell membrane in iron deficiency anemia. 131 72

The occurrence of auto-antibodies in patients with the autoimmune disease pernicious anaemia and in patients with active duodenal ulcers was investigated. In order to characterize antigenic structures, various cellular and subcellular fractions were prepared from pig gastric mucosa and from a homogenate of duodenal mucosa. By means of an enzyme-linked immunosorbent assay and immunoblotting, both the H+,K(+)-ATPase and pepsinogen/pepsin were shown to constitute the major antigens. All of the seven pernicious-anaemia sera that were tested contained auto-antibodies against both antigens, and the epitopes of the H+,K(+)-ATPase were shown to be localized on its cytoplasmic face. In 75% (18/24) of the sera from patients with duodenal ulcers, auto-antibodies were detected when using purified antigens. Six sera reacted with H+,K(+)-ATPase and twelve reacted with pepsinogen, one reacted with both antigens, and four sera reacted with the duodenal mucosal antigen. The occurrence of auto-antibodies indicates that there is a mucosal lesion and that immunological factors may be involved in the pathogenesis of the disease in some patients.
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PMID:The occurrence of auto-antibodies in patients with gastro-duodenal lesions. 169 83

A mild hereditary nonspherocytic anemia in Beagle dogs was studied. Compared to RBCs from normal dogs, RBCs from hemolytic Beagles were larger on average, contained more potassium, and exhibited an approximately 50% decrease in rate of loss of ATP induced by Ca and the ionophore, A23187. Under certain conditions, this rate of ATP loss can be taken as a measure of the Ca pump ATPase activity of intact RBCs. From RBC fractionation studies it appeared that the defective Ca pump ATPase was acquired during the relatively short life-span of the hemolytic RBC. Significant loss of Ca pump ATPase may be causally related to the hemolytic anemia. The mechanism(s) by which Ca pump ATPase activity is lost in this hemolytic anemia remain(s) to be determined.
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PMID:The activity of the red blood cell Ca pump is decreased in hemolytic anemia of the beagle dog. 252 73

The effect of parathyroid hormone on erythrocytes from newborn and adult rabbits was studied in relation to the fragility pattern in hypotonic salt solutions and the activities of Ca- and Mg-dependent ATPases. Median osmotic fragility of red blood cells from newborn rabbits was significantly higher than in red blood cells from mature rabbits. Parathyroid hormone increased the mean osmotic fragility of red blood cells from newborn and adult rabbits, but showed the greater effect on those from newborns. Similarly, the hormone stimulated to a much greater extent the Ca-ATPase, but not the Mg-ATPase in red blood cells from the newborn rabbits, in comparison with red blood cells from adult rabbits. Parathyroid hormone, which is greatly elevated in the blood of patients with chronic renal failure, may be one cause for the anaemia seen in these patients, and its effect, which is mediated by Ca-ATPase activity, is stronger on young red blood cells. Significant morphological changes in the young red blood cells, observed by scanning electron microscopy, were caused by parathyroid hormone.
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PMID:Effect of parathyroid hormone on the fragility and enzyme activities of red blood cells from young and mature rabbits. 295 52

The effect of parathyroid hormone at concentrations found in uremic patients on erythrocytes (RBC) from newborn and adult rabbits was studied in relation to the fragility pattern in hypotonic salt solutions and the activities of Ca- and Mg-dependent ATPases. Median osmotic fragility of RBC from newborn rabbits was significantly lower than in mature rabbits. Parathyroid hormone (PTH) stimulated to a greater extent the mean osmotic fragility in RBC from newborn rabbits, than in those from adults. Similarly, the hormone stimulated to a much greater extent the Ca-ATPase but not the Mg-ATPase in RBC from the newborn rabbits, in comparison to those from adult rabbits. PTH, which is greatly elevated in the blood of patients with chronic renal failure, may be one cause of the anemia seen in these patients, and its effect, which is mediated by Ca-ATPase activity, is stronger on young RBC. There were significant morphological changes in the young RBC caused by PTH, as seen with scanning electron microscopy.
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PMID:Biochemical changes associated with the osmotic fragility of young and mature erythrocytes caused by parathyroid hormone in relation to the uremic syndrome. 295 61

Simultaneous assay of blood lead (Pb-B) and red cell lead (Pb-Rbc) in 123 samples from 104 urban and suburban students, ages 10-18, shows the ratio of concentration (Pb-Rbc)/(Pb-B) to increase as the hematocrit decreases. On direct assay in 40 samples, plasma lead (Pb-P) was fixed in a narrow range. In 28 students with Pb-Rbc >40 mug/100 ml, the mean red cell 2,3-diphosphoglycerate (2,3-DPG) was 6.05+/-0.28 (+/-S.E.), significantly higher (P<.025) than the 5.25+/-0.18 of 51 students with Pb-Rbc<40 mug/100 ml, although hemoglobin values were comparable (13.83+/-0.31 versus 13.55+/-0.20). Analysis of the individual population groups showed this correlation of Pb-Rbc with 2,3-DPG to be primarily related to the intercorrelation of each parameter with hemoglobin.Rbc membrane Na/K ATPase, as per cent of total membrane ATPase, had a median value of 60% in 48 subjects. Na/K ATPase below 60% was found in 10 (77%) of the 13 students with Pb-Rbc>/=40 mug/100 ml, but in only 14 of the 35 with Pb-Rbc<40 mug/100 ml (chi(2)=5.1, df=1, P<0.05). Correlation of significant enzyme changes with Pb-Rbc, but not with Pb-B in the normal urban range of Pb-B<35 mug/100 ml suggests Pb-Rbc, increased in anemia, to be a critical factor in the hematotoxicity of lead.
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PMID:Red cell lead, whole blood lead, and red cell enzymes. 436 46

Activities of mitochondrial enzymes in blood cells from 69 patients with primary sideroblastic anemia were determined to elucidate the pathogenesis of the disease. In erythroblasts of patients with primary acquired type the activities of both delta-aminolevulinic acid synthetase and mitochondrial serine protease were inevitably decreased. The susceptibility to the protease of apo-delta-aminolevulinic acid synthetase prepared from erythroblasts of patients with this type was within the normal range, in contrast to that of pyridoxine-responsive anemia. The activities of mitochondrial enzymes such as cytochrome oxidase, serine protease, and oligomycin-sensitive ATPase, except citrate synthetase, were usually decreased in mature granulocytes of the patients. Patients with hereditary sideroblastic anemia also had decreased delta-aminolevulinic acid synthetase activity in erythroblasts, and decreased serine protease activity in both erythroblasts and mature granulocytes. Mature granulocytes obtained from patients with pyridoxine-responsive anemia before therapy had decreased cytochrome oxidase activity, however, the activity increased to a normal level when the patients were in remission. The activities of other mitochondrial enzymes in mature granulocytes were within normal range in these patients before pyridoxine therapy. The activities of these mitochondrial enzymes in lymphocytes were within normal range in all groups of patients with primary sideroblastic anemia. We suggest that patients with primary acquired, and possibly also those with hereditary sideroblastic anemia have impaired mitochondrial function in both erythroblasts and granulocytes. That only anemia is observed in these patients is because a functional abnormality of mitochondria in erythroblasts is most important because of the role of mitochondria in the formation of heme in erythrocyte development. In contrast to these two types of sideroblastic anemia, only delta-aminolevulinic acid synthetase in both erythroblasts and granulocytes seems to be impaired in patients with pyridoxine-responsive anemia.
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PMID:Multiple enzymatic defects in mitochondria in hematological cells of patients with primary sideroblastic anemia. 624 45


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