scholarly journals Decreased Glutathione Peroxidase Activity Secondary to Severe Iron Deficiency: A Possible Mechanism Responsible for the Shortened Life Span of the Iron-deficient Red Cell

Blood ◽  
1974 ◽  
Vol 43 (2) ◽  
pp. 281-289 ◽  
Author(s):  
Robert Rodvien ◽  
Amanda Gillum ◽  
Lewis R. Weintraub
Keyword(s):  
Enzyme Activity ◽  
Iron Deficiency ◽  
Glutathione Peroxidase ◽  
Peroxidase Activity ◽  
Hemoglobin Concentration ◽  
Red Cells ◽  
Red Cell ◽  
Glutathione Peroxidase Activity ◽  
Iron Deficient ◽  
Red Cell Survival

Abstract Red cell glutathione peroxidase activity decreased to 26% of initial activity following the induction of severe iron deficiency in rabbits. The fall in enzyme activity does not appear to be related to anemia per se, aging of the animals during the course of the experiment, or a generalized decrease in enzyme protein synthesis. With iron repletion, glutathione peroxidase activity did not return to initial values for 10 wk after the hemoglobin concentration had returned to normal. During this period of time, the young red cell population had a higher concentration of GSH-Px activity than the older cells. In contrast, there is no age differential in the concentration of this enzyme in normal red cells, and during the induction of iron deficiency young red cells have decreased enzyme activity as compared to older cells. Reduction in glutathione peroxidase activity may result in increased oxidative damage to the iron-deficient red cell. This, in turn, may be responsible for the previously reported membrane abnormalities and shortened red cell survival of iron-deficient red cells. It remains to be shown if glutathione peroxidase is dependent on iron for its synthesis or if the function of the enzyme is dependent on an iron-containing protein serving as an electron carrier.

scholarly journals Ethnic variation in red cell glutathione peroxidase activity

Blood ◽  
1975 ◽  
Vol 46 (1) ◽  
pp. 103-110 ◽  
Author(s):  
E Beutler ◽  
F Matsumoto
Keyword(s):  
Enzyme Activity ◽  
Glutathione Peroxidase ◽  
Peroxidase Activity ◽  
Genetic Model ◽  
The United States ◽  
European Population ◽  
Red Cell ◽  
Glutathione Peroxidase Activity ◽  
Cultured Fibroblasts ◽  
Erythrocyte Enzyme

Abstract Glutathione peroxidase activity was measured in blood and cultured fibroblasts from healthy persons of several different population groups. Individuals of Jewish ancestry and others of Mediterranean origin were found to manifest a decrease of red cell but not of leukocyte or fibroblast enzyme activity. Oriental populations differed in that the scatter in red cell enzyme activity was significantly lower than in Occidental populations. The erythrocyte enzyme of individuals with low activity was found to be less stable to heating than was the enzyme from persons with high activity. As a possible explanation for these data, a provisional genetic model is presented: a low GSH Px allele with a frequency of 0.556 in the Jewish population and of only 0.181 in the United States-Northern European population. Our results suggest that an association between GSH Px deficiency and hemolytic anemia need not represent a cause-and-effect relationship.

scholarly journals Ethnic variation in red cell glutathione peroxidase activity

Blood ◽  
1975 ◽  
Vol 46 (1) ◽  
pp. 103-110
Author(s):  
E Beutler ◽  
F Matsumoto
Keyword(s):  
Enzyme Activity ◽  
Glutathione Peroxidase ◽  
Peroxidase Activity ◽  
Genetic Model ◽  
The United States ◽  
European Population ◽  
Red Cell ◽  
Glutathione Peroxidase Activity ◽  
Cultured Fibroblasts ◽  
Erythrocyte Enzyme

Glutathione peroxidase activity was measured in blood and cultured fibroblasts from healthy persons of several different population groups. Individuals of Jewish ancestry and others of Mediterranean origin were found to manifest a decrease of red cell but not of leukocyte or fibroblast enzyme activity. Oriental populations differed in that the scatter in red cell enzyme activity was significantly lower than in Occidental populations. The erythrocyte enzyme of individuals with low activity was found to be less stable to heating than was the enzyme from persons with high activity. As a possible explanation for these data, a provisional genetic model is presented: a low GSH Px allele with a frequency of 0.556 in the Jewish population and of only 0.181 in the United States-Northern European population. Our results suggest that an association between GSH Px deficiency and hemolytic anemia need not represent a cause-and-effect relationship.

scholarly journals Excess Hemolysis in Subjects with Severe Iron Deficiency Anemia Associated and Nonassociated with Hookworm Infection

Blood ◽  
1965 ◽  
Vol 25 (1) ◽  
pp. 73-91 ◽  
Author(s):  
MIGUEL LAYRISSE ◽  
JESÚS LINARES ◽  
MARCEL ROCHE ◽  
Adelina Ojeda ◽  
Alvaro Carstens ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Cell Survival ◽  
Iron Deficiency Anemia ◽  
Red Cells ◽  
Deficiency Anemia ◽  
Intrinsic Defect ◽  
Red Cell ◽  
Hookworm Infection ◽  
Iron Treatment ◽  
Red Cell Survival

Abstract An excess hemolysis was found in subjects with iron deficiency anemia associated with hookworm infection. Red cell survival, measured with Cr51 and DFP32 in the subjects before deworming, showed a marked disproportion between the decrease of the survival and the amount of daily intestinal blood loss in most cases. Excess of hemolysis was still present after more than 90 per cent of the parasites were removed. Red cell survival became normal after correction of anemia through iron treatment. Excess of hemolysis was also present in noninfected subjects with iron deficiency anemia due to other causes. The reduction in the survival of the erythrocytes from infected subjects transfused into normal recipients shows that the hemolytic process is due to an intrinsic defect of the red cells. The low values of hemoglobinemia and the presence of haptoglobins in the plasma indicate that hemoglobin has not been liberated in excess intravascularly. Finally, the fact that the red cells from an infected patient taken after deworming survived normally in splenectomized recipients indicates that the spleen is probably the principal site of the red cell destruction. The clinical and autopsy findings suggest that splenic function is not pathologically increased, but rather that this organ is acting physiologically at a more rapid rate, "culling" the abnormal circulating red cells and thus leading to a decrease in red cell survival. The studies presented here also indicate that the hookworm infection per se does not induce hemolysis.

scholarly journals Red cell membrane stiffness in iron deficiency

Blood ◽  
1983 ◽  
Vol 62 (1) ◽  
pp. 99-106 ◽  
Author(s):  
R Yip ◽  
N Mohandas ◽  
MR Clark ◽  
S Jain ◽  
SB Shohet ◽  
...  
Keyword(s):  
Shear Stress ◽  
Iron Deficiency ◽  
Surface Area ◽  
Buoyant Density ◽  
Hemoglobin Concentration ◽  
Mean Corpuscular Hemoglobin ◽  
Red Cell ◽  
Iron Deficient ◽  
Membrane Stiffness ◽  
Rbc Deformability

The purpose of this study was to characterize red blood cell (RBC) deformability by iron deficiency. We measured RBC deformability to ektacytometry, a laser diffraction method for determining the elongation of suspended red cells subjected to shear stress. Isotonic deformability of RBC from iron-deficient human subjects was consistently and significantly lower than that of normal controls. In groups of rats with severe and moderate dietary iron deficiency, RBC deformability was also reduced in proportion to the severity of iron deficiency. At any given shear stress value, deformability of resealed RBC ghosts from both iron-deficient humans and rats was lower than that of control ghosts. However, increase of applied shear stress resulted in progressive increase in ghost deformation, indicating that ghost deformability was primarily limited by membrane stiffness rather than by reduced surface area-to-volume ratio. This was consistent with the finding that iron-deficient cells had a normal membrane surface area. In addition, the reduced mean corpuscular hemoglobin concentration (MCHC) and buoyant density of the iron-deficient rat cells indicated that a high hemoglobin concentration was not responsible for impaired whole cell deformability. Biochemical studies of rat RBC showed increased membrane lipid and protein crosslinking and reduced intracellular cation content, findings that are consistent with in vivo peroxidative damage. RBC from iron-deficient rats incubated in vitro with hydrogen peroxide showed increased generation of malonyldialdehyde, an end-product of lipid peroxidation, compared to control RBC. Taken together, these findings suggest that peroxidation could contribute in part to increased membrane stiffness in iron- deficient RBC. This reduced membrane deformability may in turn contribute to impaired red cell survival in iron deficiency.

scholarly journals Increased glutathione peroxidase activity in alpha-thalassemia

Blood ◽  
1977 ◽  
Vol 50 (4) ◽  
pp. 647-655
Author(s):  
E Beutler ◽  
F Matsumoto ◽  
D Powars ◽  
J Warner
Keyword(s):  
Glutathione Peroxidase ◽  
Peroxidase Activity ◽  
Beta Thalassemia ◽  
Red Cell ◽  
Glutathione Peroxidase Activity ◽  
Alpha Thalassemia ◽  
Thalassemia Trait ◽  
Gshpx Activity ◽  
Increased Activity ◽  
Hemoglobin H Disease

Glutathione peroxidase (GSHPx) activity was found to be greatly elevated in members of a family with alpha-thalassemia. Eleven other families with proven alpha-thalassemia were investigated, and all but one subject with hemoglobin H disease had increased red cell GSHPx. Most persons with alpha-thalassemia trait also had increased activity of red cell GSHPx. In contrast, only very modest increases in glutathione peroxidase activity were observed in subjects with various forms of beta-thalassemia.

scholarly journals Construction and activity analyses of single functional mouse peroxiredoxin 6 (Prdx6)

2019 ◽  
Vol 63 (1) ◽  
pp. 99-105 ◽  
Author(s):  
Lu-Lu Wang ◽  
Shi-Ying Lu ◽  
Pan Hu ◽  
Bao-Quan Fu ◽  
Yan-Song Li ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Glutathione Peroxidase ◽  
Phospholipase A2 ◽  
Peroxidase Activity ◽  
Glutathione Peroxidase Activity ◽  
Active Centre ◽  
Peroxiredoxin 6 ◽  
Raw264.7 Macrophages ◽  
Overlap Extension ◽  
Phospholipase A2 Activity

Abstract Introduction: Peroxiredoxin 6 (Prdx6) is a bifunctional protein with glutathione peroxidase activity and phospholipase A2 activity. Previous studies have shown a significant positive correlation between the intracellular survival ability of Brucella and Prdx6. Here, the Prdx6 enzyme with a single activity was constructed to facilitate study of the relationship between the single function of Prdx6 and Brucella infection. Material and Methods: The target open reading frame (ORF) DNAs of Prdx6 with a single active centre were prepared using gene splicing by overlap extension PCR (SOE-PCR), and the recombinant eukaryotic expression plasmids inserted by Prdx6 with the single activity centre were constructed and transfected into murine Raw264.7 macrophages. The glutathione peroxidase activity and phospholipase A2 activity of the constructed Prdx6 were examined. Results: The core centres (Ser32 and Cys47) of Prdx6 were successfully mutated by changing the 94th nucleotide from T to G and the 140th nucleotide from G to C in the two enzyme activity cores, respectively. The constructed recombinant plasmids of Prdx6 with the single active centre were transfected into murine macrophages showing the expected single functional enzyme activity, which MJ33 or mercaptosuccinate inhibitors were able to inhibit. Conclusion: The constructed mutants of Prdx6 with the single activity cores will be a benefit to further study of the biological function of Prdx6 with different enzyme activity.

Glutathione Peroxidase Activity in Iron-Deficient Rats

1981 ◽  
Vol 111 (1) ◽  
pp. 194-200 ◽  
Author(s):  
Young H. Lee ◽  
Donald K. Layman ◽  
Roma R. Bell
Keyword(s):  
Glutathione Peroxidase ◽  
Peroxidase Activity ◽  
Glutathione Peroxidase Activity ◽  
Iron Deficient

scholarly journals Brief Report: Hemozygous Erythrocyte Glutathione-Peroxidase Deficiency: Clinical and Biochemical Studies

Blood ◽  
1969 ◽  
Vol 33 (2) ◽  
pp. 164-169 ◽  
Author(s):  
T. F. NECHELES ◽  
NORMAN MALDONADO ◽  
ANTONIO BARQUET-CHEDIAK ◽  
D. M. ALLEN
Keyword(s):  
Glutathione Peroxidase ◽  
Puerto Rican ◽  
Autosomal Recessive ◽  
Red Cells ◽  
Red Cell ◽  
Hexose Monophosphate ◽  
Glutathione Peroxidase Activity ◽  
Biochemical Studies ◽  
Peroxidase Deficiency ◽  
Mode Of Inheritance

Abstract An adult Puerto Rican male is described who developed an acute hemolytic episode following the infusion of three units of stored autologous red cells. The acute episode was associated with the presence of numerous red cells containing Heinz bodies. Investigation of his red cells revealed a markedly decreased level of the enzyme glutathione peroxidase. Examination of family members revealed moderately decreased levels of red cell glutathione peroxidase activity in both parents and in a sibling suggesting an autosomal recessive mode of inheritance. Metabolic studies on the erythrocytes from this patient revealed a normal level of hexose monophosphate shunt activity under basal conditions but a lack of normal activation of this pathway in the presence of hydrogen peroxide. The results of these studies support the concept that this enzyme, glutathione peroxidase, plays a major role in mediating the normal red cell response to the presence of peroxides.

scholarly journals Selenium, glutathione and glutathione peroxidases in blood of patients with chronic liver diseases.

2003 ◽  
Vol 50 (4) ◽  
pp. 1147-1154 ◽  
Author(s):  
Jolanta Czuczejko ◽  
Bronisław A Zachara ◽  
Ewa Staubach-Topczewska ◽  
Waldemar Halota ◽  
Józef Kedziora
Keyword(s):  
Liver Disease ◽  
Glutathione Peroxidase ◽  
Chronic Liver Disease ◽  
Peroxidase Activity ◽  
Chronic Liver ◽  
Red Cell ◽  
Glutathione Peroxidase Activity ◽  
Group 2 ◽  
Cryptogenic Chronic Liver Disease ◽  
Group 1

Disturbances in the antioxidant system could play a role in pathogenesis of chronic liver disease. The aim of our study was to evaluate the levels/activities of antioxidants in blood of patients with chronic liver disease. We estimated selenium and glutathione concentrations and glutathione peroxidase activities in blood of 59 patients with chronic hepatitis B or C virus infection (group 1) and 64 patients with alcoholic, autoimmune or cryptogenic chronic liver disease (group 2). The results were compared with 50 healthy controls. Whole blood and plasma selenium and red cell glutathione concentrations were significantly lower in the patients compared with the controls. Red cell glutathione peroxidase activity was slightly reduced in both subgroups of group 1 and in group 2 with normal alanine aminotransferase values. Plasma glutathione peroxidase activity was slightly but significantly higher in patients with elevated aminotransferase values. The findings suggest that disturbances in antioxidant parameters in blood of patients with chronic liver disease may be the cause of the peroxidative damage of cells.

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