Erythrocyte Aging: Physical and Chemical Membrane Changes

Bartosz, Grzegorz

doi:10.1159/000213251

Cited by 82 publications

(44 citation statements)

References 97 publications

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“…We found an increased activity of acetylcholinesterase in the erythrocytes of Sod1 -/-mice. Acetylcholinesterase activity decreases during erythrocyte aging and has been suggested to be a marker of red cell age [29,30]. The elevated activity of this enzyme in the erythrocytes of Sod1 -/-mice may reflect their accelerated removal and resulting lower mean age.…”

Section: Discussionmentioning

confidence: 99%

“…This enzyme, located at the outer surface of the erythrocyte membrane, is not subject to intracellular oxidative stress in erythrocytes devoid of superoxide dismutase, in contrast to catalase and glutathione peroxidase, which are present inside the cell and subject to an increased steady-state level of superoxide. Both enzymes are known to be inactivated by superoxide [13], which apparently explains the lack of increase in their activities, which could be anticipated on the basis of the lower mean age of the circulating erythrocytes (the activity of these enzymes also decreases during erythrocyte aging, as in the case of acetylcholinesterase) [30,31]. Although we were not able to analyze all the parameters in the Sod +-/-heterozygotes, we compared the levels of reactive oxygen species and the reticulocyte and Heinz body counts, and also assessed splenomegaly in order to address the question of whether a decrease of SOD activity to half of the normal value yields a gene dose effect or the remaining enzyme activity in the erythrocytes of Sod +-/-mice is sufficient to afford efficient protection against superoxide.…”

Section: Discussionmentioning

confidence: 99%

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The effects of superoxide dismutase knockout on the oxidative stress parameters and survival of mouse erythrocyt

Grzelak¹,

Kruszewski²,

Macierzyńska³

et al. 2009

Cellular and Molecular Biology Letters

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Abstract:The erythrocytes of 12-month old Sod1 -/-mice showed an increased level of reactive oxygen species (ROS), as estimated by the degree of dihydroethidine and dihydrorhodamine oxidation, and the increased level of Heinz bodies. No indices of severe oxidative stress were found in the red blood cells and blood plasma of Sod1 -/-mice as judged from the lack of significant changes in the levels of erythrocyte and plasma glutathione, plasma protein thiol and carbonyl groups and thiobarbituric-acid reactive substances in the blood plasma. However, a decreased erythrocyte lifespan, increased reticulocyte count and splenomegaly were noted, indicating the importance of superoxide dismutase for maintaining erythrocyte viability. The levels of erythrocyte ROS and Sod1 +/-mice, suggesting that a superoxide dismutase activity decrease to half of its normal value may be sufficient to secure the protective effects of the enzyme.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The effects of superoxide dismutase knockout on the oxidative stress parameters and survival of mouse erythrocyt

Grzelak¹,

Kruszewski²,

Macierzyńska³

et al. 2009

Cellular and Molecular Biology Letters

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“…39,40 Lipid peroxidation increases with time during RBC aging. 1,41,42 As such, oxidation creates RBC surface ligands, which can be recognized by macrophages by mechanisms that are similar to recognition of oxLDL. 4 In vitro oxidation of RBCs results in aldehyde formation and membrane protein cross-linking, lipid peroxidation, and possibly also conjugation of lipid fragments to proteins, and protein degradation.…”

Section: Discussionmentioning

confidence: 99%

CD47 on experimentally senescent murine RBCs inhibits phagocytosis following Fcγ receptor–mediated but not scavenger receptor–mediated recognition by macrophages

Olsson

Oldenborg

2008

Blood

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IntroductionRemoval of senescent red blood cells (RBCs) from the circulation is a selective process mediated mainly by macrophages in the liver and spleen. 1 Several molecular patterns, which may be involved as ligands in recognition by macrophages, appear on the surface of senescent RBCs. Macrophages can either directly recognize these ligands, or recognition can be dependent on binding of bridging plasma proteins that may interact with the RBC ligands. [2][3][4][5][6][7] As such, these RBC ligands may include alterations in protein carbohydrate moieties, 8 loss of plasma membrane phospholipid asymmetry, [9][10][11] and/or clustering of Band 3 with subsequent binding of complement or antibodies. 12-14 Phagocytosis by macrophages can for instance be induced following ligation of receptors such as Fc␥ receptors (Fc␥R), complement receptors, or scavenger receptors (SRs). [15][16][17] Fc␥R recognizes the Fc portion of immunoglobulin G (IgG) bound to a target cell, resulting in rapid phagocytosis of the IgG-opsonized target. SRs make up a large family of receptors with a broad ligand-binding ability, where most known ligands are polyanionic molecules such as proteins, polyribonucleotides, polysaccharides, and lipids. 16 "Altered" host molecules (eg, oxidized low-density lipoprotein [oxLDL]) can be recognized by most SRs, whereas other ligands interact more specifically with SRs. 16 Oxidative damage is likely to be one important cause of RBC senescence and exposure of senescence-associated ligands. 13,18 RBCs oxidized in vitro (Ox-RBCs) are efficiently phagocytosed by macrophages in the absence of further opsonization, a process shown to be inhibited by oxLDL or other SR ligands, such as fucoidan, dextran sulfate, or poly-I, both in vivo and in vitro. 4,7,19 Phagocytosis of Ox-RBCs has also been suggested to be serum dependent, 6 and involve recognition of phosphatidylserine (PS) on the RBC surface. 9,10 Macrophage phagocytosis of target host cells is regulated by the balance between signaling through prophagocytic receptors (eg, Fc␥R or complement receptors) and inhibitory receptors. Recognition of the cell surface glycoprotein CD47 by the inhibitory receptor signal regulatory protein alpha (SIRP␣) inhibits phagocytosis of unopsonized RBCs, as well as IgG or complementopsonized RBCs, both in vivo and in vitro. 20-23 CD47 is highly expressed on RBCs, but ubiquitously expressed by most cells in the body, and can also negatively regulate phagocytosis of platelets and leukocytes. [24][25][26] The amount of CD47 on the cell surface regulates macrophage phagocytosis, since IgG-opsonized RBCs from CD47 ϩ/Ϫ mice (expressing about 50% of normal levels of CD47) are taken up faster than wild-type (WT) RBCs, but slower than CD47 Ϫ/Ϫ RBCs. 27 We have shown that the phagocytosis-inhibitory effect of CD47 does not come into play on apoptotic nucleated cells, where CD47 is clustered into patches on the apoptotic cell surface and segregated away from prophagocytic ligands such as PS or calreticulin. 25 Although older circulating RBC...

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“…Exposure of erythrocytes to oxidative stress can result in a number of membrane [14,15] and enzyme activity changes [16,17]. Some studies suggest that erythrocytes from elderly individuals are highly susceptible to oxidative stress [18,19], while others do not agree with that [20,21].…”

Section: Discussionmentioning

confidence: 99%

Age-Related Changes on Glucose Transport and Utilization of Human Erythrocytes: Effect of Oxidative Stress

Güven

Özkılıç²,

Kanıgür-Sultuybek³

et al. 1999

Gerontology

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Background: Normal aging is associated with an impairment in glucose homeostasis. Methods: In order to investigate the effect of aging on glucose transport and utilization in erythrocytes, the transport and utilization of glucose were measured in erythrocytes from 10 young (mean age 26 ± 3 years) and 10 elderly (mean age 70 ± 7 years) healthy individuals. In addition, the glucose transport and utilization were also measured in the presence of cumene hydroperoxide (CumOOH), a toxic organic hydroperoxide that is known to induce oxidative stress. Results: The levels of glucose transport and utilization were significantly lower in the elderly group than the young group (p < 0.05). The glucose transport and utilization were not altered by CumOOH treatment in either young or elderly individuals. Conclusion: These results indicate an age-related decrease in the both glucose transport and utilization in erythrocytes.

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Erythrocyte Aging: Physical and Chemical Membrane Changes

Cited by 82 publications

References 97 publications

The effects of superoxide dismutase knockout on the oxidative stress parameters and survival of mouse erythrocyt

The effects of superoxide dismutase knockout on the oxidative stress parameters and survival of mouse erythrocyt

CD47 on experimentally senescent murine RBCs inhibits phagocytosis following Fcγ receptor–mediated but not scavenger receptor–mediated recognition by macrophages

Age-Related Changes on Glucose Transport and Utilization of Human Erythrocytes: Effect of Oxidative Stress

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