Storage‐dependent remodeling of the red blood cell membrane is associated with increased immunoglobulin G binding, lipid raft rearrangement, and caspase activation

Selenium is an essential element incorporated into selenoproteins. Selenium deficiency may predispose to immune deficiency, mood disorders, and cancer. On the other hand, excessive environmental exposure to selenite may cause a variety of disorders including anemia. At least in theory, the anemia could result from accelerated suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and phosphatidylserine exposure at the erythrocyte surface. Eryptosis is triggered by an increase in the cytosolic Ca²⁺ concentration and by ceramide. The present experiments explored, whether high concentrations of selenite stimulate eryptosis. According to Fluo3 fluorescence, selenite (≥?200 μg/l sodium selenite) within 48 hours significantly increased the cytosolic Ca²⁺ concentration in human erythrocytes. According to binding of selective fluorescent antibodies, selenite (≥ 200 μg/l) significantly increased ceramide formation. Annexin V-binding demonstrated that selenite (≥200 μg/l) significantly increased phosphatidylserine exposure of erythrocytes. Forward scatter analysis further revealed that selenite (≥ 200 μg/l) significantly decreased cell volume. In contrast to selenite, selenate failed to trigger eryptosis. In conclusion, selenite triggers suicidal erythrocyte death at least partially by increasing the cytosolic Ca²⁺ concentration and by stimulating the formation of ceramide. The present study discloses novel cellular effects of this essential nutrient.

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“…Reportedly, stored erythrocytes show membrane changes and oxidative damage of cytoskeletal proteins [97,98].…”

Section: Discussionmentioning

confidence: 99%

Suicidal Death of Erythrocytes Due to Selenium-Compounds

Sopjani

Föller

Gulbins

et al. 2008

Cell Physiol Biochem

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“…Moreover, eryptosis is triggered by paclitaxel [17], amantadine [18], azathioprine [19], retinoic acid [20], chlorpromazine [21], cyclosporine [22], methylglyoxal [23], amyloid peptides [24], anandamide [25], Bay-Y5884 [26] and curcumin [27]. Mechanisms underlying eryptosis may not only affect circulating erythrocytes but may contribute to the limitation of erythrocytes during storage [28][29][30].…”

Section: Introductionmentioning

confidence: 99%

Lipopeptides in the Triggering of Erythrocyte Cell Membrane Scrambling

Wang

Mahmud²,

Föller³

et al. 2008

Cell Physiol Biochem

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Sepsis is paralleled by anemia, an effect partially resulting from eryptosis, the suicidal death of erythrocytes. Eryptosis is characterized by cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. Pathogen-induced eryptosis may partially result from interaction of bacterial cell wall components such as lipoproteins with the erythrocyte cell membrane. The present study explored, whether the synthetic lipopeptide Pam3CSK4 mimicking the acylated amino terminus of bacterial lipoproteins triggers eryptosis. According to annexin-V-binding in FACS analysis, Pam3CSK4 (1 µg/ml) stimulated phosphatidylserine exposure, an effect significantly blunted in the nominal absence of Ca 2+ . According to Fluo3 fluorescence, Pam3CSK4 increased cytosolic Ca 2+ activity and moderately stimulated erythrocytic ceramide formation, both major triggers of eryptosis. In conclusion, bacterial lipoproteins participate in the stimulation of erythrocyte cell membrane scrambling by bacterial cell wall components. Thus, lipoproteindependent suicidal erythrocyte death may contribute to the pleotropic effects of sepsis.

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“…Protein oxidation in erythrocytes is varied and leads to changes in the erythrocyte membrane, in turn leading to changes in morphology (60)(61)(62)(63). AOPP are formed by the action of chloraminated oxidants, which produce dityrosine containing cross-linked protein products (44).…”

Section: Discussionmentioning

confidence: 99%