Hemin-induced suicidal erythrocyte death

Gatidis, Sergios; Föller, Michael; Läng, Florian

doi:10.1007/s00277-009-0697-7

Cited by 30 publications

(29 citation statements)

References 74 publications

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“…However, it was reported that 4% of RBC were hemolyzed 48 hrs after the incubation with hemin at C = 10 μM8. In the latter experiments RBC were incubated in a Ringer solution.…”

Section: Discussionmentioning

confidence: 99%

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Transformation of membrane nanosurface of red blood cells under hemin action

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Черныш

Moroz

et al. 2014

Sci Rep

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Hemin is the product of hemoglobin oxidation. Some diseases may lead to a formation of hemin. The accumulation of hemin causes destruction of red blood cells (RBC) membranes. In this study the process of development of topological defects of RBC membranes within the size range from nanoscale to microscale levels is shown. The formation of the grain-like structures in the membrane (“grains”) with typical sizes of 120–200 nm was experimentally shown. The process of formation of “grains” was dependent on the hemin concentration and incubation time. The possible mechanism of membrane nanostructure alterations is proposed. The kinetic equations of formation and transformation of small and medium topological defects were analyzed. This research can be used to study the cell intoxication and analyze the action of various agents on RBC membranes.

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“…However, it was reported that 4% of RBC were hemolyzed 48 hrs after the incubation with hemin at C = 10 μM8. In the latter experiments RBC were incubated in a Ringer solution.…”

Section: Discussionmentioning

confidence: 99%

“…This was proved by the electrophoresis and electron spin resonance methods5. A variety of disorders may lead to a formation of hemin, which in turn causes hemolysis89.…”

mentioning

confidence: 98%

Transformation of membrane nanosurface of red blood cells under hemin action

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Черныш

Moroz

et al. 2014

Sci Rep

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“…malaria [49][50][51][52][53], Wilson's disease [54] and possibly metabolic syndrome [55]. Eryptosis is further stimulated by a wide variety of small molecules [56][57][58][59][60][61][62][63]. The proeryptotic effect of dicoumarol could be compounded in those clinical conditions and in the presence of those chemicals.…”

Section: Discussionmentioning

confidence: 99%

Dicoumarol Activates Ca<sup>2+</sup>-permeable Cation Channels Triggering Erythrocyte Cell Membrane Scrambling

Qadri

Kucherenko²,

Zelenak³

et al. 2011

Cell Physiol Biochem

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Dicoumarol, a widely used anticoagulant, may cause anemia, which may result from enhanced erythrocyte loss due to bleeding or due to accelerated erythrocyte death. Erythrocytes may undergo suicidal death or eryptosis, characterized by cell shrinkage and phospholipid scrambling of the cell membrane. Eryptosis may be triggered by increase of cytosolic ²⁺-activity ([Ca²⁺]_i). The present study explored, whether dicoumarol induces eryptosis. [Ca²⁺]_i was estimated from Fluo3-fluorescence, cation channel activity utilizing whole cell patch clamp, cell volume from forward scatter, phospholipid scrambling from annexin-V-binding, and hemolysis from haemoglobin release. Exposure of erythrocytes for 48 hours to dicoumarol (=10 µM) significantly increased [Ca²⁺]_i, enhanced cation channel activity, decreased forward scatter, triggered annexin-V-binding and elicited hemolysis. Following exposure to 30 µM dicoumarol, annexin-V-binding affected approximately 15%, and hemolysis 2% of treated erythrocytes. The stimulation of annexin-V-binding by dicoumarol was abrogated in the nominal absence of ²⁺. In conclusion, dicoumarol stimulates suicidal death of erythrocytes by stimulating Ca²⁺ entry and subsequent triggering of ²⁺ dependent cell membrane scrambling.

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“…Several clinical conditions associated with anemia have been shown to be paralleled by accelerated eryptosis [16], such as iron deficiency [1], phosphate depletion [17], Hemolytic Uremic Syndrome [18], sepsis [19], malaria [20][21][22], or Wilson's disease [23]. Moreover, eryptosis may be triggered by a wide variety of endogeneous substances and xenobiotics, such as antiA IgG antibodies [24], cordycepin [25], hemin [26], amiodarone [27], methylglyoxal [28], amyloid peptides [29], anandamide [30], lipopetides [31] retinoic acid [32], paclitaxel [33], amantadine [34], chlorpromazine [35], ciglitazone [36]. cyclosporine [37], Bay-5884 [38], curcumin [39], valinomycin [40], listeriolysin [41], aluminium [42], bismuth [43], mercury [44], copper [23], cadmium [45], selenium [46], vanadate [47], gold [48] and arsenic [49].…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of Thymol on Suicidal Erythrocyte Death

Mahmud

Mauro²,

Föller

et al. 2009

Cell Physiol Biochem

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The antibacterial plant component thymol has antioxidant activity. Oxidative stress is known to activate Ca²⁺-permeable cation channels with subsequent Ca²⁺ entry, activation of Ca²⁺-sensitive K⁺ channels, cell shrinkage, cell membrane scrambling and phosphatidylserine exposure at the erythrocyte surface. Cell shrinkage and phosphatidylserine exposure are typical features of suicidal erythrocyte death or eryptosis. Eryptotic cells are cleared from circulating blood thus causing anemia and may adhere to the vascular wall thus interfering with the microcirculation. The present experiments explored whether thymol interacts with eryptosis. Annexin V-binding was utilized to determine phosphatidylserine exposure, forward scatter to detect alterations of cell volume and Fluo3 fluorescence to depict changes of the cytosolic Ca²⁺ activity. Oxidative stress (30 min. 0.3 mM tert-butylhydroperoxide), energy depletion (48 h glucose removal) and isotonic cell shrinkage (48 h replacement of extracellular Cl^- with gluconate) significantly increased annexin V-binding and decreased the forward scatter, effects significantly blunted in the presence of thymol 2.5 - 20 μg/ml. Thymol is a potent inhibitor of suicidal erythrocyte death particularly following oxidative stress. In conclusion, thymol may be useful incounteracting anemia and impairment of microcirculation.

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Hemin-induced suicidal erythrocyte death

Cited by 30 publications

References 74 publications

Transformation of membrane nanosurface of red blood cells under hemin action

Transformation of membrane nanosurface of red blood cells under hemin action

Dicoumarol Activates Ca<sup>2+</sup>-permeable Cation Channels Triggering Erythrocyte Cell Membrane Scrambling

Inhibitory Effect of Thymol on Suicidal Erythrocyte Death

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