Tannic Acid Induced Suicidal Erythrocyte Death

Abed, Majed; Herrmann, Tabea; Alzoubi, Kousi; Pakladok, Tatsiana; Läng, Florian

doi:10.1159/000354510

Cited by 41 publications

(32 citation statements)

References 152 publications

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“…Eryptosis is further triggered by a wide variety of xenobiotics and is enhanced in a variety of clinical disorders [9,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43]. …”

Section: Introductionmentioning

confidence: 99%

Stimulation of Suicidal Erythrocyte Death by Increased Extracellular Phosphate Concentrations

Voelkl

Alzoubi

Mamar

et al. 2013

Kidney Blood Press Res

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109

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Background/Aim: Anemia in renal insufficiency results in part from impaired erythrocyte formation due to erythropoietin and iron deficiency. Beyond that, renal insufficiency enhances eryptosis, the suicidal erythrocyte death characterized by phosphatidylserine-exposure at the erythrocyte surface. Eryptosis may be stimulated by increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i). Several uremic toxins have previously been shown to stimulate eryptosis. Renal insufficiency is further paralleled by increase of plasma phosphate concentration. The present study thus explored the effect of phosphate on erythrocyte death. Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, and [Ca²⁺]_i from Fluo3-fluorescence. Results: Following a 48 hours incubation, the percentage of phosphatidylserine exposing erythrocytes markedly increased as a function of extracellular phosphate concentration (from 0-5 mM). The exposure to 2 mM or 5 mM phosphate was followed by slight but significant hemolysis. [Ca²⁺]_i did not change significantly up to 2 mM phosphate but significantly decreased at 5 mM phosphate. The effect of 2 mM phosphate on phosphatidylserine exposure was significantly augmented by increase of extracellular Ca²⁺ to 1.7 mM, and significantly blunted by nominal absence of extracellular Ca²⁺, by additional presence of pyrophosphate as well as by presence of p38 inhibitor SB203580. Conclusion: Increasing phosphate concentration stimulates erythrocyte membrane scrambling, an effect depending on extracellular but not intracellular Ca²⁺ concentration. It is hypothesized that suicidal erythrocyte death is triggered by complexed CaHPO₄.

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Section: Introductionmentioning

confidence: 99%

Stimulation of Suicidal Erythrocyte Death by Increased Extracellular Phosphate Concentrations

Voelkl

Alzoubi

Mamar

et al. 2013

Kidney Blood Press Res

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109

101

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“…The mitoxantrone concentrations required for the stimulation of eryptosis are within the range of mitoxantrone concentrations required for the antineoplastic activity of the substance [46]. At least in theory, the erythrocytes could be sensitized to the effect of mitoxantrone by parallel exposure to further eryptosis triggering xenobiotics [28,39,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73]. Moreover, the sensitivity to mitoxantrone may be increased in patients suffering from disorders with enhanced eryptosis [28], such as diabetes [34,74,75], dehydration [76], renal insufficiency [77,78], hemolytic uremic syndrome [79], sepsis [80], malaria [81], sickle cell disease [81], Wilson's disease [82], iron deficiency [83], malignancy [84], phosphate depletion [85], and metabolic syndrome [65].…”

Section: Discussionmentioning

confidence: 99%

Mitoxantrone-Induced Suicidal Erythrocyte Death

Arnold

Bissinger

Läng

2014

Cell Physiol Biochem

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Background/Aims: Mitoxantrone, a cytotoxic drug used for the treatment of malignancy and multiple sclerosis, is at least in part effective by triggering apoptosis. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a type of suicidal cell death. Hallmarks of eryptosis are cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signalling involved in eryptosis include Ca²⁺-entry, ceramide formation and oxidative stress. Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, formation of reactive oxidant species (ROS) from 2′,7′-dichlorodihydrofluorescein-diacetate fluorescence, and ceramide abundance from binding of fluorescent antibodies in flow cytometry. Results: A 48 hours exposure to mitoxantrone was followed by significant decrease of forward scatter (≥ 5 μg/ml mitoxantrone) and increase of annexin-V-binding (≥ 10 μg/ml mitoxantrone), effects paralleled by significant increases of ROS formation (25 μg/ml mitoxantrone) and ceramide abundance (25 μg/ml mitoxantrone). The effect of mitoxantrone was not significantly modified by nominal absence of extracellular Ca²⁺ but significantly blunted by the antioxidant N-acetylcysteine (1 mM). Conclusions: Mitoxantrone triggers cell membrane scrambling, an effect not requiring entry of extracellular Ca²⁺ but at least partially due to formation of ROS and ceramide.

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“…Eryptosis may be stimulated by a wide variety of xenobiotics [15,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66] and excessive eryptosis is further observed in several clinical conditions including diabetes, renal insufficiency, hemolytic uremic syndrome, sepsis, malaria, sickle cell disease, Wilson's disease, iron deficiency, malignancy, phosphate depletion, and metabolic syndrome [15]. …”

Section: Introductionmentioning

confidence: 99%

Stimulation of Erythrocyte Cell Membrane Scrambling by Gedunin

Lupescu¹,

Bissinger²,

Warsi³

et al. 2014

Cell Physiol Biochem

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Background/Aims: Gedunin, an inhibitor of heat shock protein HSP90, triggers apoptosis of tumor cells and is thus effective against malignancy. Moreover, the drug has antimalarial potency. In analogy to apoptosis of nucleated cells, erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i). The present study explored whether gedunin stimulates eryptosis. Methods: Forward scatter was determined to estimate cell volume, annexin V binding to identify phosphatidylserine-exposing erythrocytes, hemoglobin release to depict hemolysis, and Fluo3-fluorescence to quantify [Ca²⁺]_i. Results: A 48 h exposure of human erythrocytes to gedunin significantly increased [Ca²⁺]_i (12 µM), significantly decreased forward scatter (24 µM) and significantly increased annexin-V-binding (12 µM). The effect of gedunin (24 µM) on annexin-V-binding was virtually abrogated by removal of extracellular Ca²⁺. Conclusion: Gedunin stimulates suicidal erythrocyte death or eryptosis, an effect mainly if not exclusively due to stimulation of Ca²⁺ entry.

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Tannic Acid Induced Suicidal Erythrocyte Death

Cited by 41 publications

References 152 publications

Stimulation of Suicidal Erythrocyte Death by Increased Extracellular Phosphate Concentrations

Stimulation of Suicidal Erythrocyte Death by Increased Extracellular Phosphate Concentrations

Mitoxantrone-Induced Suicidal Erythrocyte Death

Stimulation of Erythrocyte Cell Membrane Scrambling by Gedunin

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