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Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
Published on: January 21, 2020
Arsenic-induced suicidal erythrocyte death
Hasan Mahmud1, Michael Föller, Florian Lang
1Department of Physiology, University of Tübingen, Gmelinstr. 5, 72076 Tübingen, Germany.
Archives of Toxicology
|July 19, 2008
Summary
Arsenic exposure triggers suicidal erythrocyte death (eryptosis) by increasing calcium, ceramide, and depleting ATP. This cell shrinkage and phosphatidylserine exposure occurs without red blood cell lysis.
Area of Science:
- Toxicology
- Hematology
- Cell Biology
Background:
- Environmental arsenic exposure is linked to anemia.
- Anemia may arise from suicidal erythrocyte death, known as eryptosis.
- Eryptosis involves red blood cell shrinkage and phosphatidylserine exposure.
Purpose of the Study:
- To investigate if arsenic exposure stimulates eryptosis in human erythrocytes.
- To elucidate the mechanisms by which arsenic might induce eryptosis.
Main Methods:
- Human erythrocytes were exposed to arsenic trioxide.
- Phosphatidylserine exposure was measured using annexin V-binding.
- Cell volume was assessed by forward scatter.
- Cytosolic calcium levels were determined using Fluo3-fluorescence.
- Ceramide formation was quantified using fluorescent antibodies.
- Intracellular ATP concentration was measured.
- Effects of extracellular calcium removal and amiloride were tested.
Main Results:
- Arsenic trioxide significantly increased phosphatidylserine exposure and cell shrinkage.
- Arsenic significantly elevated cytosolic calcium levels and ceramide formation.
- Arsenic significantly decreased intracellular ATP concentration.
- These effects were attenuated by removing extracellular calcium or using amiloride.
Conclusions:
- Arsenic exposure induces suicidal erythrocyte death (eryptosis).
- Arsenic triggers eryptosis by increasing intracellular calcium, stimulating ceramide formation, and depleting ATP.
- Calcium influx through cation channels plays a key role in arsenic-induced eryptosis.
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