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Updated: May 27, 2026

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

Published on: January 21, 2020

Apigenin-induced suicidal erythrocyte death.

Mohanad Zbidah¹, Adrian Lupescu, Kashif Jilani

¹Department of Physiology, University of Tuebingen, Gmelinstraße 5, 72076 Tuebingen, Germany.

Journal of Agricultural and Food Chemistry

|December 3, 2011

Summary

Apigenin, a natural flavone, triggers suicidal erythrocyte death (eryptosis) by increasing intracellular calcium, depleting ATP, and promoting ceramide formation. This process involves cell shrinkage and phosphatidylserine exposure, indicating a novel effect of apigenin on red blood cells.

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Last Updated: May 27, 2026

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Area of Science:

* Hematology
* Biochemistry
* Cell Biology

Background:

* Apigenin, a flavone found in fruits and vegetables, is known to induce apoptosis and inhibit cancerogenesis.
* Eryptosis, or suicidal erythrocyte death, is characterized by cell shrinkage and phosphatidylserine exposure, and can be triggered by increased cytosolic calcium, ceramide formation, and ATP depletion.
* The study investigates the potential of apigenin to induce eryptosis.

Purpose of the Study:

* To explore the effects of apigenin on eryptosis in erythrocytes.
* To determine if apigenin influences key eryptosis triggers such as intracellular calcium levels, ceramide formation, and ATP concentration.

Main Methods:

* Erythrocyte apoptosis was assessed by measuring intracellular calcium activity using Fluo3-fluorescence.
* Cell volume was determined by forward scatter, and phosphatidylserine exposure was quantified using annexin V binding.
* Hemolysis was measured by hemoglobin release, ceramide formation was detected using antibodies, and cytosolic ATP levels were quantified via luciferin-luciferase assay.

Main Results:

* Apigenin exposure (≥ 1 μM) for 48 hours significantly increased intracellular calcium and decreased cell volume.
* Higher concentrations of apigenin (15 μM) led to increased ceramide formation and decreased ATP concentration.
* Apigenin (≥ 5 μM) significantly increased phosphatidylserine exposure, an effect blunted by calcium removal, while hemolysis remained unaffected.

Conclusions:

* Apigenin stimulates calcium entry, ceramide formation, and ATP depletion in erythrocytes.
* These effects collectively trigger suicidal erythrocyte death (eryptosis), characterized by cell shrinkage and phosphatidylserine exposure.
* Apigenin exhibits novel effects on erythrocytes, inducing eryptosis through specific biochemical pathways.