Send to

Choose Destination
See comment in PubMed Commons below
Toxins (Basel). 2013 Apr 19;5(4):703-16. doi: 10.3390/toxins5040703.

Carmustine-induced phosphatidylserine translocation in the erythrocyte membrane.

Author information

Department of Physiology, University of Tuebingen, Gmelinstr. 5, Tuebingen D-72076, Germany.


The nitrosourea alkylating agent, carmustine, is used as chemotherapeutic drug in several malignancies. The substance triggers tumor cell apoptosis. Side effects of carmustine include myelotoxicity with anemia. At least in theory, anemia could partly be due to stimulation of eryptosis, the suicidal death of erythrocytes, characterized by cell shrinkage and breakdown of phosphatidylserine asymmetry of the cell membrane with phosphatidylserine exposure at the erythrocyte surface. Stimulators of eryptosis include increase of cytosolic Ca²⁺ activity ([Ca²⁺]i). The present study tested whether carmustine triggers eryptosis. To this end [Ca²⁺]i was estimated from Fluo3 fluorescence, cell volume from forward scatter, phosphatidylserine exposure from annexin V binding, and hemolysis from hemoglobin release. As a result a 48 h exposure to carmustine (≥25 µM) significantly increased [Ca²⁺]i, decreased forward scatter and increased annexin V binding. The effect on annexin V binding was significantly blunted in the absence of extracellular Ca²⁺. In conclusion, carmustine stimulates eryptosis at least partially by increasing cytosolic Ca²⁺ activity.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
    Loading ...
    Support Center