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Toxins (Basel). 2013 Apr 19;5(4):703-16. doi: 10.3390/toxins5040703.

Carmustine-induced phosphatidylserine translocation in the erythrocyte membrane.

Author information

1
Department of Physiology, University of Tuebingen, Gmelinstr. 5, Tuebingen D-72076, Germany. kashif_cbc@yahoo.com

Abstract

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.

PMID:
23604064
PMCID:
PMC3705288
DOI:
10.3390/toxins5040703
[Indexed for MEDLINE]
Free PMC Article
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