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Silver ion‐induced suicidal erythrocyte death
Author(s) -
Sopjani Mentor,
Föller Michael,
Haendeler Judith,
Götz Friedrich,
Lang Florian
Publication year - 2009
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1438
Subject(s) - ion , chemistry , medicine , toxicology , medical emergency , biology , organic chemistry
Abstract Owing to its antibiotic activity, silver is used for water purification, wound care and a wide variety of implants. Silver metal and silver compounds ionize in solution, and silver ions interfere with the function of a wide variety of proteins. In mammalian cells, silver ions may trigger apoptosis by stimulation of cytochrome c release from mitochondria. The present study explored the effect of AgNO 3 on eryptosis, the suicidal death of erythrocytes, cells devoid of mitochondria. Similar to apoptosis of nucleated cells, eryptosis is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the cell surface. Eryptosis is triggered by energy depletion, cellular depletion of nitric oxide (NO) and activation of protein kinase C (PKC). Phosphatidylserine exposure was determined by annexin V‐binding, cell volume by forward scatter, cellular ATP by a luciferin–luciferase assay kit, and hemolysis by photometry. A 48 h exposure to AgNO 3 (≥100 n m ) but not to NaNO 3 significantly enhanced the percentage of annexin V‐binding cells, slightly but significantly decreased forward scatter and significantly decreased cytosolic ATP. Furthermore, inhibition of PKC by staurosporine and donation of NO by sodium nitroprusside significantly blunted silver‐induced eryptosis. In conclusion, AgNO 3 triggers cell membrane scrambling, an effect attributed to ATP depletion, PKC activation and decrease of cellular NO. Copyright © 2009 John Wiley & Sons, Ltd.