Apoptosis, organotin-induced

Batel R, Bihari N, Rinkevich B, Dapper J, Schaecke H, Schroeder HC, Mueller WE. 1993. Modulation of organotin-induced apoptosis by water pollutant methyl mercury in a human lymphoblastoid tumor cell hne and a marine sponge. Mar Ecol Progr Ser 93 245-251. 

Inhibition of macromolecular synthesis, mitochondrial energy metabolism, and reduction of DNA synthesis, as well as direct interaction with the cell membrane (increase in cytosolic Ca2+ concentration), have been implicated in organotin-induced cytotoxicity [169, 170]. Promotion of oxidative and DNA damage in vivo has been detected [171]. Oxidative damage and increased concentration of intracellular calcium ions seem to be the major factors contributing to triorga-notin-induced apoptosis in many cell lines [172]. 

Although toxic agents have the potential to cause necrosis, some of them can interfere with intracellular signaling pathways and induce apoptosis instead of necrosis. It seems that organotin(IV) compounds exert their toxic effects involving all these processes. The precise balance of these actions and their outcomes may differ radically from one cell type to another and among different organisms. 

The effects of different OTC in human immune tissue were studied in isolated tonsil B cells. Non-stimulated B cells were killed by 100 nM concentration of all tested OTC after 8 h in vitro culture. Organotin derivatives also decreased the proliferation of tonsillar B lymphocytes stimulated with Staphylococcus aureus Cowan 1 and IL-2, when present at 100 nM and higher concentrations. Increased phosphatidylserine exposure demonstrated that 100 nM concentration of triphenyltin chloride and dibutyltin dichloride induced B cells to die by apoptosis . ... 

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