Tributyltin stimulates apoptosis in rat thymocytes

Tak Yee Aw, Pierluigi Nicotera, Luigi Manzo, Sten Orrenius

Research output: Contribution to journalArticlepeer-review


Treatment of rat thymocytes with micromolar concentrations of tributyltin caused a rapid increase in the cytosolic free Ca2+ concentration that was inhibited by Ni2+, which blocks Ca2+ influx through membrane channels. The elevation of cytosolic Ca2+ was associated with extensive DNA fragmentation, which was prevented by pretreatment of the cells with either of the intracellular Ca2+ chelators quin-2 or 1,2-bis(2-amino-phenoxy) ethane-N′,N′,N′,N′,-tetraacetic acid. Loss of thymocyte viability, which followed DNA fragmentation, was also prevented by the two Ca2+ chelators or by removing extracellular Ca2+ with ethylene glycol bis(β-aminoethyl ether)N,N′-tetraacetic acid. The pattern of DNA fragmentation was characteristic of that produced by agents which activate a Ca2+- and Mg2+-dependent endogenous endonuclease during apoptosis or programmed cell death. Additional studies showed that other organotin compounds, including trimethyltin, triphenyltin, and dibutyltin had minimal effects on cytosolic Ca2+, DNA fragmentation, and cell viability. These results are consistent with a greater susceptibility of thymocytes to tributyltin and provide a basis for understanding its selective immunotoxicity in vivo.

Original languageEnglish
Pages (from-to)46-50
Number of pages5
JournalArchives of Biochemistry and Biophysics
Issue number1
Publication statusPublished - Nov 15 1990

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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