Abstract:
:The evolving role of mitochondria as a target for different death-inducing noxae prompted us to investigate trimethyltin (TMT)-dependent effects on mitochondrial functionality. For this purpose, we used a homogeneous cell culture model represented by undifferentiated PC12 cells. Mitochondria isolated from PC12 cells treated with TMT for 6, 12 and 24h, showed a time-dependent inhibition of ADP-stimulated oxygen consumption using succinate or glutamate/malate as substrate. Using a fluorescent assay, the effect of TMT on mitochondrial membrane potential (delta Psi) in PC12 cells was also determined. After 24h in culture, a strong loss of mitochondrial membrane potential (delta Psi) was observed in TMT-treated cells. Collapse of mitochondrial membrane potential correlated with an increased expression of bax/bcl-2 ratio, as evaluated by polymerase chain reaction. Western blotting and spectrophotometric analysis showed that cytochrome c release and activation of caspase 3 were concurrently induced. Our findings suggest that inhibition of mitochondrial respiration represents the early toxic event for cell death in PC12 due to trimethyltin.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Misiti F,Orsini F,Clementi ME,Lattanzi W,Giardina B,Michetti Fdoi
10.1016/j.neuint.2007.11.008subject
Has Abstractpub_date
2008-05-01 00:00:00pages
1092-9issue
6eissn
0197-0186issn
1872-9754pii
S0197-0186(07)00314-2journal_volume
52pub_type
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