Selenium is an essential trace element in mammals and is thought to play a chemopreventive role in human cancer, possibly by inducing tumor cell apoptosis. Mitochondria play a pivotal role in the induction of apoptosis in many cell types. The effects of selenite on mitochondrial function were therefore investigated. Selenite induced the oxidation and cross-linking of protein thiol groups, mitochondrial permeability transition (MPT), a decrease in the mitochondrial membrane potential, and the release of cytochrome c in mitochondria isolated from rat liver. Induction of the MPT by selenite was prevented by cyclosporin A, EGTA, or N-ethylmaleimide. These results thus indicate that selenite induces the MPT as a result of direct modification of protein thiol groups, resulting in the release of cytochrome c and a loss of mitochondrial membrane potential.
|Number of pages||8|
|Journal||Biochemical and biophysical research communications|
|Publication status||Published - 2002|
Bibliographical noteFunding Information:
This work was supported by grant KOSEF 2000-2-20900-008-5 from the Korea Science and Engineering Foundation to I.Y. Kim.
- Cytochrome c
- MPT, mitochondrial permeability transition
- Mitochondrial membrane potential
- Thiol oxidation
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology