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Published on: July 22, 2013
Dysfunction of rat liver mitochondria by selenite: induction of mitochondrial permeability transition through
Tae-soo Kim1, Dae-won Jeong, Byung Yup Yun
1Laboratory of Cellular and Molecular Biochemistry, Graduate School of Biotechnology, Korea University, 1 5-Ka, Anam-Dong, Sungbuk-Ku, Seoul 136-701, Republic of Korea.
Abstract:
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.
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