Dysfunction of rat liver mitochondria by selenite: Induction of mitochondrial permeability transition through thiol-oxidation

Tae Soo Kim, Dae Won Jeong, Yup Yun Byung, Ick Young Kim

Research output: Contribution to journalArticle

42 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1130-1137
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume294
Issue number5
DOIs
Publication statusPublished - 2002 Jul 6

Fingerprint

Selenious Acid
Mitochondria
Liver Mitochondrion
Sulfhydryl Compounds
Liver
Rats
Permeability
Oxidation
Mitochondrial Membrane Potential
Cytochromes c
Cytochromes a
Apoptosis
Membranes
Ethylmaleimide
Mammals
Egtazic Acid
Trace Elements
Selenium
Cyclosporine
Tumors

Keywords

  • Apoptosis
  • Cytochrome c
  • Mitochondria
  • Mitochondrial membrane potential
  • MPT, mitochondrial permeability transition
  • Selenite
  • Thiol oxidation

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Dysfunction of rat liver mitochondria by selenite : Induction of mitochondrial permeability transition through thiol-oxidation. / Kim, Tae Soo; Jeong, Dae Won; Byung, Yup Yun; Kim, Ick Young.

In: Biochemical and Biophysical Research Communications, Vol. 294, No. 5, 06.07.2002, p. 1130-1137.

Research output: Contribution to journalArticle

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