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Cited by 51Mitochondrial Function and PathologySelenium in Biological SystemsCell death mechanisms and regulation

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

Kim, Tae-soo, Jeong, Dae-won, Yun, Byung Yup, Kim, Ick Young·2002·Biochemical and Biophysical Research Communications
DOI 10.1016/s0006-291x(02)00612-5
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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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Research works printed but not linked: 41

  1. Hengartner, 2000, The biochemistry of apoptosis, Nature, 407, 770, 10.1038/35037710 · DOI · Paper page
  2. Vaux, 1999, Cell death in development, Cell, 96, 245, 10.1016/S0092-8674(00)80564-4 · DOI
  3. Thompson, 1995, Apoptosis in the pathogenesis and treatment of disease, Science, 267, 1456, 10.1126/science.7878464 · DOI · Paper page
  4. Johnstone, 2002, Apoptosis. A link between cancer genetics and chemotherapy, Cell, 108, 153, 10.1016/S0092-8674(02)00625-6 · DOI
  5. Green, 2000, Apoptotic pathways: paper wraps stone blunts scissors, Cell, 102, 1, 10.1016/S0092-8674(00)00003-9 · DOI
  6. Zamzami, 2001, The mitochondrion in apoptosis: how Pandora's box opens, Nat. Rev. Mol. Cell. Biol., 2, 67, 10.1038/35048073 · DOI
  7. Joza, 2001, Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death, Nature, 410, 549, 10.1038/35069004 · DOI
  8. Green, 1998, Mitochondria and apoptosis, Science, 281, 1309, 10.1126/science.281.5381.1309 · DOI
  9. Hirsch, 1997, Role of the mitochondrial permeability transition pore in apoptosis, Biosci. Rep., 17, 67, 10.1023/A:1027339418683 · DOI
  10. Susin, 1999, Molecular characterization of mitochondrial apoptosis-inducing factor, Nature, 397, 441, 10.1038/17135 · DOI · Paper page
  11. Yang, 1998, Induction of the mitochondrial permeability transition causes release of the apoptogenic factor cytochrome c, Free Radic. Biol. Med., 24, 624, 10.1016/S0891-5849(97)00367-5 · DOI
  12. Bossy-Wetzel, 1998, Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization, EMBO J., 17, 37, 10.1093/emboj/17.1.37 · DOI · Paper page
  13. Bindoli, 1997, Influence of the redox state of pyridine nucleotides on mitochondrial sulfhydryl groups and permeability transition, Arch. Biochem. Biophys., 342, 22, 10.1006/abbi.1997.9986 · DOI
  14. Morin, 2001, Curcumin induces the mitochondrial permeability transition pore mediated by membrane protein thiol oxidation, FEBS Lett., 495, 131, 10.1016/S0014-5793(01)02376-6 · DOI
  15. Kowaltowski, 1997, Mitochondrial membrane protein thiol reactivity with N-ethylmaleimide or mersalyl is modified by Ca2+: correlation with mitochondrial permeability transition, Biochim. Biophys. Acta, 1318, 395, 10.1016/S0005-2728(96)00111-9 · DOI
  16. Wudarczyk, 1996, Relation between the activities reducing disulfides and the protection against membrane permeability transition in rat liver mitochondria, Arch. Biochem. Biophys., 327, 215, 10.1006/abbi.1996.0112 · DOI
  17. Rayman, 2000, The importance of selenium to human health, Lancet, 356, 233, 10.1016/S0140-6736(00)02490-9 · DOI · Paper page
  18. Kim, 2001, Se-methylselenocysteine induces apoptosis through caspase activation in HL-60 cells, Carcinogenesis, 22, 559, 10.1093/carcin/22.4.559 · DOI
  19. Zhu, 2000, In vitro effects of Se-allylselenocysteine and Se-propylselenocysteine on cell growth, DNA integrity, and apoptosis, Biochem. Pharmacol., 60, 1467, 10.1016/S0006-2952(00)00461-5 · DOI
  20. Jung, 2001, Se-Methylselenocysteine induces apoptosis mediated by reactive oxygen species in HL-60 cells, Free Radic. Biol. Med., 31, 479, 10.1016/S0891-5849(01)00604-9 · DOI
  21. Seko, 1997, Active oxygen generation as a possible mechanism of selenium toxicity, Biomed. Environ. Sci., 10, 333
  22. Shen, 2001, Superoxide radical-initiated apoptotic signalling pathway in selenite-treated HepG(2) cells: mitochondria serve as the main target, Free Radic. Biol. Med., 30, 9, 10.1016/S0891-5849(00)00421-4 · DOI · Paper page
  23. Yang, 2000, Intracellular thiol depletion causes mitochondrial permeability transition in ebselen-induced apoptosis, Arch. Biochem. Biophys., 380, 319, 10.1006/abbi.2000.1939 · DOI
  24. Stewart, 1999, Selenium compounds have disparate abilities to impose oxidative stress and induce apoptosis, Free Radic. Biol. Med., 26, 42, 10.1016/S0891-5849(98)00147-6 · DOI
  25. Sakurai, 2000, Mitochondrial permeability transition induced by 1-hydroxyethyl radical, Free Radic. Biol. Med., 28, 273, 10.1016/S0891-5849(99)00236-1 · DOI
  26. Li, 1999, Protein kinase C δ targets mitochondria, alters mitochondrial membrane potential, and induces apoptosis in normal and neoplastic keratinocytes when overexpressed by an adenoviral vector, Mol. Cell. Biol., 19, 8547, 10.1128/MCB.19.12.8547 · DOI
  27. Cormier, 2001, In vitro effects of nicotine on mitochondrial respiration and superoxide anion generation, Brain Res., 900, 72, 10.1016/S0006-8993(01)02254-5 · DOI
  28. McCord, 1969, Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein), J. Biol. Chem., 244, 6049, 10.1016/S0021-9258(18)63504-5 · DOI · Paper page
  29. Ichas, 1998, From calcium signaling to cell death: two conformations for the mitochondrial permeability transition pore. Switching from low- to high-conductance state, Biochim. Biophys. Acta, 1366, 33, 10.1016/S0005-2728(98)00119-4 · DOI
  30. Schild, 2001, Distinct Ca2+ thresholds determine cytochrome c release or permeability transition pore opening in brain mitochondria, FASEB J., 15, 565, 10.1096/fj.00-0551fje · DOI
  31. Bernardi, 1993, Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore. I. Evidence for two separate Me2+ binding sites with opposing effects on the pore open probability, J. Biol. Chem., 268, 1005, 10.1016/S0021-9258(18)54033-3 · DOI
  32. Ganther, 1999, Selenium metabolism, selenoproteins and mechanisms of cancer prevention: complexities with thioredoxin reductase, Carcinogenesis, 20, 1657, 10.1093/carcin/20.9.1657 · DOI
  33. Petronilli, 1994, The voltage sensor of the mitochondrial permeability transition pore is tuned by the oxidation-reduction state of vicinal thiols. Increase of the gating potential by oxidants and its reversal by reducing agents, J. Biol. Chem., 269, 16638, 10.1016/S0021-9258(19)89437-1 · DOI
  34. Coulter, 2000, Mitochondrially targeted antioxidants and thiol reagents, Free Radic. Biol. Med., 28, 1547, 10.1016/S0891-5849(00)00255-0 · DOI
  35. Sakurai, 2001, Alloxan-induced mitochondrial permeability transition triggered by calcium, thiol oxidation, and matrix ATP, J. Biol. Chem., 276, 26942, 10.1074/jbc.M102029200 · DOI
  36. Fagian, 1990, Membrane protein thiol cross-linking associated with the permeabilization of the inner mitochondrial membrane by Ca2+ plus prooxidants, J. Biol. Chem., 265, 19955, 10.1016/S0021-9258(17)45467-6 · DOI
  37. Shen, 1999, Sodium selenite-induced oxidative stress and apoptosis in human hepatoma HepG2 cells, Int. J. Cancer, 81, 820, 10.1002/(SICI)1097-0215(19990531)81:5<820::AID-IJC25>3.0.CO;2-F · DOI
  38. Shen, 2000, Dual role of glutathione in selenite-induced oxidative stress and apoptosis in human hepatoma cells, Free Radic. Biol. Med., 28, 1115, 10.1016/S0891-5849(00)00206-9 · DOI
  39. Cho, 1999, Induction of apoptosis by selenite and selenodiglutathione in HL-60 cells: correlation with cytotoxicity, Biochem. Mol. Biol. Int., 47, 781
  40. Stewart, 1997, Induction of differentiation and apoptosis by sodium selenite in human colonic carcinoma cells (HT29), Cancer Lett., 117, 35, 10.1016/S0304-3835(97)00212-7 · DOI
  41. Zhu, 1996, Apoptosis induced by selenium in human glioma cell lines, Biol. Trace Elem. Res., 54, 123, 10.1007/BF02786259 · DOI

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Metadata

Authors
Kim, T.-S., Jeong, D.-W., Yun, B. Y., & Kim, I. Y.
Affiliations
Korea University (KR)
Corresponding author
Kim, Ick Young
ORCID
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2002-06
Volume
294
Issue
5
Pages
1130-1137
ISSN
0006-291X (ISSN-L)
DOI
10.1016/s0006-291x(02)00612-5
OpenAlex
W2070953417
Cited by
51
References
1
Citations by year
2024: 1 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2018: 2 · 2016: 1 · 2014: 4 · 2013: 1 · 2012: 1
FWCI
1.62
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biochemical and Biophysical Research Communications (publishedVersion)
  • PubMed (publishedVersion)
Funders
Korea Science and Engineering Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
selenite, selenium, mitochondrial permeability transition, thiol oxidation, cytochrome c release, mitochondrial membrane potential, liver mitochondria, cyclosporine, apoptosis, chemoprevention
MeSH terms
Mitochondrial Permeability Transition Pore, Animals, Cytochrome c Group, Dose-Response Relationship, Drug, Ion Channels, Membrane Potentials, Mitochondria, Liver, Oxidation-Reduction, Sulfhydryl Compounds, Superoxides, Anticarcinogenic Agents, Sodium Selenite, Mitochondrial Proteins, Mitochondrial Membrane Transport Proteins, Rats

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