Selenium-induced apoptosis

Ick Young Kim, Tae Soo Kim, Youn Wook Chung, Daewon Jeong

Research output: Chapter in Book/Report/Conference proceedingChapter

6 Citations (Scopus)


Selenium is both an essential and a toxic trace element. It has been reported to induce cell growth and cell proliferation, but also cell death by necrosis or apoptosis. The biological action of selenium is dependent on both its specific chemical form and concentration. At high levels, selenium induces oxidation and cross-linking of protein thiol groups and generation of reactive oxygen species, ultimately leading to cell death. Indeed, a shift to a more oxidizing environment induced by selenium is thought to be largely responsible for selenium-induced apoptotic cell death. Selenium compounds capable of oxidizing thiol groups and generating the superoxide anion (O2 •-) also trigger loss of the mitochondrial function and release of proapoptotic proteins, such as cytochrome c, from mitochondria into the cytosol. In addition, some selenium compounds activate caspase-3, which in turn contributes to morphological changes in the cell and DNA fragmentation characteristic of the late stage of apoptosis. The serial events of selenium-induced apoptosis are thus thought to include the generation of an oxidizing intracellular environment followed by induction of mitochondrial dysfunction, cytochrome c release, caspase-3 activation, and DNA fragmentation.

Original languageEnglish
Title of host publicationSelenium
Subtitle of host publicationIts Molecular Biology and Role in Human Health, Second Edition
PublisherSpringer US
Number of pages7
ISBN (Electronic)9780387338279
ISBN (Print)0387338268, 9780387338262
Publication statusPublished - 2006

Bibliographical note

Publisher Copyright:
© 2006 Springer Science+Business Media, LLC. All rights reserved.

ASJC Scopus subject areas

  • General Medicine


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