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.
|Title of host publication||Selenium|
|Subtitle of host publication||Its Molecular Biology and Role in Human Health, Second Edition|
|Number of pages||7|
|ISBN (Print)||0387338268, 9780387338262|
|Publication status||Published - 2006|
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© 2006 Springer Science+Business Media, LLC. All rights reserved.
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