In:
FEBS Letters, Wiley, Vol. 567, No. 2-3 ( 2004-06-04), p. 189-196
Abstract:
Stimulation of cells with tumor necrosis factor‐α (TNF‐α) results in the increase in generation of H 2 O 2 in mitochondria that leads to apoptosis. The effect of H 2 O 2 produced by TNF‐α on the redox status of selenocysteine (SeCys) residue essential for mitochondrial thioredoxin reductase (TrxR2) was investigated in HeLa cells. TNF‐α caused accumulation of oxidized TrxR2 with a thioselenide bond. The conditional induction of SeCys‐deficient TrxR2 resulted in the increased production of H 2 O 2 and apoptosis. These results suggest that the SeCys residue of TrxR2 plays a critical role in cell survival by serving as an electron donor for Trx‐II and subsequent peroxiredoxin‐III, which is a primary line of defense against H 2 O 2 in mitochondria.
Type of Medium:
Online Resource
ISSN:
0014-5793
,
1873-3468
DOI:
10.1016/j.febslet.2004.04.055
Language:
English
Publisher:
Wiley
Publication Date:
2004
detail.hit.zdb_id:
1460391-3
SSG:
12
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