| Literature DB >> 17113580 |
Yan Chen1, Jiyang Cai, Dean P Jones.
Abstract
Mitochondrial thioredoxin (mtTrx) can be oxidized in response to inducers of oxidative stress; yet the functional consequences of the oxidation have not been determined. This study evaluated the redox status of mtTrx and its association to oxidant-induced apoptosis. Results showed that mtTrx was oxidized after exposure to peroxides and diamide. Overexpression of mtTrx protected against diamide-induced oxidation and cytotoxicity. Oxidation of mtTrx was also achieved by knocking down its reductase; and lead to increased susceptibility to cell death. The data indicate that the redox status of mtTrx is a regulatory mechanism underlying the vulnerability of mitochondria to oxidative injury.Entities:
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Year: 2006 PMID: 17113580 PMCID: PMC1761693 DOI: 10.1016/j.febslet.2006.11.007
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124