Journal
FEBS LETTERS
Volume 580, Issue 28-29, Pages 6596-6602Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2006.11.007
Keywords
thioredoxin; mitochondria; oxidative stress; redox; thioredoxin reductase
Funding
- NEI NIH HHS [EY07892, R01 EY007892] Funding Source: Medline
- NIEHS NIH HHS [ES09047, R21 ES014668, ES014668, R01 ES009047] Funding Source: Medline
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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. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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