Mitochondrial thioredoxin in regulation of oxidant-induced cell death

FEBS Lett. 2006 Dec 11;580(28-29):6596-602. doi: 10.1016/j.febslet.2006.11.007. Epub 2006 Nov 14.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Death / drug effects
  • Diamide / pharmacology
  • Gene Expression / drug effects
  • Humans
  • Membrane Potentials / drug effects
  • Mitochondria / drug effects*
  • Mitochondrial Membranes / drug effects
  • Oxidants / pharmacology*
  • Oxidation-Reduction / drug effects
  • Oxidative Stress / drug effects
  • Peroxides / pharmacology
  • Thioredoxin Reductase 2
  • Thioredoxin-Disulfide Reductase / deficiency
  • Thioredoxins / metabolism*
  • Time Factors
  • tert-Butylhydroperoxide / pharmacology

Substances

  • Oxidants
  • Peroxides
  • Diamide
  • Thioredoxins
  • tert-Butylhydroperoxide
  • TXNRD2 protein, human
  • Thioredoxin Reductase 2
  • Thioredoxin-Disulfide Reductase