Both Thioredoxin 2 and Glutaredoxin 2 Contribute to the Reduction of the Mitochondrial 2-Cys Peroxiredoxin Prx3

We show that the mitochondrial 2-Cys peroxiredoxin is substrate for thioredoxin 2, but can be reduced by glutaredoxin 2 via the dithiol reaction mechanism

Eva-Maria Hanschmann; Maria Elisabet Lönn; Lena Dorothee Schütte; Maria Funke; José R. Godoy; Susanne Eitner; Christoph Hudemann; Christopher Horst Lillig


Scholarcy highlights

  • SFB593-N01 and by a grant from the von Behring-Rontgen Foundation. 1 Present address: Centre for Vascular Research, School of Medical Sciences signaling and metabolic pathways
  • The results presented here provide strong evidence that both mitochondrial redox systems, glutaredoxin 2 and thioredoxin 2, contribute to the redox state of the typical 2-Cys Prx3 in vivo, but not to the reduction of the atypical 2-Cys Prx5, which appears to rely on the Trx system for the reduction of the disulfide formed during its reaction cycle
  • In contrast to Prx3, Grx2 was not able to support the reduction of catalytically oxidized Prx5 efficiently. These data prove that, in vitro, both mitochondrial redoxins can serve as reductants for the typical 2-Cys Prx 3 in a dithiol reaction mechanism, but that the reduction of the catalytic disulfide in the atypical 2-Cys Prx 5 is restricted to the Trx system
  • In this study we have analyzed the potential contribution of Grx2 to the reduction of the catalytic disulfide of Prxs in mitochondria
  • Our results suggest that both mitochondrial thioldisulfide reductase systems, Grx2 and Trx2, contribute to the reduction of the catalytic disulfide in the typical 2-Cys Prx3 in vivo
  • It is not surprising that Grx2 is able to reduce the catalytic disulfide in Prx3, earlier studies excluded Grxs as electron donors
  • This study introduces glutaredoxin 2 as a novel electron donor for Prx3, yielding further insights into essential redox signaling mechanisms in the compartment with the highest prevalence for reactive oxygen species, mitochondria

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