Literature DB >> 19128239

Peroxiredoxin 5 confers protection against oxidative stress and apoptosis and also promotes longevity in Drosophila.

Svetlana N Radyuk1, Katarzyna Michalak, Vladimir I Klichko, Judith Benes, Igor Rebrin, Rajindar S Sohal, William C Orr.   

Abstract

Peroxiredoxin 5 is a distinct isoform of the peroxiredoxin gene family. The antioxidative and anti-apoptotic functions of peroxiredoxin 5 have been extensively demonstrated in cell culture experiments. In the present paper, we provide the first functional analysis of peroxiredoxin 5 in a multicellular organism, Drosophila melanogaster. Similar to its mammalian, yeast or human counterparts, dPrx5 (Drosophila peroxiredoxin 5) is expressed in several cellular compartments, including the cytosol, nucleus and the mitochondrion. Global overexpression of dPrx5 in flies increased resistance to oxidative stress and extended their life span by up to 30% under normal conditions. The dprx5(-/-) null flies were comparatively more susceptible to oxidative stress, had higher incidence of apoptosis, and a shortened life span. TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) analysis revealed that the dprx5(-/-) null mutant had discernible tissue-specific apoptotic patterns, similar to those observed in control flies exposed to paraquat. In addition, apoptosis was particularly notable in oenocytes. During development the dPrx5 levels co-varied with ecdysone pulses, suggesting inter-relationship between ecdystreroids and dPrx5 expression. The importance of dPrx5 for development was further underscored by the embryonic lethal phenotype of progeny derived from the dprx5(-/-) null mutant. Results from the present study suggest that the antioxidant and anti-apoptotic activities of dPrx5 play a critical role in development and aging of the fly.

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Year:  2009        PMID: 19128239      PMCID: PMC2842572          DOI: 10.1042/BJ20082003

Source DB:  PubMed          Journal:  Biochem J        ISSN: 0264-6021            Impact factor:   3.857


  43 in total

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Authors:  Y Zhou; K H Kok; A C Chun; C M Wong; H W Wu; M C Lin; P C Fung; H Kung; D Y Jin
Journal:  Biochem Biophys Res Commun       Date:  2000-02-24       Impact factor: 3.575

4.  Peroxiredoxin II is essential for sustaining life span of erythrocytes in mice.

Authors:  Tae-Hoon Lee; Sun-Uk Kim; Seong-Lan Yu; Sue Hee Kim; Do Sim Park; Hyung-Bae Moon; So Hee Dho; Ki-Sun Kwon; Hyun Jeong Kwon; Ying-Hao Han; Sangkyun Jeong; Sang Won Kang; Hee-Sup Shin; Kyung-Kwang Lee; Sue Goo Rhee; Dae-Yeul Yu
Journal:  Blood       Date:  2003-02-13       Impact factor: 22.113

5.  The peroxiredoxin gene family in Drosophila melanogaster.

Authors:  S N Radyuk; V I Klichko; B Spinola; R S Sohal; W C Orr
Journal:  Free Radic Biol Med       Date:  2001-11-01       Impact factor: 7.376

6.  Identification of a new type of mammalian peroxiredoxin that forms an intramolecular disulfide as a reaction intermediate.

Authors:  M S Seo; S W Kang; K Kim; I C Baines; T H Lee; S G Rhee
Journal:  J Biol Chem       Date:  2000-07-07       Impact factor: 5.157

7.  Molecular cloning and characterization of the mouse peroxiredoxin V gene.

Authors:  T H Lee; S J Kim; S W Kang; K K Lee; S G Rhee; D Y Yu
Journal:  Biochem Biophys Res Commun       Date:  2000-04-13       Impact factor: 3.575

8.  Mice with targeted mutation of peroxiredoxin 6 develop normally but are susceptible to oxidative stress.

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9.  Mitochondrial and cytosolic expression of human peroxiredoxin 5 in Saccharomyces cerevisiae protect yeast cells from oxidative stress induced by paraquat.

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10.  Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression.

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  44 in total

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Review 4.  The Multifaceted Impact of Peroxiredoxins on Aging and Disease.

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Review 6.  Involvement of redox state in the aging of Drosophila melanogaster.

Authors:  William C Orr; Svetlana N Radyuk; Rajindar S Sohal
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Review 10.  Functions and evolution of selenoprotein methionine sulfoxide reductases.

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Journal:  Biochim Biophys Acta       Date:  2009-05-04
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