Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila

Alexander P. Runko, Anthony Griswold, Kyung Tai Min

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

In Friedreich's ataxia, reduction of the mitochondria protein frataxin results in the accumulation of iron and reactive oxygen species, which leads to oxidative damage, neurodegeneration and a diminished lifespan. Recent studies propose that frataxin might play a role in the antioxidative process. Here we show that overexpression of Drosophila frataxin in the mitochondria of female transgenic animals increases antioxidant capability, resistance to oxidative stress insults, and longevity. This suggests that Drosophila frataxin may function to protect the mitochondria from oxidative stresses and the ensuing cellular damage.

Original languageEnglish (US)
Pages (from-to)715-719
Number of pages5
JournalFEBS Letters
Volume582
Issue number5
DOIs
StatePublished - Mar 5 2008
Externally publishedYes

Fingerprint

Mitochondria
Oxidative stress
Drosophila
Oxidative Stress
Friedreich Ataxia
Genetically Modified Animals
Reactive Oxygen Species
Animals
Iron
Antioxidants
frataxin
Proteins

Keywords

  • Drosophila
  • Frataxin
  • Friedreich's ataxia
  • Oxidative stress

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila. / Runko, Alexander P.; Griswold, Anthony; Min, Kyung Tai.

In: FEBS Letters, Vol. 582, No. 5, 05.03.2008, p. 715-719.

Research output: Contribution to journalArticle

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