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

Authors: Runko AP; Griswold AJ; Min KT
Year: 2008
Journal: FEBS letters
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.
Reference

Integration:

Created on May 15, 2013, 12:31 a.m.
Not linked
Integrated: False

No notes
Species: Fruit fly

Experiments: 0
Interventions:

fh overexpression

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