GSBS Student Publications

Title

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

Publication Date

2008-02-09

UMMS Affiliation

Graduate School of Biomedical Sciences; Porter Neuroscience Research Center; Department of Biochemistry and Molecular Pharmacology

Document Type

Article

Disciplines

Life Sciences | Medicine and Health Sciences

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.

DOI of Published Version

10.1016/j.febslet.2008.01.046

Source

FEBS Lett. 2008 Mar 5;582(5):715-9. Epub 2008 Feb 5. Link to article on publisher's site

Journal/Book/Conference Title

FEBS letters

Related Resources

Link to Article in PubMed

PubMed ID

18258192

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