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Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila
Author(s) -
Runko Alexander P.,
Griswold Anthony J.,
Min Kyung-Tai
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.01.046
Subject(s) - frataxin , oxidative stress , mitochondrion , neurodegeneration , microbiology and biotechnology , oxidative phosphorylation , reactive oxygen species , biology , ataxia , transgene , drosophila melanogaster , drosophila (subgenus) , antioxidant , biochemistry , aconitase , gene , neuroscience , medicine , disease
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.