Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila
Graduate School of Biomedical Sciences; Porter Neuroscience Research Center; Department of Biochemistry and Molecular Pharmacology
Life Sciences | Medicine and Health Sciences
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
FEBS Lett. 2008 Mar 5;582(5):715-9. Epub 2008 Feb 5. Link to article on publisher's site
Runko AP, Griswold AJ, Min K. (2008). Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila. GSBS Student Publications. https://doi.org/10.1016/j.febslet.2008.01.046. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/1447