Runko Alexander P, Griswold Anthony J, Min Kyung-Tai
Porter Neuroscience Research Center, MSC 3705, NINDS, NIH, Bethesda, MD 20892, USA.
FEBS Lett. 2008 Mar 5;582(5):715-9. doi: 10.1016/j.febslet.2008.01.046. Epub 2008 Feb 5.
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.
在弗里德赖希共济失调症中，线粒体蛋白酵母铁硫蛋白的减少会导致铁和活性氧的积累，进而引发氧化损伤、神经退行性变并缩短寿命。最近的研究表明酵母铁硫蛋白可能在抗氧化过程中发挥作用。在此我们发现，在雌性转基因动物的线粒体中过表达果蝇酵母铁硫蛋白可增强抗氧化能力、提高对氧化应激损伤的抵抗力并延长寿命。这表明果蝇酵母铁硫蛋白可能具有保护线粒体免受氧化应激及随之而来的细胞损伤的功能。
