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Effects of deleting mitochondrial antioxidant genes on life span

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Date
2007-04
Author
Ünlü, Ercan Selçuk
Koç, Ahmet
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Abstract
Reactive oxygen species (ROS) damage biomolecules, accelerate aging, and shorten life span, whereas antioxidant enzymes mitigate these effects. Because mitochondria are a primary site of ROS generation and also a primary target of ROS attack, they have become a major focus area of aging studies. Here, we employed yeast genetics to identify mitochondrial antioxidant genes that are important for replicative life span. In our studies, it was found that among the known mitochondrial antioxidant genes (TTR1, CCD1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, PRX1), deletion of only three genes, SOD1 (Cu, Zn superoxide dismutase), SOD2 (Manganese-containing superoxide dismutase), and CCS1 (Copper chaperone), shortened the life span enormously. The life span decreased 40% for Δsod1 mutant, 72% for Δsod2 mutant, and 50% for Δccs1 mutant. Deletion of the other genes had little or no effect on life span.
URI
http://doi.org/10.1196/annals.1395.055
http://hdl.handle.net/11147/2269
Collections
  • Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik [290]
  • Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection [3276]
  • WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection [2953]


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