Effects of deleting mitochondrial antioxidant genes on life span.

Authors: Unlu ES; Koc A

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 Deltasod1 mutant, 72% for Deltasod2 mutant, and 50% for Deltaccs1 mutant. Deletion of the other genes had little or no effect on life span.

Keywords: Antioxidants/*metabolism; Cell Aging; Dose-Response Relationship, Drug; *Gene Deletion; *Gene Expression Regulation, Fungal; Genes, Fungal; *Genes, Mitochondrial; Mitochondria/*metabolism; Mutation; Oxidative Stress; Reactive Oxygen Species; Saccharomyces cerevisiae/metabolism; Saccharomyces cerevisiae Proteins; Superoxide Dismutase/genetics; Time Factors
Journal: Annals of the New York Academy of Sciences
Volume: 1100
Pages: 505-9
Date: April 27, 2007
PMID: 17460215
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Citation:

Unlu ES, Koc A (2007) Effects of deleting mitochondrial antioxidant genes on life span. Annals of the New York Academy of Sciences 1100: 505-9.


Study Lifespan Factors:
  • SOD2 SuperOxide Dismutase 2


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