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Effects of Deleting Mitochondrial Antioxidant Genes on Life Span
Author(s) -
UNLU ERCAN SELCUK,
KOC AHMET
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1395.055
Subject(s) - sod2 , superoxide dismutase , sod1 , reactive oxygen species , antioxidant , biology , mutant , gene , genetics , mitochondrion , dismutase , biochemistry
: 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 Δ sod1 mutant, 72% for Δ sod2 mutant, and 50% for Δ ccs1 mutant. Deletion of the other genes had little or no effect on life span.