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Effects of deleting mitochondrial antioxidant genes on life span.
Ann N Y Acad Sci. 2007 Apr; 1100:505-9.AN

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.

Authors+Show Affiliations

Department of Biology, Izmir Institute of Technology, 35430 Urla, Izmir, Turkey.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17460215

Citation

Unlu, Ercan Selcuk, and Ahmet Koc. "Effects of Deleting Mitochondrial Antioxidant Genes On Life Span." Annals of the New York Academy of Sciences, vol. 1100, 2007, pp. 505-9.
Unlu ES, Koc A. Effects of deleting mitochondrial antioxidant genes on life span. Ann N Y Acad Sci. 2007;1100:505-9.
Unlu, E. S., & Koc, A. (2007). Effects of deleting mitochondrial antioxidant genes on life span. Annals of the New York Academy of Sciences, 1100, 505-9.
Unlu ES, Koc A. Effects of Deleting Mitochondrial Antioxidant Genes On Life Span. Ann N Y Acad Sci. 2007;1100:505-9. PubMed PMID: 17460215.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of deleting mitochondrial antioxidant genes on life span. AU - Unlu,Ercan Selcuk, AU - Koc,Ahmet, PY - 2007/4/27/pubmed PY - 2007/5/31/medline PY - 2007/4/27/entrez SP - 505 EP - 9 JF - Annals of the New York Academy of Sciences JO - Ann N Y Acad Sci VL - 1100 N2 - 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. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/17460215/Effects_of_deleting_mitochondrial_antioxidant_genes_on_life_span_ L2 - https://doi.org/10.1196/annals.1395.055 DB - PRIME DP - Unbound Medicine ER -