Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

Permanent URI for this collectionhttps://hdl.handle.net/11147/9

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Author: search.filters.author.Koç, AhmetSubject: search.filters.subject.Antioxidant genes

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  • Article
    Citation - WoS: 18
    Citation - Scopus: 19
    Assessment of Chronological Lifespan Dependent Molecular Damages in Yeast Lacking Mitochondrial Antioxidant Genes
    (Elsevier Ltd., 2010) Demir, Ayşe Banu; Koç, Ahmet; Koç, Ahmet; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    The free radical theory of aging states that oxidative damage to biomolecules causes aging and that antioxidants neutralize free radicals and thus decelerate aging. Mitochondria produce most of the reactive oxygen species, but at the same time have many antioxidant enzymes providing protection from these oxidants. Expecting that cells without mitochondrial antioxidant genes would accumulate higher levels of oxidative damage and, therefore, will have a shorter lifespan, we analyzed oxidative damages to biomolecules in young and chronologically aged mutants lacking the mitochondrial antioxidant genes: G. RX2, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, and PRX1. Among these mutants, ccp1Δ, trx3Δ, grx5Δ, prx1Δ, mutants were sensitive to diamide, and ccs1Δ and sod2Δ were sensitive to both diamide and menadione. Most of the mutants were less viable in stationary phase. Chronologically aged cells produced higher amount of superoxide radical and accumulated higher levels of oxidative damages. Even though our results support the findings that old cells harbor higher amount of molecular damages, no significant difference was observed between wild type and mutant cells in terms of their damage content. © 2010 Elsevier Inc.
  • Article
    Citation - WoS: 59
    Citation - Scopus: 60
    Effects of Deleting Mitochondrial Antioxidant Genes on Life Span
    (John Wiley and Sons Inc., 2007) Ünlü, Ercan Selçuk; Koç, Ahmet; Koç, Ahmet; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    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.