Demir, Ayşe BanuKoç, Ahmet2017-06-112017-06-112010Demir, A. B., & Koç, A. (2010). Assessment Of Chronological Lifespan Dependent Molecular Damages İn Yeast Lacking Mitochondrial Antioxidant Genes. Biochemical And Biophysical Research Communications, 400(1), 106–110.http://linkinghub.elsevier.com/retrieve/pii/S0006291X10015056https://hdl.handle.net/11616/7083Biochemical and Biophysical Research Communications 400 (2010) 106–110The 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: GRX2, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, and PRX1. Among these mutants, ccp1D, trx3D, grx5D, prx1D, mutants were sensitive to diamide, and ccs1D and sod2D 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.eninfo:eu-repo/semantics/openAccessChronological agingMolecular damageMitochondriaAntioxidant geneOxidative stressArticle400110611010.1016/j.bbrc.2010.08.019