Assessment of chronological lifespan dependent molecular damages in yeast lacking mitochondrial antioxidant genes

摘要: The free radical theory of aging states that oxidative damage to biomolecules causes and antioxidants neutralize radicals thus decelerate aging. Mitochondria produce most the reactive oxygen species, but at same time have many antioxidant enzymes providing protection from these oxidants. Expecting cells without mitochondrial genes would accumulate higher levels and, therefore, will a shorter lifespan, we analyzed damages in young chronologically aged mutants lacking genes: GRX2, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, PRX1. Among mutants, ccp1Δ, trx3Δ, grx5Δ, prx1Δ, were sensitive diamide, ccs1Δ sod2Δ both diamide menadione. Most less viable stationary phase. Chronologically produced amount superoxide accumulated damages. Even though our results support findings old harbor molecular damages, no significant difference was observed between wild type mutant terms their content.