Abstract:
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:
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.
