Oxidative stress and the senescence acceleration in senescence-accelerated mouse P10 (SAMP10)

Abstract It has been hypothesized that oxidative stress, which is an imbalance between endogenous levels of oxygen radicals and antioxidant defense systems, is the main cause of aging. Senescence-accelerated mouse prone 10 (SAMP 10), which is a strain of aging-promoting model mice, shows learning and memory impairment with age, and atrophy is observed in the cerebral cortex and limbic system. The oxygen radical production in SAM mice brain tissues increases with age. The slope of the age-dependent increase was steeper in SAMP10 than control mice. Antioxidant enzyme levels in the liver of SAMP10 were higher than those in the control mice at young age, but at old age, antioxidant enzyme levels were lower and/or similar to the levels of control mice. These results suggest that oxidative stress is strongly involved in the cause of senescence acceleration of SAMP10 and that SAMP10 is a model animal suitable for the study of normal aging.